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Date: 2002/05/06 19:19:54, Link
Author: niiicholas
testing, testing, 1 2 3...

Wow, this looks like a spiffy software package, all the code tags are right above there...

Curious green ideas sleep furiously

...well, it's sticking all of the tags at the *end* of the line, regardless of the cursor position.

Trying smilies:
:0  ???  :D

Trying a URL:
Talkorigins webpage link test

...hey, that worked pretty well..

A graphic:

...hmm, it stuck the code at the end of the post, I'll move it up.

I won't even trying the Flash movie posting option...


Date: 2002/05/17 02:35:38, Link
Author: niiicholas

Wes has kindly made me a moderator on this forum.  I'd like to briefly mention a few things for background's sake.  As other things come up they will be added to this thread (or the thread can be bumped if someone needs an introduction).

First, the title of the forum.  Here is the reference (from Wes):


"The time has come," the Walrus said, "to speak of many things.  Of shoes and ships and sealing wax, of cabbages and kings."

-- Lewis Carroll


1) This is a public-viewing, but restricted posting forum.  Posting access is granted by (I think) either Wes or me, basically if we feel like the poster will contribute to the purpose of this particular forum, detailed below.

2) The purpose of this forum is to give ID skeptics a place to gather references, citations, bits of arguments, etc., in one place, either just for reference, or for a possible future article or FAQ.  

The idea is to do things on a thread-specific basis.  A random example thread title might be "Examples of co-option in evolution", and the person who starts the thread says something like:

"I would like this thread to focus on well-documented examples of cooption in evolution.  The reason, of course, is that antievolutions frequently assert, without documentation, that change-of-function is a very low probability event, and use this pseudo-argument to brush off the "what about cooption?" objection to the arguments of Behe and Dembski regarding the nonevolution of functional complexity.

The best way to rebut the IDists' assertion is simply to list the numerous examples of cooption in evolution, with references.  So, if you come across a good example, mention it and if possible cite what references you have; others may be able follow up suggestions of places to look, e.g. "I think I read an essay by Gould on this once".

Additional things worth posting in a thread like this:

- links to other threads discussing cooption
- links to high-quality webpages
- links to the Pubmed abstracts of specific papers
- references on the topic generally, e.g. papers on the topic of the fate of gene duplications, for example.
- images and highly relevant quotes can be posted also

Both molecular and macro cases are welcome, part of the point of this thread is to show that the same process occurs commonly in both realms.

See how this would work?  The potential topics are endless, but hopefully when you run across something, e.g. "Hey, a new article on the evolution of blood-clotting!", you can check the forum to see if there is already a thread on blood-clotting, and add the reference there.

3) Discussions of the above are welcome in this forum, however if very long-winded debates develop they are better put in the general ID discussion.  Also, active debates with internet IDists should be conducted in the general ID discussion (where they have a chance to fight back); I think a good policy would be to stick a link to a debate thread in the relevant thread here.  The main focus here is on "collaborative informational resource gathering/displaying" -- hopefully it will develop into a high-quality resource for ID skeptics across the net.

Have fun,


Date: 2002/05/17 21:43:08, Link
Author: niiicholas
Here is a fantastic recent example from your friend and mine, Jonathan Wells.

There You Go Again:
A Response to Kenneth R. Miller
Jonathan Wells
Discovery Institute
April 9, 2002


The believers in Darwinian evolution who currently dominate our educational establishment think that all students--even those headed for careers in auto mechanics or real estate--should believe, as they do, that all of us are descended from ape-like creatures through genetic accidents and survival of the fittest.

Promoters of this doctrine have recently been urging the Ohio State School Board to adopt science standards that would require all high school graduates to memorize Darwinian theory without questioning it, and without being exposed to any of the mounting evidence against it. To help in this campaign, the promoters enlisted the support of Brown University biology professor Kenneth R. Miller, who represented them before the Board on March 11.

Miller is not a disinterested scientific expert. As the co-author of an introductory biology textbook that has been purchased for use in the Ohio public school system, he has a substantial personal stake in the controversy. In 2000, I published a book, Icons of Evolution, criticizing the way biology textbooks--including Miller’s--systematically distort the scientific evidence to provide support for Darwin’s theory. In his appearance before the Ohio State School Board, Miller attempted to respond to some of my criticisms.

In his eagerness to defend Darwinian orthodoxy, however, Miller bungled the attempt.

It takes a rather amazing amount of gall for Wells to accuse Ken Miller of not being a "disinterested scientific expert" because of Miller's interest in his textbook, when Wells obviously has (at the very least) a similar level of interest in his own book Icons.

Also interesting in the above quote is how Wells appears to (now) be denying the common descent of humans and apes, whereas if you read Icons of Evolution carefully one finds quotes like (paraphrase) "it is clear that the human species has a history".  AFAICT Wells actually does believe in some kind of guided evolution (i.e. he disagrees only with the "genetic accidents and survival of the fittest" bit), that's probably what he would say about the first sentence if pressed, but it is interesting how he managed not to distinguish his view from the special creationist view.

Returning to the fold under pressure, perhaps...

Date: 2002/05/17 22:00:37, Link
Author: niiicholas

Following my own suggestion, here is a thread devoted to collection material/links/references relevant to blood-clotting and the claims IDists make about it.  As there is not yet a single webpage anywhere that has gathered all of the relevant material in a single place, this might as well be it.  Perhaps at some point it could be edited into a FAQ, or could inspired someone to write a FAQ (since much of the hard work of finding the references, IDist quotes, etc., would be done).

Specifically relevant would be things like:

1) blood-coagulation/clotting (or hemolyph coagulation for you invertebrates out there), especially e.g. webpages/literature that describe the basics in an easily understandable manner such that a FAQ reader could be referred there

2) references to articles/lit. on the evolution of blood clotting

3) Links to/quotes of antievolutionist assertions regarding blood-clotting, with commentary on problems if you are inspired

4) Links to the various webpages already out there rebutting IDist claims.

Awhile ago I did a search and dug up a pretty good starting reference list, I'll post that in a moment.


Date: 2002/05/17 22:09:17, Link
Author: niiicholas
These are the results of a computer search last year on terms like "evolution blood coagulation."  I was pretty careful checking abstracts etc. to avoid including "false hits" -- (e.g., "evolution" has a chemical meaning unrelated to biological evolution).

For fun, I added asterisks (*) to refer to papers that Behe referenced in Darwin's Black Box.  The others are the ones he missed, or that were published 1996 or later.

I'll quote the whole URL in code brackets, hopefully they'll fit.

Code Sample

Banyai, L., Varadi, A. and Patthy, L. (1983). “Common evolutionary origin of the fibrin-binding structures of fibronectin and tissue-type plasminogen activator.” FEBS Letters, 163(1): 37-41. Link:

Bazan, J. F. (1990). “Structural design and molecular evolution of a cytokine receptor superfamily.” Proceedings of the National Academy of Sciences of the United States of America, 87(18): 6934-6938. Link:

Blake, C. C. F., Harlos, K. and Holland, S. K. (1987). “Exon and Domain Evolution in the Proenzymes of Blood Coagulation and Fibrinolysis.” Cold Spring Harbor Symposia on Quantitative Biology: The Evolution of Catalytic Function, LII: 925-932. Link:

Crabtree, G. R. (1986). “The Molecular Genetics of Fibrinogen.” Journal of Cellular Biochemistry Supplement(10 PART A): 229.  

Crabtree, G. R., Comeau, C. M., Fowlkes, D. M., Fornace, A. J., Jr., Malley, J. D. and Kant, J. A. (1985). “Evolution and structure of the fibrinogen genes: Random insertion on introns or selective loss?” Journal of Molecular Biology, 185(1): 1-20.  

Di Cera, E., Dang, Q. D. and Ayala, Y. M. (1997). “Molecular mechanisms of thrombin function.” Cell Mol Life Sci, 53(9): 701-730.  

Doolittle, R. F. (1985). “More homologies among the vertebrate plasma proteins.” Biosci Rep, 5(10-11): 877-884. Link:

Doolittle, R. F. (1990). “The Structure and Evolution of Vertebrate Fibrinogen A Comparison of the Lamprey and Mammalian Proteins,” in ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY: FIBRINOGEN, THROMBOSIS, COAGULATION, AND FIBRINOLYSIS. C. Y. Liu and Chien, S. New York, Plenum Press. 281. Link:

Doolittle, R. F. (1992). “A detailed consideration of a principal domain of vertebrate fibrinogen and its relatives.” Protein Science, 1(12): 1563-1577. Link:

Doolittle, R. F. (1992). “Early Evolution of the Vertebrate Fibrinogen Molecule.” Biophysical Journal, 61(2 PART 2): A410.  

Doolittle, R. F. (1992). “Early Evolution of the Vertebrate Fibrinogen Molecule.” FASEB Journal, 6(1): A410.  

Doolittle, R. F. (1992). “Stein and Moore Award address. Reconstructing history with amino acid sequences.” Protein Science, 1(2): 191-200. Link:

*Doolittle, R. F. (1993). “The Evolution of Vertebrate Blood Coagulation - a Case of Yin and Yang.” Thrombosis and Haemostasis, V70(N1): 24-28. Link:

Doolittle, R. F. and Feng, D. F. (1987). “Reconstructing the Evolution of Vertebrate Blood Coagulation from a Consideration of the Amino Acid Sequences of Clotting Proteins.” Cold Spring Harbor Symposia on Quantitative Biology: The Evolution of Catalytic Function, LII: 869-874. Link:

Doolittle, R. F., G., Spraggon and J., Everse S. (1997). “Evolution of vertebrate fibrin formation and the process of its dissolution.” Ciba Found Symp, 212: 4-17; discussion 17-23. Link:

Doolittle, R. F. and Riley, M. (1990). “The amino-terminal sequence of lobster fibrinogen reveals common ancestry with vitellogenins.” Biochemical and Biophysical Research Communications, 167(1): 16-19. Link:

Edgington, T. S., Curtiss, L. K. and Plow, E. F. (1985). “A linkage between the hemostatic and immune systems embodied in the fibrinolytic release of lymphocyte suppressive peptides.” Journal of Immunology, 134(1): 471-477.  

Ghidalia, W., Vendrely, R., Montmory, C., Coirault, Y., Samama, M., Lucet, B., Bellay, A. M. and Vergoz, D. (1989). “Overall study of the in vitro plasma clotting system in an invertebrate, Liocarcinus puber (Crustacea Decapoda): Considerations on the structure of the Crustacea plasma fibrinogen in relation to evolution.” Journal of Invertebrate Pathology, 53(2): 197-205.  

Hervio, L. S., Coombs, G. S., Bergstrom, R. C., Trivedi, K., Corey, D. R. and Madison, E. L. (2000). “Negative selectivity and the evolution of protease cascades: the specificity of plasmin for peptide and protein substrates.” Chemistry & Biology, V7(N6): 443-452.  

Hewett-Emmett, D., Czelusniak, J. and Goodman, M. (1981). “The evolutionary relationship of the enzymes involved in blood coagulation and hemostasis.” Annals of the New York Academy of Sciences, 370(20): 511-527.  

Holland, S. K., Harlos, K. and Blake, C. C. F. (1987). “Deriving the generic structure of the fibronectin type II domain from the prothrombin Kringle 1 crystal structure.” EMBO (European Molecular Biology Organization) Journal, 6(7): 1875-1880.  

Jordan, R. E. (1983). “Antithrombin in vertebrate species: conservation of the heparin-dependent anticoagulant mechanism.” Archives of Biochemistry and Biophysics, 227(2): 587-595.  

Kant, J. A., Fornace, A. J., Jr., Saxe, D., Simon, M. J., McBride, O. W. and Crabtree, G. R. (1985). “Evolution and organization of the fibrinogen locus on chromosome 4: Gene duplication accompanied by transposition and inversion.” Proceedings of the National Academy of Sciences of the United States of America, 82(8): 2344-2348.  

Kornblihtt, A. R., Pesce, C. G., Alonso, C. R., Cramer, P., Srebrow, A., Werbajh, S. and Muro, A. F. (1996). “The fibronectin gene as a model for splicing and transcription studies.” FASEB Journal, 10(2): 248-257.  

Laki, K. (1972). “Our ancient heritage in blood clotting and some of its consequences.” Annals of the New York Academy of Sciences, 202(4): 297-307.  

Neurath, H. (1984). “Evolution of proteolytic enzymes.” Science, 224(4647): 350-357. Link:

Neurath, H. (1986). “The Versatility of Proteolytic Enzymes.” Journal of Cellular Biochemistry, 32(1): 35-50.  

Neurath, H. (1986). “The Versatility of Proteolytic Enzymes.” Journal of Cellular Biochemistry Supplement(10 PART A): 229.  

Oldberg, A. and Ruoslahti, E. (1986). “Evolution of the fibronectin gene: Exon structure of cell attachment domain.” Journal of Biological Chemistry, 261(5): 2113-2116.  

Opal, S. M. (2000). “Phylogenetic and functional relationships between coagulation and the innate immune response.” Critical Care Medicine, V28(N9 SUPPS): S77-S80.  

Pan, Y. and Doolittle, R. F. (1991). “Distribution of Introns in Lamprey Fibrinogen Genes.” Journal of Cellular Biochemistry Supplement(15 PART D): 75.  

Pan, Y. and Doolittle, R. F. (1992). “cDNA sequence of a second fibrinogen alpha chain in lamprey: an archetypal version alignable with full-length beta and gamma chains.” Proceedings of the National Academy of Sciences of the United States of America, 89(6): 2066-2070. Link:

Patthy, L. (1985). “Evolution of the Proteases of Blood Coagulation and Fibrinolysis by Assembly from Modules.” Cell, 41(3): 657-664. Link:

Patthy, L. (1990). “Evolution of blood coagulation and fibrinolysis.” Blood Coagulation and Fibrinolysis, 1(2): 153-166. Link:

Patthy, L. (1990). “Evolutionary Assembly of Blood Coagulation Proteins.” Seminars in Thrombosis and Hemostasis, 16(3): 245-259. Link:

Patthy, L. (1999). “Genome evolution and the evolution of exon-shuffling—a review.” Gene, 238(1): 103-114. Link:

Roberts, Lewis R., Nichols, Lanita A. and Holland, Lene J. (1995). “CDNA and amino-acid sequences and organization of the gene encoding the B-beta subunit of fibrinogen from Xenopus laevis.” Gene (Amsterdam), 160(2): 223-228.  

Sosnoski, D. M., Emanuel, B. S., Hawkins, A. L., Van Tuinen, P., Ledbetter, D. H., Nussbaum, R. L., Kaos, F. T., Schwartz, E., Phillips, D. and et al. (1988). “Chromosomal localization of the genes for the vitronectin and fibronectin receptors .alpha. subunits and for platelet glycoproteins IIb and IIIa.” Journal of Clinical Investigation, 81(6): 1993-1998.  

Wang, Y. Z., Patterson, J., Gray, J. E., Yu, C., Cottrell, B. A., Shimizu, A., Graham, D., Riley, M. and Doolittle, R. F. (1989). “Complete sequence of the lamprey fibrinogen .alpha. chain.” Biochemistry, 28(25): 9801-9806.  

Xu, X. and Doolittle, R. F. (1990). “Presence of a vertebrate fibrinogen-like sequence in an echinoderm.” Proceedings of the National Academy of Sciences of the United States of America, 87(6): 2097-2101. Link:

Zhang, Y. L., Hervio, L., Strandberg, L. and Madison, E. L. (1999). “Distinct contributions of residue 192 to the specificity of coagulation and fibrinolytic serine proteases.” Journal of Biological Chemistry, V274(N11): 7153-7156. Link:

Zimmermann, E. (1983). “[The evolution of the coagulation system from primitive defense mechanisms].” Behring Institute Mitteilungen, 82(73): 1-12.  

Many of these articles are however tough to get (unless you're at UCSD, unsurprisingly), so I've only read a few.

Others are welcome to add stuff as they see fit.

Thanks, nic

Date: 2002/05/17 23:18:58, Link
Author: niiicholas
Quote (Wesley R. Elsberry @ May 17 2002,19:19)
In this ARN forum topic, the issue of arguing concerning optimality was raised.  The person bringing this up cited Dembski, but several of his ideas seem to stem from Paul Nelson's presentation back at the 1997 NTSE conference.

Basically, ID advocates object to optimality arguments by biologists when these venture into the realm of contrasting natural mechanisms with supposed supernatural mechanisms.  Paul Nelson made the observation that such argumentation presupposes certain "theological themata".  Nelson also asserted that in order to argue that some state observed in nature was sub-optimal, one would have to reliably know what the absolute optimal state was, and calculate an optimality deficit figure.

I responded to Nelson's assertion that knowledge of absolute optimality was a necessary part of a sub-optimality argument some time ago on <a href="" target="_blank">the newsgroup</a>.  The response can be seen here, but the essential message is that a valid sub-optimality argument can be warranted on a strictly relative basis, with no need for absolute optimality to be known.

I also responded to William Dembski's essay on optimality argumentation, pointing out several problems in his argumentation.  Dembski's essay is here, and my response is here.

I agree that there are plenty of cases when the assertion "this biological design is suboptimal relative to what someone with foresight would have designed for this purpose" is a perfectly legimate inference, although of course sometimes things will be ambiguous.

I was interested in this little bit here:


Basically, ID advocates object to optimality arguments by biologists when these venture into the realm of contrasting natural mechanisms with supposed supernatural mechanisms.  Paul Nelson made the observation that such argumentation presupposes certain "theological themata".  

I take this to be a reference to the IDist counterargument, "'God wouldn't have done it that way' is a theological argument".

It seems to me that this criticism is only correct insofar as the attributes of God are really up-for-grabs; for most antievolutionists it is in fact rather clear what kind of God is being hypothesized, and once that hypothesis has been suggested then it seems to me perfectly fair for a skeptic to point out where facts disagree with the hypothesis.

However, the IDists have really argued themselves into a pickle on this one.  Recall that ID "officially" says that nothing is known about the designer, i.e. whether it is supernatural or natural ID.  Therefore, if a skeptic points out that a suboptimal design is well explained by the foresight-lacking mechanism of natural selection, whereas an intelligent designer using foresight would easily have avoided the suboptimality, then the IDists have no recourse to the "that's a theological argument" line.  The only way they can use this argument (which would still have the problems mentioned above) is if they admit that they are bringing God into it as the designer!

g'night, nic

Date: 2002/05/24 19:42:53, Link
Author: niiicholas
Some good discussion and links on a article discussing the homology between a blood-clotting protein and a cone-snail venom protein (!!!) was posted on this II thread.


Date: 2002/05/24 20:25:51, Link
Author: niiicholas
Some more stuff I've gathered on the mysterious missing Hagemann factor case:

1) I went and re-checked Darwin's Black Box and Behe does indeed include the component as part of the IC blood-clotting system.***

2) Here is the abstract of the Robinson et al. paper that Wes cited:


Robinson, A. Jean, Kropatkin, Mona, and Aggeler, Paul M.  1969.   Hageman Factor (Factor XII) Deficiency in Marine Mammals. Science 166:1420-1422.

Hematologic and coagulation studies were conducted on Atlantic bottlenose dolphins and killer whales. Hematologic values were similar to those in man. These animals differed from other mammals in that the Hageman factor (factor XII) was absent and this absence caused marked prolongation of coagulation. Levels of VIII and V were high and those of VII and X were low compared with levels in man.

The paper mentions at the end a longish list of birds, reptiles, etc. that don't have Hagemann factor either, surprise suprise, although it mentions that at least some of these have other factors that may compensate...

Also of interest are the names of the orcas: "Orky" "Snorky" "Corky". Don't see those names as headers in scientific tables every day...

3) The conclusions of the Robinson et al. (1969) paper are backed up by this recent paper:


Pubmend citation

Thromb Res 1998 Apr 1;90(1):31-7

Whale Hageman factor (factor XII): prevented production due to pseudogene conversion.

Semba U, Shibuya Y, Okabe H, Yamamoto T.

In Southern blot analysis of the Hind III-digested whale genomic DNA obtained from the livers of two individual whales, we detected a single band with a size of five kilobase pairs which hybridized to full length guinea pig Hageman factor cDNA. We amplified two successive segments of the whale Hageman factor gene by polymerase chain reaction (PCR), and sequenced the PCR products with a combined total of 1367 base pairs. Although all of the exon-intron assemblies predicted were identical to those of the human Hageman factor gene, there were two nonsense mutations making stop codons and a single nucleotide insertion causing a reading frame shift. We could not detect any message of the Hageman factor gene expression by northern blot analysis or by reverse transcription-polymerase chain reaction (RT-PCR) analysis. These results suggest that in the whale, production of the Hageman factor protein is prevented due to conversion of its gene to a pseudogene. The deduced amino acid sequence of whale Hageman factor showed the highest homology with the bovine molecule among the land mammals analyzed so far.

In other words, this is a classic textbook-style case of pseudogene production, as well as being yet another bit of evidence supporting the whale-artiodactyl connection that has been suggested by various molecular studies and supported by recently discovered transitional fossils, see J. G. M. Thewissen's whale evolution page here.

4) It should be pointed out that while Behe includes Hageman factor (= Factor XII) as part of the IC blood-clotting system in DBB, the likely ID defense will be to take the "eternally receding IC system" approach wherein they declare this part non-essential and therefore not "part" of the IC "system" (if it's not part of the system, what it is a part of?).  

According to this t.o. POTM, it is indeed questionable how necessary Factor XII is for blood-clotting:


In this view, 3 factors included in the older scheme
(Factor XII = Hageman, prekallikrein and HMK) are now excluded, since deficiencies do not cause clinical disease, although they are associated with long clotting times in vitro. The role of XI isn't clear, since deficieny isn't invariably associated with disease.

...although one wonders if "deficiencies" means "complete absense", as it is apparent that Factor XII does play some important roles, e.g. the introduction to Semba et al. (1998) states:


Hageman factor (factor XII) is an initiation factor of plasma protease cascades, such as the intrinsic blood coagulation pathway and the plasma kinin system [1 and 2]. Important roles of the plasma kinin system in inflammatory responses in infection have been demonstrated. Microbial proteases such as Pseudomonas aeruginosa elastase, and negatively charged bacterial components such as endotoxin are capable of activating Hageman factor and prekallikrein [3, 4, 5 and 6].

...sounds like a handy thing to have around for sure.  Certainly on the above quote we can say that Hageman factor is necessary for "Hageman factor-dependent cascade activation", which just goes to show that just about anything can be considered "essential for function" depending on where one draws the lines of the "system".  

An even better feature of Semba et al. (1998) is that they propose a hypothesis for why Hagemann factor has been lost in marine mammals:


Saito et al. reported that all marine mammals examined by them did not possess coagulation activities equivalent to Hageman factor and prekallikrein [8]. Their explanation of this observation is as follows: the lack of these initiation factors of the intrinsic blood coagulation pathway must be advantageous to the marine mammals in prevention of disseminated intravascular coagulation syndrome which might occur in the semi-static state of blood circulation in the skin and the lungs under high hydrostatic pressure.


3. Discussion
The present study demonstrates that the Hageman factor gene converted to a pseudogene by the point mutations in exons coding for the protease domain in the whale. This conversion explains the absence of Hageman factor in whale plasma [8]. Messenger RNA of whale Hageman factor was not also detected in the liver mRNA fraction even by Southern blot analysis of the RT-PCR products. This result suggests very high instability of whale Hageman factor mRNA. Since only the 3' half of the whale Hageman factor gene has been analyzed so far, final conclusions about the mechanism of the blocked expression of the whale Hageman factor gene message cannot yet be drawn.

Participation of the intrinsic blood coagulation pathway in the disseminated intravascular coagulation syndrome has been suspected. The whale may dive to depths of 1000 m, where a semi-static state of blood circulation in the skin and the lungs might occur due to the high hydrostatic pressure. The fact that the initiation factor of the intrinsic blood coagulation system is not produced in the whale would support the clinical suspicion about the participation of this system in the disseminated intravascular coagulation syndrome.

We have been postulating that Hageman factor and the plasma kinin system play important roles in the host defense of land mammals. However, our hypothesis does not explain why Hageman factor-deficient individuals are not suffering from infectious deseases. Therefore, there may be an opposite hypothesis: the plasma kinin system does not play an essential role in host defense. From a superficial point of view, the present study might support this opposite hypothesis. However, Saito et al. reported that a significant amount of high-molecular weight kininogen was present in whale plasma [8]. This concentration corresponds to 30% of that in human plasma. We presently confirmed this using dolphin plasma (data not shown). If we take into account that the significant amount of high-molecular weight kininogen is present even in whale plasma, we could speculate that the important roles of the plasma kinin system are compensated by an unknown system(s) in Hageman factor-deficient individuals as well as in the marine mammals.

The deduced amino acid sequence of whale Hageman factor closely resembles that of the bovine molecule including the Pro-rich region where almost no homology is observed among the human, guinea pig, and bovine molecules [16]. Recently, Shimamura et al. [19] described their opinion that whales (including dolphins and porpoises), ruminants (cows, chevrotains, deer, sheep), and hippopotamuses form a monophyletic group. This is based on their analyses of two retroposons in the genomes of 15 mammalian species. Our present data support their opinion.

So, we appear to have parts being lost, perhaps "parts" being replaced or compensated for, and generally a lot of evolution going on.  One wonders how any of this would be explained on a "IDdidit" just-so story.


PS: Looking up 'related articles' in Pubmed reveals that decreased Factor XII activity is associated with increased miscarriage in humans:


PubMed link

Fertil Steril 2002 Feb;77(2):353-6

Coagulation factor XII activity, but not an associated common genetic polymorphism (46C/T),is linked to recurrent miscarriage.

Iinuma Y, Sugiura-Ogasawara M, Makino A, Ozaki Y, Suzumori N, Suzumori K.

Department of Obstetrics and Gynecology, Nagoya City University Medical School, Mizuho-ku, Nagoya 467-8601, Japan.

OBJECTIVE: To investigate whether a factor XII genetic polymorphism is associated with first-trimester embryonal loss. DESIGN: Prospective case-control study. SETTING; Nagoya City University Hospital. PATIENT(S): Eighty-three patients with a history of two or more unexplained first-trimester recurrent miscarriages and 67 controls with no obstetric complications or history of miscarriage. MAIN OUTCOME MEASURE(S): Plasma factor XII activity, a genetic polymorphism (46 C-->T) of factor XII, lupus anticoagulant, and beta(2)glycoprotein I dependent anticardiolipin antibodies. RESULT(S): Ten of the 83 patients and 1 of the 67 controls had decreased factor XII activity; the difference in frequency was statistically significant. Wild-type (CC), heterozygote (CT), and homozygote (TT) allele patterns were observed in 8, 36, and 39 patients, respectively, compared with 11, 20, and 36 of the patients and controls, respectively. The mean (+/- SD) corresponding factor XII activity was 154.8 +/- 44.8%, 112.7 +/- 30.2%, and 66.2 +/- 29.2% in patients and 164.6 +/- 26.7%, 114.3 +/- 28.1%, and 70.4 +/- 18.1% in controls. The two groups did not differ in the frequency of the T allele or categories of factor XII activity. CONCLUSION(S): Factor XII activity overall, but not the 46C/T common genetic polymorphism, is associated with recurrent miscarriage.
(bold added)

...which sure seems to imply that it is important for something.

Further support:


Pubmed link

Fertil Steril 2001 May;75(5):916-9

Factor XII but not protein C, protein S, antithrombin III, or factor XIII is a predictor of recurrent miscarriage.

Ogasawara MS, Aoki K, Katano K, Ozaki Y, Suzumori K.

Department of Obstetrics and Gynecology, Nagoya City University Medical School, Nagoya, Japan.

OBJECTIVE: To investigate whether a decrease in the values of protein C (PC), protein S (PS), antithrombin III (ATIII), factor XII (FXII), or factor XIII (FXIII) has predictive value for subsequent miscarriages. DESIGN: Prospective study. SETTING: Nagoya City University Medical School. PATIENT(S): A total of 536 patients with a history of two or more first-trimester miscarriages. INTERVENTION(S): One hundred and twelve patients treated with low-dose aspirin were excluded from the analysis. MAIN OUTCOME MEASURE(S): The subsequent pregnancy outcome of 424 patients was compared for abnormal and normal levels of each parameter. RESULT(S): There were no differences in the subsequent miscarriage rates between abnormal and normal values of PC, PS, ATIII, and FXIII. However, the rate with abnormal FXII is significantly higher than that with normal FXII. CONCLUSION(S): A decrease in FXII (but not in PC, PS, ATIII, or FXIII) predicts subsequent miscarriage in patients with a history of first-trimester recurrent miscarriages.

Here is another example of why missing Factor XII is not a good thing:


Ann Thorac Surg 2002 Jan;73(1):286-8

Huge left atrial thrombus with mitral stenosis in congenital factor XII deficiency.

Hasegawa T, Uematsu M, Tsukube T, Takemura Y, Okita Y.

Department of Surgery, Division II, Kobe University School of Medicine, Japan.

Factor XII deficiency has been reported to be a risk factor for thromboembolism as a result of inactivation of fibrinolysis. We describe a case of a huge left atrial thrombus with mitral stenosis, which was successfully removed surgically in a Factor XII deficient patient.

pubmed link

...and yet the ancestors of whales clearly had Hageman Factor, but lost it.  How is this possible unless Behe's argument about IC is fundamentally flawed?


*** Added in edit, Dec. 2002:

Actually, Behe did not.  It looks like it is on pp. 82 and 84, but on p. 86 Behe limits the system to only four components.  This was pointed out to me by DNAunion here:

On p. 86, Behe writes,


”Leaving aside the system before the fork in the pathway, where some details are less well known, the blood-clotting system first the definition of irreducible complexity. … The components of the system (beyond the fork in the road) are fibrinogen, prothrombin, Stuart factor, and proaccelerin. Just as none of the parts of the Foghorn [Leghorn] system is used for anything except controlling the fall of the telephone pole, so none of the cascade proteins are used for anything except controlling the formation of a blood clot. Yet in the absence of any one of the components, blood does not clot, and the system fails.” (Michael Behe, Darwin’s Black Box: The Biochemical Challenge to Evolution, Free Press, 1996, p86)

(copying from DNAunion)

Ken Miller, here,



Consider, for example, the intricate cascade of proteins involved in the clotting of vertebrate blood. This has been cited as one of the principal examples of the kind of complexity that evolution cannot generate, despite the elegant work of Russell Doolittle (Doolittle and Feng 1987; Doolittle 1993) to the contrary. A number of proteins are involved in this complex pathway, as described by Behe:

When an animal is cut, a protein called Hagemann factor (XII) sticks to the surface of cells near the wound. Bound Hagemann factor is then cleaved by a protein called HMK to yield activated Hagemann factor. Immediately the activated Hagemann factor converts another protein, called prekallikrein, to its active form, kallikrein. (Behe 1996a, 84)

How important are each of these proteins? In line with the dogma of irreducible complexity, Behe argues that each and every component must be in place before the system will work, and he is perfectly clear on this point:

. . . none of the cascade proteins are used for anything except controlling the formation of a clot. Yet in the absence of any of the components, blood does not clot, and the system fails. (Behe 1996a, 86)

As we have seen, the claim that every one of the components must be present for clotting to work is central to the "evidence" for design. One of those components, as these quotations indicate, is Factor XII, which initiates the cascade. Once again, however, a nasty little fact gets in the way of intelligent design theory. Dolphins lack Factor XII (Robinson, Kasting, and Aggeler 1969), and yet their blood clots perfectly well. How can this be if the clotting cascade is indeed irreducibly complex? It cannot, of course, and therefore the claim of irreducible complexity is wrong for this system as well. I would suggest, therefore, that the real reason for the rejection of "design" by the scientific community is remarkably simple – the claims of the intelligent design movement are contradicted time and time again by the scientific evidence.

...the second quote is pretty clearly out-of-context and Miller should have noted that Behe left himself some wiggle room in DBB concerning everything "before the fork" -- most of the cascade.  Behe only explicitly includes four parts in the IC system.

Date: 2002/05/24 21:25:14, Link
Author: niiicholas
A recent post on by Dunk discussing some recent (2002) literature, with quotes:

Here is the google link


Date: 2002/05/24 22:27:00, Link
Author: niiicholas
An attempt to list the major relevant articles/books in the ID blood-clotting discussion:

Code Sample

Darwin's Black Box : The Biochemical Challenge to Evolution
by Michael J. Behe

Behe and the Blood Clotting Cascade (1997)
T.O. POTM on blood-clotting pointing out the sequence patterns

A Delicate Balance
by Russell F. Doolittle
Originally published in the February/ March 1997 issue of Boston Review

Behe Responds to the Boston Review
Letter to the Boston Review
by Michael J. Behe
(listed as copyright 1999, Behe originally posted the material to the Boston Review discussion bord in Spring 1997)

Finding Darwin's God, Miller (1999) link

In Defense of the Irreducibility of the Blood Clotting Cascade (July 31, 2000)
Response to Russell Doolittle, Ken Miller and Keith Robison
by Michael J. Behe

Design on the Defensive, (Fall (?) 2000)
Ken Miller's page responding to Behe's review of Miller's book

(Ken Miller evolution page:

Miller's response to Behe's (2000) "In defense of the IC of the Blood Clotting Cascade."
Introduction to Miller's argument on blood-clotting:
...linked from Miller's 'Design on the Defensive' (

The Evolution of Vertebrate Blood Clotting
Miller's "original draft" (longer description than in the book) on the evolution of blood-clotting. Linked from the above reference:

Comments on Ken Miller's Reply to My Essays (Behe, January 2001)
A response to Ken Miller, but blood-clotting isn't mentioned.

There may be additional relevant online articles, I will add them if anyone suggests them.

Thanks, nic

Date: 2002/05/24 23:23:13, Link
Author: niiicholas
Jonathan Wells has a very interesting report on the debate before the Ohio Board of Education.  

Ken Miller's take, and further debates online about some of the points, are linked from here:


Date: 2002/05/24 23:28:42, Link
Author: niiicholas
Here is a muddled page in support of Behe's IC blood-clotting argument, I list it as it draws heavily from Behe's chapter & gives a sense of Behe's specific arguments there (including Behe's inclusion of Hageman factor in the IC system):

Irreducible Complexity? Blood Clotting! at, by Robert Harsh


Date: 2002/05/24 23:51:37, Link
Author: niiicholas
A somewhat interesting but mildly confused article in Geology News, "Geoscience at the BA: Clots have been with us for 400 million years", reporting on a talk by Colin Davidson (Imperial College School of Medicine) on the evolution of blood-clotting, especially regarding the role of large (genome or chromosome) duplications.  I say the article is confused as punctuated equilibrium is invoked as having something to do with the situation, which AFAICT it doesn't, and as none of the connections of blood-clotting to more ancient protease cascade systems are discussed.  The interesting quotes concern gene duplication:


Evolution at molecular level

The basic tenets of molecular biology make understanding evolution at the molecular level possible. Genes are encoded by DNA, also known as nucleic acid, and composed of long strings of four biochemical units termed bases (shortened to A, G, C, and T). The linear order or sequence of these bases encodes special signals for starting and stopping as well code-script read in triplets for amino acids.

These chains of amino acids - of which there are 20 - form proteins and are the products of most (but not all) genes. We can, therefore, determine the determine the protein amino acid sequence of genes by decoding the triplet DNA sequences and compare it to any other gene. The more evolutionarily similar two organisms, the greater the similarity of amino acid sequences when comparing homologous genes. This is because there has been less time for the natural mutation process - such as inborn errors in DNA replication - to act on a gene's DNA sequence. When comparing most human and chimpanzee proteins one finds 98 to 100% identity, but the same proteins shared with bacteria the identity drops between 30 to 60% or less.

Proteins also exist in the genomes of most organisms that share a high degree of identity, and who share a common ancestor. The best understood mechanism of gene duplication occurs during the production of gametes in sexual organisms. This process is called meiosis in which the two sets of chromosomes - one from each parent - line up and the threads of DNA cross, break and rejoin so that DNA is exchanged between parental chromosomes - so generating diversity.

Usually this is an equal and reciprocal exchange, but occasionally the result is unequal and one of the chromosomes acquires a little more DNA containing an extra gene,or part of one. If the gamete with extra DNA acquires an entire gene it is referred to as "gene duplication by unequal crossover".

In blood clotting, two of the similar proteases, Factor VII (FVII) and X (FX), are within close proximity on chromosome 13 in humans indicating that unequal crossover played a role in the evolution of blood clotting.

Complete genome duplication

Another mechanism of gene duplication is through complete genome duplication. The entire genome of brewer's yeast Saccharomyces cerevisiae has been sequenced, and provides evidence of complete genome duplication by the genetic redundancy and conserved arrangement of the remaining duplicated genes. One way that genome duplication can occur is through polyploidy and subsequent degeneration back to a lower ploidy state. (Polyploidy is where the cell nucleus contains multiple sets of chromosomes.  Humans are diploid meaning we have two copies of each chromosome but the toad Xenopus laevis has four copies of each chromosome and therefore an additional two copies of each gene.)

Such duplicated genes can take one of two career paths. The majority of gene duplicates enter "early retirement" as the constant mutational pressure results in amino acid substitutions that render the protein non-functional. In the rare event that the amino acid substitution is beneficial, the duplicated gene can participate in natural selection and acquire a new function or interaction within an existing pathway - such as blood clotting.

" It appears that the physiologically important 'extrinsic' pathway as we know it mammals evolved by two rounds of genome or chromosomal duplication and one tandem duplication prior to a last common ancestor with fish ~400 MYA and after the origin of the vertebrates ~520 MYA. This brief window of evolutionary time indicates that a flurry of duplication events occurred to generate the clotting pathway and supports the theories of punctuated evolution.

"The evolutionary time frame of blood clotting evolution is supported by investigations into other gene families such as Hox genes and the genes of the MHC. Investigations in other systems support the two large-scale duplication of the ancestral vertebrate genome as well. The debatable issue is when both duplications occurred." says Davidson.

However, in the conclusion Davidson is also quoted as saying:


Fundamental evolutionary event

"Vertebrates are one of the planet's most diverse and successful group of animals colonizing both the water and land. Vertebrates share common developmental physiology, and anatomy and are distinguished from invertebrates by complex systems such as immune, nervous, endocrine and blood clotting systems.

"Since blood transports and mediates many of the above vertebrate innovations it seems certain that the protective function of blood clotting was a fundamental evolutionary event. A more primitive state of blood clotting than that found in jawless vertebrates is likely not present in any living creature and died with the primitive vertebrates in the Cambrian.

"The origin of vertebrate blood clotting, like the origin of life must have been a rare event, yet without protection from bleeding it would not have been possible for the radiation of vertebrates from fish to dinosaurs and ultimately humans."

I think it is a mistake to compare the origin of blood-clotting to the origin of life, or even to imply that it is rare: it is apparent that a similar system has arisen in arthropods at least (see Miller's (1999) discussion of the evolution of decapod blood-clotting), and it seems quite likely various clotting systems will be discovered in other complex metazoans (perhaps descended from a primitive ancestral system, but still with considerable independent evolution in each lineage, as e.g. with eyes).  One can even argue that the pitch of trees is a clotting system. Perhaps Davidson is a wee bit vertebrate-biased.


Date: 2002/05/25 00:35:53, Link
Author: niiicholas
An interesting paragraph from a recent article that continues the debate between Behe and Shanks & Joplin, regarding the (chemical) specificity necessary for ICness vs. "simple interactive" systems or what-have-you.

Niall Shanks and Karl Joplin, "Behe, Biochemistry, and the Invisible Hand," Philo, Volume 4, Number 1.


Regarding blood-clotting & specificity, they write:


Behe bolsters his attack on the BZ reaction with a truly bizarre argument derived from the fact that the reagents in the BZ reaction have a wide variety of uses—in Behe’s terminology, they have low specificity. For example, one ingredient, sodium bromate, is a general purpose oxidizing agent, and ingredients other than the ones we mentioned can be substituted. In our reaction, we mentioned the use of cerium ions, but iron or manganese ions will work just as well. He points out that the reaction is easy to set up and runs over a wide range of concentrations.21

If this is the case, then mousetraps are not irreducibly complex either. The steel used in their construction has a wide range of uses, as does the wood used for the base. You can substitute plastic for wood, and any number of metals for the spring and hammer. Mousetraps are easy to make (which is why they are cheap) and will work with metals manifesting a wide range of tensile strengths. But the fact that they are easy to make does not mean they assemble just by chance. Mousetraps need a maker just as much as the BZ system needs chemical mechanisms governed by the laws of chemistry. Either the BZ system is an irreducibly complex system, or the complexity of mousetraps is not a model for irreducible complexity. Take your pick, for you cannot have it both ways.

This matter is made all the more acute because crucial components of Behe’s own examples of irreducible complexity have multiple uses and lack substrate specificity (interact with a wide variety of substrates). For example, plasminogen (a component of the irreducibly complex blood-clotting cascade) has been documented to play a role in a wide variety of physiological processes, ranging from tissue remodeling, cell migration, embryonic development, and angiogenesis, as well as wound healing.22 And though Behe tells us that plasmin (the activated form of plasminogen), “. . . acts as scissors specifically to cut up fibrin clots,”23 we learn in one of the very papers he cites that, “Plasmin has a relatively low substrate specificity and is known to degrade several common extracellular-matrix glycoproteins in vitro.”24


22. See Thomas H. Bugge, Keith W. Kombrinck, Matthew J. Flick, Cynthia C. Daugherty, Mary J. Danton, Jay L. Degan, “Loss of Fibrinogen Rescues Mice for the Pleiotropic Effects of Plasminogen Deficiency,” Cell 87 (1996): 709–19.

23. See Behe, Darwin’s Black Box, 88.

24. See Bugge, et al., “Loss of Fibrinogen Rescues Mice,” 709.

Blood-clotting comes up again here:


In our original article we pointed to the gene coding for the protein p53. Lab mice have been created in which this gene has been knocked out. In support of our claims about the existence of redundancy in biochemical systems, we pointed out that, though this protein was involved in a number of important biochemical and biological processes, its removal did not result in a catastrophic disruption of the developmental process. There was redundancy, and other proteins could conspire to do the work of the missing protein.

Behe acknowledges this case, but draws his reader’s attention to the blood-clotting cascade originally discussed in his book:

Yet contrast this case [p53] with that of mice in which the gene for either fibrinogen, tissue factor, or prothrombin has been knocked out. . . . The loss of any one of those proteins prevents clot formation—the clotting cascade is broken. Thus Shanks and Joplin’s concept of redundant complexity does not apply to all biochemical systems.41

Again, suppose this point is right. What is its relevance when the role of redundant complexity lies in its ability to account, in natural, evolutionary terms, for the origins of irreducible complexity? And origins, as Behe points out, is the central issue. Loss of functional genes reduces redundancy to yield an irreducibly complex system. All Behe’s example shows is that further losses at this point can catastrophically disrupt the system.

We also think, however, that Behe has oversold the irreducible complexity of the blood-clotting cascade. The cascade itself has features that manifest redundant complexity. The real situation is thus more complex than Behe’s carefully massaged description would lead you to believe. Plasminogen deficient (Plg-/-)—hence plasmin deficient—mice have been studied. As noted earlier, plasmin is needed for clot degradation (it cuts up the fibrin), yet:

Plasmin is probably one member of a team of carefully regulated and specialized matrix-degrading enzymes, including serine-, metallo-, and other classes of proteases, which together serve in matrix remodeling and cellular reorganization of wound fields. . . . However, despite slow progress in wound repair, wounds in Plg-/- mice eventually resolve with an outcome that is generally comparable to that of control mice. Thus an interesting and unresolved question is what protease(s) contributes to fibrin clearance in the absence of Plg?42

Behe cited this very paper, so we must assume that he, too, knows that parts of his clotting-cascade are redundantly complex. In this case, healing delayed is not healing denied!


41. See Behe, “Self-Organization and Irreducible Complexity,” 161.

42. See Bugge, et al. “Loss of Fibrogen Rescues Mice,” 717.

...Bugge et al. rides again!  (This was a paper which Doolittle misread, or at least oversimplified, in his Boston review article, which gave Behe an opportunity to dodge the real issue, namely how Doolittle has been able to predict the presence of blood-clotting proteins in various species (with simpler systems, no less) unless Doolittle's model for the evolution of blood-clotting has significant validity.)

Brief commentary on Shanks & Joplin: while they have introduced the useful notion of "redundant complexity", and in the above 2001 Philo paper have tied the concept to the "scaffolding" model for the origin of IC (i.e., reduce redundancy and you end up with IC), I don't think that they have a general solution to the origin of IC unless they incorporate cooption/change of function into their analysis.  I can only think of a few examples where "loss of scaffolding" explains the origin of an IC system, but many where cooption of a part/system to a new function explains it.  Perhaps more importantly, the processes are not mutually exclusive and so in some cases both processes might operate in succession.


Date: 2002/05/26 00:55:42, Link
Author: niiicholas
Ooh, another great opportunity for collaboration.  This is a huge topic with a lot of literature, so unless one happens to be a biochemist who did their PhD. on the topic it is hard for one person to scrape together the diverse information & references that are necessary to explain the problems with Paul Nelson's pseudoargument to the public.  I think Ken Miller's replies had some difficulty in this regard (and I don't even recall the statement "universal genetic code" being in the actual Evolution series -- is this just me missing it or is it actually there?)

The most complete presentation of Nelson v. common descent that I can recall was a longish talk that I recall listening to online -- but I can't find it at the moment.  Is there a good online essay where Paul Nelson actually lays out the argument from "the genetic code isn't quite universal" to the conclusion "common descent is false [to some unspecified degree]"?

Anyhow, Nelson's argument went like this:

- the code was thought to be universal, and this was crowning evidence for common descent because the code couldn't change because intermediate stages are fatal so it must have come from a common ancestor

[actually, it was just one of many pieces of evidence, but whatever]

- but it's not quite universal, therefore either:

(a) the code can change after all
(b) common descent is false

- Nelson doesn't like (a), citing a (single) paper that criticizes another (single) scientist's proposal about how a codon assignment could change.

- therefore evolutionists are dogmatically clinging to an auxilliary hypothesis that is shielding their main theory from rigorous testing.

I'm sure I'm oversimplifying, I heard the talk last year, but that's basically it.

However, I recall doing some digging on these arguments for an ARN post or two, I will see if I can find them...

Hmm, as usual the ARN UBB search engine is proving useless.  Well, here's some general points regarding "deviant/noncanonical genetic codes":

(1) Deviant genetic codes are most common in critters/organelles with small or otherwise weird genomes, e.g. ciliates (which Nelson specifically mentions IIRC):


Pubmed link

The molecular basis of nuclear genetic code change in ciliates

Quote: "Most changes in the genetic code involve termination: this may be because stop codons are rare, occurring only once per gene, and so changes in termination are likely to be less deleterious than change in sense codons. This would be particularly true for those species of ciliates whose genes reside on gene-sized chromosomes and/or have short 3' untranslated regions. In addition, termination is a competition for stop-codon-containing ribosomal A sites between release factors and tRNAs. Consequently, relatively small changes either in the tRNAs or in eRF1 may shift this balance toward partial or complete readthrough in some cases. For instance, Bacillus subtilis uses in-frame UGA codons extensively to encode tryptophan; however, this readthrough is inefficient, and UGA is also used as a stop codon [33, 34] . The abundance of stop codon reassignments relative to amino acid codon reassignment, however, could also be an observer bias. In-frame stop codons are much easier to detect in protein coding sequences than amino acid replacements, especially if the latter have similar properties."

(2) Some organisms, extant today, have ambiguous codon assignments (i.e. one codon codes for both an amino acid and 'stop' at the same time, proving that this is not necessarily a fatal situation, contra Paul Nelson.

[I've seen this stated in an article somewheres, if anyone else finds examples they might post them.  They pretty clearly refute the "transitional stages impossible" contention.]

(3) Deciding whether or not the code is optimal, how optimal, and how much a potential "frozen accident" is by no means a simple question as Nelson seems to assume.

The below paper argues for optimality in at least one sense, but note the back-and-forth, and how what constitutes "optimal" may be different for different organisms at different times (& which may thus result in the evolution of code deviants).


Pubmed link -- free online BTW

Mol Biol Evol 2000 Apr;17(4):511-8

Early fixation of an optimal genetic code.

Freeland SJ, Knight RD, Landweber LF, Hurst LD.

Department of Ecology, Princeton University, University of Bath, Bath, England.

The evolutionary forces that produced the canonical genetic code before the last universal ancestor remain obscure. One hypothesis is that the arrangement of amino acid/codon assignments results from selection to minimize the effects of errors (e.g., mistranslation and mutation) on resulting proteins. If amino acid similarity is measured as polarity, the canonical code does indeed outperform most theoretical alternatives. However, this finding does not hold for other amino acid properties, ignores plausible restrictions on possible code structure, and does not address the naturally occurring nonstandard genetic codes. Finally, other analyses have shown that significantly better code structures are possible. Here, we show that if theoretically possible code structures are limited to reflect plausible biological constraints, and amino acid similarity is quantified using empirical data of substitution frequencies, the canonical code is at or very close to a global optimum for error minimization across plausible parameter space. This result is robust to variation in the methods and assumptions of the analysis. Although significantly better codes do exist under some assumptions, they are extremely rare and thus consistent with reports of an adaptive code: previous analyses which suggest otherwise derive from a misleading metric. However, all extant, naturally occurring, secondarily derived, nonstandard genetic codes do appear less adaptive. The arrangement of amino acid assignments to the codons of the standard genetic code appears to be a direct product of natural selection for a system that minimizes the phenotypic impact of genetic error. Potential criticisms of previous analyses appear to be without substance. That known variants of the standard genetic code appear less adaptive suggests that different evolutionary factors predominated before and after fixation of the canonical code. While the evidence for an adaptive code is clear, the process by which the code achieved this optimization requires further attention.

...and also note the rather unambiguous first sentence of the introduction of this article:


All known nonstandard genetic codes appear to be secondarily derived minor modifications of the canonical code (Osawa 1995).

Here is their conclusion FYI:


The Mechanism of Adaptive Code Evolution

This leads to the question of the evolutionary mechanisms responsible for an adaptive canonical code. The many models of precanonical code evolution, reviewed extensively elsewhere (Knight, Freeland, and Landweber 1999 ), permit two major possibilities: that an adaptive code was selected from a large pool of variants, or that an adaptive code arose de novo by code expansion (or simplification) within adaptive, error-minimizing constraints. Individual codon reassignments, necessary for adaptive code shuffling, are certainly possible, but the question remains unresolved, and two lines of evidence increasingly favor the latter explanation.

First, the notion of code expansion from a simpler primordial form, although still lacking in detail, is now associated with a diverse body of empirical and phylogenetic evidence (Knight, Freeland, and Landweber 1999 ). It seems unlikely that clear patterns of biosynthetic relatedness would be found in a code which had undergone extensive codon assignment shuffling. Additionally, while adaptive code structure is unlikely to be an artifact of a stereochemically determined code, empirical evidence suggests that stereochemistry is not without a role. For example, RNA molecules artificially selected to bind Arginine contain disproportionately many CGN/AGR codons (Knight and Landweber 1998 ). If all or most amino acids show stereochemical affinities for their corresponding codons, this would suggest that natural selection worked in concert with stereochemical interactions and biosynthetic expansion to produce the canonical code de novo, "choosing" the current 20 amino acids as those that satisfied criteria for both stereochemical affinity and error minimization. This interpretation would thus offer a novel insight into the selection of the proteinaceous amino acids from the near-infinite possibilities of both prebiotic syntheses and biosynthetic modification.


We have presented comprehensive evidence that the standard genetic code is a product of natural selection to minimize the phenotypic impact of genetic error; the arrangement of codon assignments meets, to an extraordinary degree, the predictions of the adaptive hypothesis and cannot be explained as an artifact of stereochemistry, biosynthetically mediated code expansion, or analytical methodology. However, the process by which an adaptive code evolved at present remains unclear, and yet its resolution may be of key importance to our understanding of the amino acid components universal to life.

This is the Osawa reference which looks to be key:

Osawa, S. 1995. The evolution of the genetic code. Oxford University Press, Oxford, England.

Anyhow, as usual when one begins to investigate the actual biology of an ID argument, one finds that the IDists are taking a thoroughly myopic view instead of looking at the broad range of evidence that is necessary.

Thanks, nic

Date: 2002/05/28 15:10:09, Link
Author: niiicholas
I came across a new article on the evolution of photosynthesis; there are a number of articles on this topic, I will post them as I rediscover them, others may have come across interesting stuff also.


Reaction centres: the structure and evolution of biological solar power
Peter Heathcote b, Paul K. Fyfe a and Michael R. Jones a
Trends in Biochemical Sciences 2002, 27:79-87


Reaction centres are complexes of pigment and protein that convert the electromagnetic energy of sunlight into chemical potential energy. They are found in plants, algae and a variety of bacterial species, and vary greatly in their composition and complexity. New structural information has highlighted features that are common to the different types of reaction centre and has provided insights into some of the key differences between reaction centres from different sources. New ideas have also emerged on how contemporary reaction centres might have evolved and on the possible origin of the first chlorophyll–protein complexes to harness the power of sunlight.

[...I'll quote the last part of the review to give a sense of where things are at...]

Common structural blueprint

The crystallographic information summarized in Fig. 4 highlights structural features that are common to all types of reaction centre [3,10,25] . At the heart of each complex is a core domain consisting of an arrangement of two sets of five transmembrane  helices. This protein scaffold encases six (bacterio)chlorin and two quinone cofactors that are arranged in two pseudosymmetric membrane-spanning branches. These cofactors catalyse the photochemical transmembrane electron transfer reaction that is the key to the photosynthetic process. Added to this basic structural blueprint are a variety of protein–cofactor structures, such as antenna complexes, the oxygen-evolving complex or Fe–S centres, which represent further adaptations. In particular, in the PSII reaction centre and all known Type I reaction centres, the core electron transfer domain is flanked by two homologous antenna domains, each consisting of a bundle of six membrane-spanning  helices binding antenna pigments [24], and antenna chlorophylls are also bound to the ten-helix core ( Fig. 4). These antenna domains are not present in purple bacteria such as Rhodobacter sphaeroides or green filamentous bacteria such as Chloroflexus.

Which is the oldest reaction centre?

The realization that all reaction centres are based on a common design has provoked much discussion over the evolutionary links between the different complexes and the nature of the ancestral reaction centre. This is a challenging topic because it is clear that chlorophyll-based photosynthesis is a very old process that appeared during the first few hundred million years of evolution [38]. One approach to this problem has been to examine which of the five distinct groups of photosynthetic bacteria represents the oldest photosynthetic lineage, through phylogenetic studies of both photosynthetic and non-photosynthetic proteins. However, such studies have produced conflicting results, with green filamentous bacteria, heliobacteria and purple bacteria all being identified as the oldest lineage in different studies [39–42] . The problem of tracing the evolutionary development of modern day photosystems is not helped by some of the variety and complexity exhibited by photosynthetic organisms, which indicates some interchange of photosynthetic components by lateral gene transfer between groups during the course of evolution [41,43] . At present, it is probably prudent to conclude that the use of this approach requires additional data and a more extensive analysis.

Primordial reaction centre: Type I, Type II or both?

Setting aside the question of which is the oldest photosynthetic organism, several models have been proposed to account for the development of modern day reaction centres from simpler ancestors [41]. Most recently, a new evolutionary scheme for contemporary reaction centres has been proposed that envisages the ancestral reaction centre as homodimeric, with the three-domain antenna–core–antenna organization seen in extant Type I complexes [37]. It is proposed that this ancestral reaction centre had two membrane-spanning electron transfer chains, each terminating in a loosely bound quinone that could dissociate when reduced and move into the membrane pool, and that it occupied a membrane that had already developed a fully functional anaerobic respiratory chain, in accordance with the 'respiration early' hypothesis [44]. Therefore, the ancestral reaction centre proposed had a mixed character, with the three-domain organization and (possibly) symmetric electron transfer characteristic of contemporary Type I reaction centres but a capacity to reduce the intramembrane quinone pool, as seen in contemporary Type II reaction centres [37].

The future ... and the dim, distant past

The increasingly detailed crystallographic information now available for the cyanobacterial Type I and Type II reaction centres is provoking renewed interest in the detailed mechanism of these elegant transducers of energy. In particular, the first crystallographic glimpses of the machinery for oxygen evolution are both intriguing and exciting, and will trigger much re-evaluation of our current understanding of a reaction that is of obvious importance to aerobes such as ourselves. It is also becoming apparent that a detailed understanding of quinone chemistry of the homodimeric reaction centres from heliobacteria and green sulfur bacteria might help to focus ideas about the nature of the ancestral reaction centre and the evolutionary route that has led to contemporary complexes.

Finally, peering even further back in evolutionary time, an intriguing question that remains relatively unexplored concerns the origins of the ancestral reaction centre. What was the function of this (bacterio)chlorophyll-containing membrane protein before it evolved into a system capable of harnessing light energy? One suggestion is that early organisms used pigment–protein complexes to protect themselves against the ultraviolet (UV) radiation that bathed the surface of the planet before the development of the atmospheric ozone layer [45]. Such proteins might originally have operated by absorbing high-energy UV photons and dissipating the energy through internal conversion between the (bacterio)chlorophyll Soret absorbance transition and the visible-region absorbance bands, before emitting the energy as a much more benign visible or near-infrared photon [45]. Light-activated electron transfer might originally have developed as an extension to this photoprotective function, excited state energy being converted first into the energy of a charge separated state (similar to the P870+HA- state formed in the purple bacterial reaction centre) and subsequently lost as heat as the charge-separated state recombines (as occurs in purple bacterial reaction centres when forward electron transfer from HA- is blocked). Another suggestion is that photosynthetic function evolved from bacteriochlorophyll-containing proteins involved in infrared thermotaxis [46]. Whatever the truth, addressing these questions requires a journey back to an early stage in the evolution of life, and presents a fascinating challenge.

[37] Baymann F. et al. (2001) Daddy, where did PS(I) come from?
Biochim. Biophys. Acta, 1507:291-310. MEDLINE Cited by

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Date: 2002/05/29 23:30:40, Link
Author: niiicholas

This would seem to be as good a place as any to collect links/references to things like Johnson's

- works
- reviews of his works
- interviews
- online talks

...etc.  I think there is already at least one fairly comprehensive PJ links page on the web so maybe we could just 'high-grade' particularly interesting things here.

E.g., I started this thread because I just heard about this link:

Berkeley’s Radical
An Interview with Phillip E. Johnson

Johnson bares his soul & gives quite a detailed history of his own 'evolution'.


You have said there is no natural explanation for the rise of genetic information. How important is that question in the debate?

PJ: The Wedge of Truth is all about those issues. The scientific key is, "No natural processes create genetic information." As soon as we get that out, there’s only one way the debate can go because Darwinists aren’t going to come up with a mechanism. They’ll start out talking about the peppered moth, and when that self-destructs, then they’ll say, "Oh, self-organizing systems, or the fourth law of thermodynamics," and other nonsense, which is just covering up ignorance.

Genetic information is the issue, but it isn’t the final issue. After you make that breakthrough, then you see other ways in which the theory is questionable. Darwinists will say, "Oh, well, maybe the mechanism has some problems, but the "fact of evolution"—common ancestry—is not in question. We distinguish the fact of evolution from the mechanism of evolution."

But that’s a bogus distinction because the "fact"—common ancestry—incorporates the mechanism. It’s just a matter of "now you see it, now you don’t." They are saying the mechanism by which a father and mother give birth to children is the same mechanism by which our "bacterial ancestors" gave birth to human beings. They say it’s all a process of natural reproduction and naturally occurring variation in the offspring.

Biologists affiliated with the Intelligent Design movement nail down the distinction by showing that DNA mutations do not create evolution in any significant sense. Instead, they make birth defects, so the whole thing is false from the get-go. There is no way you can establish that a bacterium is the parent of a complex animal. There is no mechanism to make the change, no historical or fossil evidence that such a change ever occurred, and there’s no way to duplicate the process in a lab.

Once you get that in the debate, then we will be poised for a metaphysical and intellectual reversal that is every bit as profound as the one with Copernicus. People will say, "My gosh, we’ve been completely misled by this fundamental truth of the creation story of our culture. We can no longer understand the world that way."

How do you change the way people regard the authority of science? Get them to think of it as a much more limited thing. Science is very reliable when scientists stick to the kinds of things that can be tested by refutable experiments, but much of what they tell us is outside that. When they have to fake the mechanisms, it becomes a very dubious philosophy. That raises the question of why so many very brilliant people were misled for so long and did such a good job of rationalizing these things.

When the mechanism of Darwinism becomes discredited, it’s like a train that’s been turned around. You can say, "Well, that’s interesting, but the train is still in the same place. The world, Yale, Berkeley, are still there. The New York Times is still telling us what to think. So why isn’t everything different?" Well, it is different, but you can’t see it yet. The train is turned in the opposite direction. It’s going to start out very slowly, but it’s moving on the logical tracks towards something very different, and when we get there, our great-great-grand-children will see how different things are.

Not a man with small goals, PJ.

Note also the "scientific key" to the whole ID argument (according to Johnson): "No natural processes create genetic information."  Hmm.  I think I'll start a thread.


Date: 2002/05/30 00:02:55, Link
Author: niiicholas

While reading this interview with Phil Johnson, leader of the ID movement:

Berkeley’s Radical
An Interview with Phillip E. Johnson

...I was struck by this section:


You have said there is no natural explanation for the rise of genetic information. How important is that question in the debate?

PJ: The Wedge of Truth is all about those issues. The scientific key is, "No natural processes create genetic information." As soon as we get that out, there’s only one way the debate can go because Darwinists aren’t going to come up with a mechanism. They’ll start out talking about the peppered moth, and when that self-destructs, then they’ll say, "Oh, self-organizing systems, or the fourth law of thermodynamics," and other nonsense, which is just covering up ignorance.

Genetic information is the issue, but it isn’t the final issue. After you make that breakthrough, then you see other ways in which the theory is questionable. Darwinists will say, "Oh, well, maybe the mechanism has some problems, but the "fact of evolution"—common ancestry—is not in question. We distinguish the fact of evolution from the mechanism of evolution."

But that’s a bogus distinction because the "fact"—common ancestry—incorporates the mechanism. It’s just a matter of "now you see it, now you don’t." They are saying the mechanism by which a father and mother give birth to children is the same mechanism by which our "bacterial ancestors" gave birth to human beings. They say it’s all a process of natural reproduction and naturally occurring variation in the offspring.

Biologists affiliated with the Intelligent Design movement nail down the distinction by showing that DNA mutations do not create evolution in any significant sense. Instead, they make birth defects, so the whole thing is false from the get-go. There is no way you can establish that a bacterium is the parent of a complex animal. There is no mechanism to make the change, no historical or fossil evidence that such a change ever occurred, and there’s no way to duplicate the process in a lab.

Once you get that in the debate, then we will be poised for a metaphysical and intellectual reversal that is every bit as profound as the one with Copernicus. People will say, "My gosh, we’ve been completely misled by this fundamental truth of the creation story of our culture. We can no longer understand the world that way."

How do you change the way people regard the authority of science? Get them to think of it as a much more limited thing. Science is very reliable when scientists stick to the kinds of things that can be tested by refutable experiments, but much of what they tell us is outside that. When they have to fake the mechanisms, it becomes a very dubious philosophy. That raises the question of why so many very brilliant people were misled for so long and did such a good job of rationalizing these things.

When the mechanism of Darwinism becomes discredited, it’s like a train that’s been turned around. You can say, "Well, that’s interesting, but the train is still in the same place. The world, Yale, Berkeley, are still there. The New York Times is still telling us what to think. So why isn’t everything different?" Well, it is different, but you can’t see it yet. The train is turned in the opposite direction. It’s going to start out very slowly, but it’s moving on the logical tracks towards something very different, and when we get there, our great-great-grand-children will see how different things are.

Note that the "scientific key" to the whole ID argument (according to Johnson) is this: "No natural processes create genetic information."  

This strikes me as easily and trivially refutable by numerous examples.  Anything that starts with genetic information amount X, and ends up with genetic information amount X+Y, should qualify.  The classic case would be X=information in a genome before a gene duplicates & diverges under selection, and X+Y being the information in the genome after this has occurred.

Another less-often considered example should be (IMO) when a mutation (let's say "beneficial to at least part of the population" to avoid the obvious objection) arises in a *population*.  Here,

X=information in the genomes of a population
Y=information in the beneficial mutation

I realize that "information" has no single definition in biology, one could also argue that "new information" would arise through novel combinations of alleles, etc.  For the purposes of this thread, I suggest the following working definition:

Genetic information=functional DNA that encodes useful/beneficial proteins or regulatory sequences this is what the IDers mean by "genetic information" (except of course when they are challenged on the topic, wherein they promptly begin the obfuscation and goal-post moving, rather like eternally elusive creationist definition of "kind").

So, let's use this thread to accumulate examples of natural processes increasing "genetic information" in the above-described sense.  Other things that might be relevant, e.g. studies of the increase of Shannon information in selective algorithms, could also be posted, just note the form of information as relevant.


PS: I'll start off with one of my favorite examples:

Sdic, sperm dynein intermediate chain, a new gene which evolved over the past few million years by the duplication, fusion, and modification of two genes that are now on each side of Sdic on the chromosome.

Here is a brief introduction from Ian Musgrave:


My second favorite example is the Sdic gene, where the annexin and dynenin intermediate chain genes were duplicated in tandem, then the intervening sequences deleted to form a single new gene, (the Sperm specific dynenin intermediate chain gene Sdic). The good thing about this example is that a previously non-coding part of the sequence became the protein coding sequence, and the protein coding sequence has a non-coding role.

Capy P. (1998 Dec 10). Evolutionary biology. A plastic genome [news; comment] Nature, 396, 522-3.

Nurminsky DI, Nurminskaya MV, De Aguiar D, and Hartl DL. (1998 Dec 10). Selective sweep of a newly evolved sperm-specific gene in Drosophila [see comments] Nature, 396, 572-5.

Here is the Nurminsky et al. 1998 article:


pubmed link

Nature 1998 Dec 10;396(6711):572-5

Selective sweep of a newly evolved sperm-specific gene in Drosophila.

Nurminsky DI, Nurminskaya MV, De Aguiar D, Hartl DL.

Harvard University, Department of Organismic & Evolutionary Biology, Cambridge, Massachusetts 02138, USA.

The pattern of genetic variation across the genome of Drosophila melanogaster is consistent with the occurrence of frequent 'selective sweeps', in which new favourable mutations become incorporated into the species so quickly that linked alleles can 'hitchhike' and also become fixed. Because of the hitchhiking of linked genes, it is generally difficult to identify the target of any putative selective sweep. Here, however, we identify a new gene in D. melanogaster that codes for a sperm-specific axonemal dynein subunit. The gene has a new testes-specific promoter derived from a protein-coding region in a gene encoding the cell-adhesion protein annexin X (AnnX), and it contains a new protein-coding exon derived from an intron in a gene encoding a cytoplasmic dynein intermediate chain (Cdic). The new transcription unit, designated Sdic (for sperm-specific dynein intermediate chain), has been duplicated about tenfold in a tandem array. Consistent with the selective sweep of this gene, the level of genetic polymorphism near Sdic is unusually low. The discovery of this gene supports other results that point to the rapid molecular evolution of male reproductive functions.

Since then, this article has been published:


Pubmed link

Nurminsky D, Aguiar DD, Bustamante CD, Hartl DL.
Chromosomal effects of rapid gene evolution in Drosophila melanogaster.
Science. 2001 Jan 5;291(5501):128-30.

Rapid adaptive fixation of a new favorable mutation is expected to affect neighboring genes along the chromosome. Evolutionary theory predicts that the chromosomal region would show a reduced level of genetic variation and an excess of rare alleles. We have confirmed these predictions in a region of the X chromosome of Drosophila melanogaster that contains a newly evolved gene for a component of the sperm axoneme. In D. simulans, where the novel gene does not exist, the pattern of genetic variation is consistent with selection against recurrent deleterious mutations. These findings imply that the pattern of genetic variation along a chromosome may be useful for inferring its evolutionary history and for revealing regions in which recent adaptive fixations have taken place.

This article is a good review of the general topic of the evolution of new genes:


pubmed link

Curr Opin Genet Dev 2001 Dec;11(6):673-80

Evolution of novel genes.

Long M.

Department of Ecology and Evolution, The University of Chicago, 1101 East 57th Street, Chicago Illinois 60637, USA.

Much progress in understanding the evolution of new genes has been accomplished in the past few years. Molecular mechanisms such as illegitimate recombination and LINE element mediated 3' transduction underlying exon shuffling, a major process for generating new genes, are better understood. The identification of young genes in invertebrates and vertebrates has revealed a significant role of adaptive evolution acting on initially rudimentary gene structures created as if by evolutionary tinkers. New genes in humans and our primate relatives add a new component to the understanding of genetic divergence between humans and non-humans.

Have fun,

Date: 2002/05/30 00:51:24, Link
Author: niiicholas
Here is a whole double issue of JME with a large group of articles devoted to evolution-of-genetic-code issues:

Volume 53 - Number 4/5, 2001


Lluís Ribas de Pouplana, James R. Brown, Paul Schimmel
Structure-Based Phylogeny of Class IIa tRNA Synthetases in Relation to an Unusual Biochemistry
Article in: PDF | HTML-Frames

David H. Ardell, Guy Sella
On the Evolution of Redundancy in Genetic Codes
Article in: PDF | HTML-Frames

Yoshikazu Nakamura
Molecular Mimicry Between Protein and tRNA
Article in: PDF | HTML-Frames

Shigehiko Kanaya, Yuko Yamada, Makoto Kinouchi, Yoshihiro Kudo, Toshimichi Ikemura
Codon Usage and tRNA Genes in Eukaryotes: Correlation of Codon Usage Diversity with Translation Efficiency and with CG-Dinucleotide Usage as Assessed by Multivariate Analysis
Article in: PDF | HTML-Frames

Robin D. Knight, Laura F. Landweber, Michael Yarus
How Mitochondria Redefine the Code
Article in: PDF | HTML-Frames

Shin-ichi Yokobori, Tsutomu Suzuki, Kimitsuna Watanabe
Genetic Code Variations in Mitochondria: tRNA as a Major Determinant of Genetic Code Plasticity
Article in: PDF | HTML-Frames

Funny that Paul Nelson's views were not included, eh?

I just received a good private message on this topic from a new poster & I encouraged him to post it in the general discussion, I'll then post a link to it from this thread.


Date: 2002/05/30 01:14:38, Link
Author: niiicholas
One more article.

Here's the short version of the case as I now understand it.

- In the beginning, scientists thought the genetic code was universal (maybe; this is the standard line, whether all relevant experts also assumed this initially seems to me to be uncertain, at least I've not seen any analysis of the topic).

- in the 1980's it was documented that this was not the case

- In the late 1980's Osawa proposed the "codon disappearence" theory for the evolution of code changes, described in the Schultz & Yarus (1996) article referenced below thusly:


Codon reassignment to new amino acids within large, complex, relatively modern genomes (Osawa et al. 1992) poses interesting mechanistic problems. Osawa and Jukes have proposed (1989), and reaffirm in recent publications (1992; Osawa and Jukes 1995), that during codon reassignment every example of a codon in an entire genome must mutate or otherwise disappear as a result of mutational change in genomic GC content. Subsequent to its total disappearance, a codon can be captured by, e.g., an anticodon mutation in a dispensable tRNA, thereby reappearing with a new identity. We will call this the ``codon disappearance'' theory, after its characteristic intermediate state.

- In the mid-1990's another theory was proposed, apparently right in Schultz & Yarus' 1996 article:


We find the absolute disappearance of hundreds, thousands, or tens of thousands of examples of a codon by mutation pressure alone, in diverse independent cases, an improbable evolutionary scenario. Total disappearance should be an extremely slow occurrence, because mutation pressure and genetic drift in large populations are among the weakest evolutionary forces, producing only very slow changes in genomic composition. Furthermore, back mutation increases in effectiveness as the goal is approached because of the accumulation of codons related to the disappearing codon by single mutation. Finally, complete disappearance of codons in eukaryotes would be hindered by coherent areas of varied GC content along chromosomes (Sharp and Lloyd 1993; Ikemura and Wada 1991). Because codon choice follows GC content, such areas can provide sheltered enclaves for particular codons (Santos and Tuite 1995).

Though total disappearance is difficult to prove, mutation pressure certainly causes codon frequencies to change. Evolution to very low frequencies and inefficient translational function is well supported (e.g., Kano et al. 1993). But we argue that mutation and drift in codon frequency over entire genomes are vulnerable to being overtaken by faster evolutionary processes such as selection. Thus the question: Are there plausible faster processes, perhaps selection-driven processes, for codon reassignment?

Schultz and Yarus characterized a nonanticodon tRNA site (1994a,b) where particular nucleotide sequences allow a tRNA to read an unusual near-cognate codon. More generally, several sites are known where single mutations in nonanticodon nucleotides (reviewed in Yarus and Smith 1995) enhance tRNA ability to read (at least) two codons, (at least) one of which is forbidden by normal base-pairing and wobble rules. Schultz and Yarus suggested (1994c) that such equivocal adapters could catalyze codon reassignment for one of the codons being ambiguously read. (For clarity in what follows, a codon read in more than one way is said to be ``ambiguous''; a tRNA which reads normal codons as well as codons not normally assigned is said to be ``equivocal.'';) In the particular case in which reassignment is initiated by a mutation that impairs normal translation of a codon, reassignment via an equivocal adapter tRNA might evolve quickly by selection for improved translation of the newly ambiguous codon. Transitional coding ambiguity could finally be resolved by, for example, loss or mutation of the original tRNA, and anticodon mutation to equivocal complementarity in the new (equivocal) tRNA, so that the amino acid of the previously equivocal tRNA is reassigned. We will call this the ``ambiguous intermediate'' theory.

Here is the reference, and some of Schultz & Yarus' (1996) lines of evidence for the ambiguous intermediate theory:


JME link
J Mol Evol 1996 May;42(5):597-601

On malleability in the genetic code.

Schultz DW, Yarus M.

To explain now-numerous cases of codon reassignment (departure from the "universal" code), we suggest a pathway in which the transformed codon is temporarily ambiguous. All the unusual tRNA activities required have been demonstrated. In addition, the repetitive use of certain reassignments, the phylogenetic distribution of reassignments, and the properties of present-day reassinged tRNAs are each consistent with evolution of the code via an ambiguous translational intermediate.


Firstly: at the heart of our proposal lies the supposition that codons are read ambiguously by two tRNAs (or a tRNA and an RF, in the case of terminators), specifying insertion of more than one amino acid (or an amino acid as well as stop). In contrast, the assumption that codons vanish before reassignment, which is characteristic of codon disappearance theory, is mandated by the assertion that codons cannot have two meanings.

In strict form, this axiom of nonambiguity contradicts chemical principle. An infinite free energy difference between reaction pathways is required to select one reactant and reject another absolutely. The strict absence of ambiguity is also contradicted by experiment. Cumulative missense translation in normal E. coli has been estimated at 4 × 10-4 per codon (Ellis and Gallant 1982). Total miscoding per peptide chain is the much larger sum over the hundreds of codons in the protein. Therefore an appreciable basal ambiguity (yielding ~ 10% of the average 250-amino-acid protein with a variant sequence) is evident, and tolerated, in wild-type cells.

Further, cells are unharmed even when this substantial basal ambiguity is increased dramatically. We have constructed strains containing equivocal E. coli tRNAs that demonstrate suppressor efficiencies of 50 to nearly 100%, making a stop codon ambiguous (Schultz and Yarus 1994a,b). Ribosomal ambiguity mutations (RAM) increase misreading of stop codons up to 100-fold in cells that remain viable (Strigini and Brickman 1973; Andersson et al. 1982). Most specifically, the general error frequency can be increased 13-fold (using 5 µg/ml streptomycin) and cells continue to grow exponentially at a rate close to controls. After more than 400 generations in streptomycin, there is no detectable decrease in cellular viability (Gallant and Palmer 1979). Thus ambiguity at a variety of codons (to >=1 error in the average 250-amino-acid protein) is well tolerated, or has no apparent phenotype. The limited ambiguity we posit as the initiating event in codon reassignment, occurring at one (or a few) codon(s) and perhaps initially quantitatively small, seems quite plausible in this context.

Nor is coding ambiguity limited to prokaryotes. Eukaryotes have basal levels of coding ambiguity which are probably similar to prokaryotes (Gallant and Palmer 1979). Normal yeast glutamine tRNAs are known to read equivocally at the first codon position (Weiss and Friedberg 1986; Edelman and Culbertson 1991). Similar ambiguities can be exploited for an organism's own purposes, as when animal and plant viruses purposefully use ambiguous stop condons to adjust the level of stop readthrough to an essential gene product. This misreading by a wild-type tRNA is known to approach 5% at stop codons within a special mRNA context (Skuzeski et al. 1991; Feng et al. 1990). Thus, during codon reassignment there seems to be no reason that all codons must invariably be read without ambiguity.

[note here that ambiguity is not exactly vanishingly rare and therefore the assumption that intermediates would be nonviable is false]

Secondly: There is no definite direction to reassignment in codon disappearance theory; dispensable RNA genes may capture unassigned codon by, e.g., random single base changes in their anticodons (Osawa and Jukes, 1989). However, we first argue that known reassignments (Table 1) are very nonrandom. We then argue the nonrandomness supports ambiguous intermediate theory because it is explicable by types of equivocal reading already demonstrated in tRNAs.


However, 14 of 14 single-nucleotide reassignments in Table 1 parallel the activities of known equivocal tRNAs. That is, all 14 changes might be mediated by tRNAs reading a single base equivocally, using G-U (anticodon-codon) wobble at the first position, or C-A or G-A mispairing at the third codon position. Equivocal C-A third-position mispairing has long been known from study of tRNA opal (UGA) suppressors (Hirsh 1971). We recently constructed two new tRNAs that demonstrate in vivo the required equivocal G-U and C-A readings (Schultz and Yarus 1994b), thereby potentially accounting for ten assignments (Table 1). This congruence, in fact, first drew our attention to the possibility that tRNAs might mediate codon reassignment. The remaining exceptional wobble, transitional G-A pairing at the third position, has also been detected in the equivocal tRNA repertoire in vitro, using cytoplasmic and chloroplast tRNA Cys (Nicotiana) as UGA suppressors (Urban & Beier, 1995). The remaining 15th case requires a more unusual first/second-position double miscoding. However, the Candida albicans tRNA translating the reassigned CUG codon has been independently shown to be capable of a similar doubly equivocal coding (Santos et al. 1993; see below). Thus 15 of 15 known reassignments can be matched with known tRNA capabilities.

Thirdly: Phylogenetic distribution of reassignment is consistent with ambiguous intermediates. Tourancheau et al. (1995) have made the initially surprising observation that UAA/UAG in ciliates have been reassigned to glutamine at least three times independently (on the basis of the rRNA tree), instead of depending on a common ancestral reassignment. This striking phylogenetic cluster of identical but independent reassignments has no apparent explanation in the codon disappearance scheme. However, such a cluster is easily explained within the ambiguous intermediate mechanism by a tendency to equivocal reading of these codons inherited from an ancestor. Such an ambiguity might be conserved within a group of species if used for an important regulatory event like stop codon readthrough. These authors also found no correlation between GC content of the ciliates and reassignment, which might have been expected if evolutionary change in GC content drives the process.

Fourthly: Molecular fossil and functional evidence of translational ambiguity accompanies known cases of reassignment. We have previously pointed out that sequenced tRNAs that have captured new codons, such as the UAA and UAG reading tRNAs from the ciliate Tetrahymena thermophila (Hanyu et al. 1986), contain unusual nucleotide sequences that we have identified as enhancers of equivocal coding in E. coli (Schultz and Yarus 1994c). Thus the structure of these three related isoaccepting tRNAGln sequences suggests the existence of an ancestor that coded equivocally.


In summary: We acknowledge the significance of codon reassignment, and do not argue against change in GC content as a significant evolutionary event (e.g., Sueoka, 1993). But we do argue that codon reassignment is unlikely to be carried out entirely by the slow processes of mutation pressure and drift. Additionally, the axiom of nonambiguity fundamental to codon disappearance theory is not justified. The evident nonrandomness of known reassignments, the clustering of similar changes in phylogeny, and the properties of reassigned tRNAs, where known, are strikingly consistent with ambiguously translating intermediates. These phenomena are unexpected or contradictory to codon disappearance theory, acting in isolation.

In this connection, there is no logical incompatibility between mutational change in GC content and ambiguous intermediates. Schultz and Yarus (1994c) have noted that these may occur together. In fact, a codon which has become rare might also be expected to evolve a rare cognate tRNA. Such a rare tRNA would be more vulnerable than usual to competition during translation, including competition from an equivocal adaptor translating its codon. Thus not only might mutation pressure be overtaken by faster selection, but the initial effects of mutation pressure might facilitate the overtaking mechanism. Quantitative modeling of this process might prove rewarding.

Finally: if ambiguous intermediate theory gives a good account of modern coding changes, it thereby becomes a preferred route by which a limited ancestral code could have been transformed to the present ``universal'' genetic code. In fact, coding transitions via ambiguous intermediates would likely be easier during the formation of the code than today.

Other aspects of ambiguous intermediate and codon disappearance schemes can be compared in the previous note by Osawa and Jukes (1995), and in Schultz and Yarus (1994c), to which the interested reader is directed for references and details which do not appear here.

Date: 2002/05/30 01:49:29, Link
Author: niiicholas
Reviewing this 1993 article by Paul Nelson and Jonathan Wells:


Is Common Descent an Axiom of Biology?

[Editorial note:  The following discussion paper was written for the conference, “The Darwinian Paradigm: Problems and Prospects,” held June 22-25, 1993, at the Pajaro Dunes beach community on Monterey Bay, near Watsonville, California.  The conference was organized by Phillip Johnson.  Attendees included Michael Behe, Walter Bradley, John Angus Campbell, William Dembski, Dean Kenyon, Stephen Meyer, Paul Nelson, David Raup, Siegfried Scherer, Jonathan Wells, and Kurt Wise.]


To:                  Pajaro Dunes Conference Participants
From:              Paul Nelson and Jonathan Wells
Date:               15 June 1993
Re:                  Discussion paper for Topic Area I (homology, etc.)

...and skipping to the genetic code section, we find that Nelson & Wells are indeed assuming that the "functional invariance" thesis was dropped, without evidence, to protect common descent:


The Universal Genetic Code Argument for Common Descent

Lest it be thought that this pattern of reasoning – namely, sacrificing the auxiliary theory to save common descent – is an isolated example, we offer another, perhaps more striking case.

Most of us are familiar with the universal genetic code argument for common descent.  The argument first appeared in the mid to late 1960s, after the structure of the code was elucidated.  It is now widespread.[33]

[they quote several quotes to this effect]

...and then, they argue that "functional invariance" is highly probable and therefore scientists are unjustifiably dropping the "functional invariance theory" to protect common descent:


Postulating that such fundamental variations occurred is, however, very far from knowing how they occurred. "Direct replacements of one amino acid by another throughout proteins," argue Osawa et al., "would be disruptive in intact organisms and even in mitochondria."[45]  That is, we should not think that the body of molecular knowledge motivating functional invariance can be jettisoned at will. (Yes, if common descent is true, and variant codes exist, functional invariance has to go to the wall. Yet functional invariance still seems to be true, or at least highly probable.)  Rather, taking common descent as given, we are now faced with another novel research problem: "How could non-disruptive code changes occur?"[46]

I find this article fascinating because it exemplifies one particularly devious tactic of the ID movement: rather than taking the obvious, but difficult, route of simply arguing that common descent is true or false to some specific degree, based on this and that specific evidence, they try to make the convert the entire argument into one about the intellectual credibility of the biologists, and therefore the thesis the IDists are really trying to advance is something like "mainstream biologists are biased and would believe in evolution no matter what the evidence."  As in Nelson & Wells' conclusion:


Suppose Darwin had it right, namely, that "all the organic beings which have ever lived on this earth have descended from some one primordial form."[52]  The existence of this "one primordial form," the common ancestor, establishes a theoretical domain that logically subsumes all biological and paleontological phenomena.  That is, even if life had multiple origins, we will be unable, having assumed the truth of common descent, to provide any evidence for that possibility: all observed organisms, whether recent or extinct, will necessarily lie within what might be called the "common ancestor horizon."

If this seems counter-intuitive, try the following thought experiment. Assume the truth of common descent, and then attempt to construct an empirical argument against it. No imaginable evidence one might bring to bear, however striking – e.g., organisms for which no transitional stages seem possible, multiple genetic codes – will be able to overturn the theory. If there really was a common ancestor, then all discontinuities between organisms are only apparent, the artifacts of an incomplete history. An ideally fine-grained history would reveal the begetting relations by which all organisms have descended from the common ancestor.

If the axiom thesis is correct, then the theory of common descent will indeed be refractory to the evidential challenges thrown up by biological experience. One can see the point in Mayr's recent claim that common descent

has been gloriously confirmed by all researches since 1859. Everything we have learned about the physiology and chemistry of organisms supports Darwin's daring speculation that "all the organic beings which have ever lived on this earth have descended from some one primordial form..."[53]

One wonders what we could have learned about organisms, since 1859, that would not have confirmed common descent.

We offer the axiom thesis, not because we are persuaded of its truth, but to provide a starting point or focus for discussion. How, really, do the patterns of living things count for, or against, the notions of primary continuity (common ancestry) or primary discontinuity (polyphyly)? If common descent cannot be dislodged by the "evidence," then how should we go about evaluating it?

I propose a (new??) term for this style of argument: Argumentum ad Innuendo.

Thanks, nic

Date: 2002/05/30 20:33:50, Link
Author: niiicholas

Just a little background in case we've got any lurkers who haven't taken biochemistry lately...

In the canonical genetic code that everyone learns in textbooks there are 20 amino acids -- however, chemically many more amino acids are possible.  As I understand it there are many cases where organisms will produce an amino acid chain using the canonical code, and then post-translationally modify some of the amino acids, effectively resulting in the usage of more than 20 amino acids by the organism, although technically the normal genetic code is still used.

However, there are some cases where the canonical code has been modified to include a noncanonical amino acid *during* translation.  A few weeks ago a new example of this was published, and in the AE general discussion a new poster Ed has alerted us to how this example fits in with the 'stop codon alteration' pattern that is so common in genetic code changes.

Here is the link to Ed's post "Stop codon thievery"

I'll quote Ed's post for the sake of thoroughness:

A very recent example of a "stop" codon being
sometimes coopted for another use is the subject of two papers and a "perspective" (1-3) in the 24 May 2002 issue of Science. These all are reporting on the "new" amino acid "pyrrolysine", which is coded for by the (usually) stop codon UAG in a certain methanogenic archaeon's mRNA. To quote from (1):


The way in which pyrrolysine is encoded bears striking parallels to the encoding of the 21st amino acid, selenocysteine. Selenocysteine is found in Archaea, eubacteria and animals, including mammals . Both nonstandard amino acids are encoded by the RNA nucleotide triplets (codons) that signify a command to stop translation of mRNA into protein (UGA is the "stop codon" encoding selenocysteine). The notion that at least 22 amino acids are directly encoded by the nucleotide sequence of mRNA reflects the greater richness of the genetic code than is apparent from the standard textbook account.

Originally, the coding problem was defined in terms of how the 20 common amino acids could be specified by four RNA nucleotides. As the triplet nature of the genetic code began to unfold in the early 1960s, it might have been tempting to speculate that some of the 64 possible codons encoded the many rare amino acids found in proteins. However, it became clear that 20 is the correct number of amino acids, and that the great majority of nonstandard amino acids are created by chemical modifications of standard amino acids after translation. In 1986 came the surprise discovery that the nonstandard amino acid selenocysteine is directly specified by the genetic code and is not created by posttranslational modification. Selenocysteine is now joined by pyrrolysine, and together these two amino acids demonstrate that the genetic code can be expanded by redefining the meaning of a stop codon.   {references omitted}

Reference (1) goes into some depth, with references, as to how the stop signal is subverted in the case of selenocysteine, the only other non-canonical amino acid known to be specified by the code and not built by modification after translation. In the selenocysteine case, only a minority of the UGA codons are used to code the amino acid: most are still stop codons. Signals elsewhere in the mRNA determine which. It is still unknown just how the UAG coding pyrrolysine works, however.

(1) Atkins JF, Gesteland R. Science 2002 May 24;296(5572):1409-10
(2) G. Srinivasan et al., Science 296, 1459 (2002).
(3) B. Hao et al., Science 296, 1462 (2002).

Thanks Ed, keep it up!


Date: 2002/05/31 01:31:35, Link
Author: niiicholas
Another classic case is the evolution of antifreeze genes from proteases in arctic & subarctic fish, which has happened independently at least a couple of times:

I believe this article is freely available online from PNAS:

Proc. Natl. Acad. Sci. USA
Vol. 94, pp. 3485-3487, April 1997

Origin of antifreeze protein genes: A cool tale in molecular evolution
John M. Logsdon Jr. and W. Ford Doolittle


Where do new genes come from? Duplication, divergence, and exon shuffling are the expected answers, so it is especially exciting when new genes are cobbled together from DNA of no related function (or no function at all). In this issue, Chen et al. (1) describe an antifreeze glycoprotein (AFGP) gene in an Antarctic fish that has arisen (in part) from noncoding DNA. Further, they show that a very similar AFGP from an Arctic fish is the product of some completely unrelated molecular processes (2). Together, these papers shed light on a number of key issues in molecular evolution.

In the late 1960s Arthur DeVries showed that freezing resistance in Antarctic fish was due to blood serum glycoproteins that lowered their freezing temperature below that of the subzero sea surrounding them (3, 4). The ensuing years have witnessed a great deal of work on AFPs (antifreeze proteins; not all are glycoproteins) in a number of phylogenetically diverse fish species, much of it by DeVries and his colleagues (5-7), revealing a number of types differing in their structure and amino-acid composition. These proteins, despite their diversity, function in similar ways to deter ice crystal growth (7, 8). But where did they come from, and how did they arise?

Birth of a Gene

In the first of the two papers, Chen et al. (1) demonstrate that an AFGP gene from the Antarctic notothenioid Dissostichus mawsoni derives from a gene encoding a pancreatic trypsinogen. The relationship of these two genes is not simply one of duplication and divergence (9), co-option/recruitment (10), or exon shuffling (11), processes that have been appreciated by molecular evolutionists for some time now. Instead, the novel portion of the AFGP gene (encoding the ice-binding function) derives from the recruitment and iteration of a small region spanning the boundary between the first intron and second exon of the trypsinogen gene (Fig. 1). This newborn segment was expanded and then iteratively duplicated (perhaps by replication slippage or unequal crossing-over) to produce 41 tandemly repeated segments. Nonetheless, the contemporary AFGP gene retains, as its birthmark, sequences at both ends which are nearly identical to trypsinogen. Retention of the 5 end of the trypsinogen gene may be significant, since this region encodes a signal peptide used for secretion from the pancreas into the digestive tract. Chen et al. (1) hypothesize that an early version of the notothenioid AFGP gene may have had its first function preventing freezing in the intestinal fluid, with this function later expanded into the circulatory system by way of its expression in the liver.

Here is Figure 1:


Figure 1. Comparison of gene structures and their sequence similarities. The regions shown represent genomic regions encompassed by sequenced cDNAs, and are not to scale. Exons are shown as large boxes; introns are shown as thinner boxes; inferred initiation and termination codons are indicated. Untranslated regions are hatched, and regions encoding putative signal peptides are stippled. Regions in different genes that are the same color share sequence similarity, but only regions of the same color shade are homologous; dotted lines delineate regions of clear homology between Dissostichus trypsinogen and AFGP genes. The open region of the trypsinogen gene is absent in AFGP. The segment below the double-headed arrow represents expansion of a sequence element present in the Dissostichus trypsinogen gene that appears to have given rise to the canonical AFGP repeat; its subsequent tandem iteration is shown by thin dashed lines. AFGP repeats are numbered and discontinuities are indicated for presentation. Regions between the AFGP repeats (spacers; indicated as either yellow or black) are the presumed sites of posttranslational cleavage. A discontinuity in the intron Dissostichus AFGP gene is shown to represent an internal segment not present in the homologous trypsinogen gene intron.


Thanks, nic

Date: 2002/05/31 01:44:19, Link
Author: niiicholas
Interesting...scrolling down to the bottom of the PNAS article, there is a link to a Science article that cited it.  Guess what?  Plants have evolved antifreeze proteins as well:

A Carrot Leucine-Rich-Repeat Protein That Inhibits Ice Recrystallization

Dawn Worrall, Luisa Elias, David Ashford, Maggie Smallwood, * Chris Sidebottom, Peter Lillford, Julia Telford, Chris Holt, Dianna Bowles


It appears that proteins have been coopted to antifreeze activity from other functions quite recently in evolution (20). In plants, pathogenesis-related proteins such as the (1-3)endoglucanase and chitinase of winter rye (5) and the PGIP-related carrot protein have been recruited. The cell wall is modified in response to both low temperature and pathogen attack (21). Because ice crystallizes in the apoplast, proteins involved in such cell wall modification are well suited for cooption into antifreeze activity if their protein structures permit.

PGIPs belong to a large family of proteins known as the leucine-rich-repeat (LRR) proteins (22). LRR proteins contain 10 to 30 repeated units of a ~24-amino acid peptide containing regularly spaced leucine residues. The carrot AFP consensus sequence is similar to the motif found in other LRR proteins (Fig. 3B). One LRR protein exhibits an unusual nonglobular protein structure with a solvent-exposed parallel  sheet (23), and this structure has been compared with the related parallel  sheet found in pectin-degrading enzymes such as pectate lyase (22). In this context, it may be relevant that fish AFPIII contains a  sheet on its presumptive ice-binding face (24) and that the AFPII ice-binding face may also contain a  sheet structure (25).

The co-option of an LRR protein into antifreeze function in carrot suggests an additional common structural feature of AFPs. Of the seven AFPs known (1, 2), four contain repeated sequences. Thus, a repetitive structure may correlate with antifreeze activity.

The carrot AFP can be stably produced in tobacco plants grown under normal greenhouse conditions. The RI properties of this protein may be useful for improving food storage and protecting crop plants against cold temperatures.

Thanks, nic

Date: 2002/06/11 00:44:21, Link
Author: niiicholas
This thread is for accumulating examples of cooption/change of function from the literature, and citations of the importance of this process in the literature.

The purpose of examining this is that Behe and Dembski both fail to give cooption the attention it absolutely deserves.  In particular the occurence of cooption disproves Behe's IC argument.

Thanks, nic

Date: 2002/06/11 01:03:11, Link
Author: niiicholas
I was struck by this passage from Maynard Smith's The Theory of Evolution.  It almost sounds like it was written to respond to Behe, except that it was written in 1958 (I think; I have the 1993 Canto edition which is the fourth edition):

Discussing the origin of feathers, Maynard Smith writes  (pp. 303-304):


This example will help to explain one of the difficulties often encountered in explaining evolution in terms of natural selection.  It often seems that a perfected organ, although efficient at performing its function, is far too complex to have arisen by one or a few mutations, and yet is such that any intermediate stage between the absence of the organ and its full development would be incapable of performing this function. Thus it is inconceivable that the flight feathers of a bird could have arisen by a single mutation, but the intermediate stages between a scale and a feather would be useless for flight.  In this case the difficulty disappears once it is realized that during the early stages of the evolution of feathers, the latter were probably of selective advantage because they conserved heat, and only later did they become functional in flight.

This is a very common feature of evolution; a new structure evolves at first because it confers advantage by performing one function, but in time it reaches a threshold beyond which it can effectively perform a different function. We saw earlier that something of this kind occurred during the evolution of the elephant's trunk.  The flying membranes of bats and of pterodactyls were probably used in gliding before they were of any use in flapping flight, and, as Spurway has pointed out, small membranes along the sides of the body are found in some arboreal mammals which do not even glide, and these folds of skin render such animals more difficult to see by eliminating the shadows they would otherwise case.  Similarly, lungs were a selective advantage to fish living in stagnant waters, enabling them to breathe air, long before the descendants of these fish walked on land; in modern teleost fishes the lung has lost its function as a breathing organ, and has been transformed into a hydrostatic organ, the swim bladder.  These examples show that there is no reason to suppose that even the most complex structures underwent a long period of evolution and elaboration before they could function, and so confer selective advantage; rather their function may have changed once or even several times in the course of evolution.

(bold added)

This long-standing hypothesis regarding the origin of feathers has been strengthened by recent discoveries of fossil dinosaurs with non-flight feathers.  E.g. the fantastic pictures here:


Date: 2002/06/11 01:24:42, Link
Author: niiicholas
Found this key Darwin quote on the ISCID forum:

Chapter 6 of Origin of Species

Here is the link:

Note especially how closely Darwin ties the change-of-function argument to his "organs of extreme perfection" line which is so often quoted by antievolutionists.  Why don't they ever acknowledge that Darwin himself listed numerous cases of homologous structures being adapted for wildly different functions?


If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. But I can find out no such case. No doubt many organs exist of which we do not know the transitional grades, more especially if we look to much-isolated species, round which, according to my theory, there has been much extinction. Or again, if we look to an organ common to all the members of a large class, for in this latter case the organ must have been first formed at an extremely remote period, since which all the many members of the class have been developed; and in order to discover the early transitional grades through which the organ has passed, we should have to look to very ancient ancestral forms, long since become extinct.

We should be extremely cautious in concluding that an organ could not have been formed by transitional gradations of some kind. Numerous cases could be given amongst the lower animals of the same organ performing at the same time wholly distinct functions; thus the alimentary canal respires, digests, and excretes in the larva of the dragon-fly and in the fish Cobites. In the Hydra, the animal may be turned inside out, and the exterior surface will then digest and the stomach respire. In such cases natural selection might easily specialise, if any advantage were thus gained, a part or organ, which had performed two functions, for one function alone, and thus wholly change its nature by insensible steps. Two distinct organs sometimes perform simultaneously the same function in the same individual; to give one instance, there are fish with gills or branchiae that breathe the air dissolved in the water, at the same time that they breathe free air in their swimbladders, this latter organ having a ductus pneumaticus for its supply, and being divided by highly vascular partitions. In these cases, one of the two organs might with ease be modified and perfected so as to perform all the work by itself, being aided during the process of modification by the other organ; and then this other organ might be modified for some other and quite distinct purpose, or be quite obliterated.

The illustration of the swimbladder in fishes is a good one, because it shows us clearly the highly important fact that an organ originally constructed for one purpose, namely flotation, may be converted into one for a wholly different purpose, namely respiration.

[note: Darwin gets this one backwards, Maynard-Smith's version is the currently accepted one]


In considering transitions of organs, it is so important to bear in mind the probability of conversion from one function to another, that I will give one more instance. Pedunculated cirripedes have two minute folds of skin, called by me the ovigerous frena, which serve, through the means of a sticky secretion, to retain the eggs until they are hatched within the sack. These cirripedes have no branchiae, the whole surface of the body and sack, including the small frena, serving for respiration. The Balanidae or sessile cirripedes, on the other hand, have no ovigerous frena, the eggs lying loose at the bottom of the sack, in the well-enclosed shell; but they have large folded branchiae. Now I think no one will dispute that the ovigerous frena in the one family are strictly homologous with the branchiae of the other family; indeed, they graduate into each other. Therefore I do not doubt that little folds of skin, which originally served as ovigerous frena, but which, likewise, very slightly aided the act of respiration, have been gradually converted by natural selection into branchiae, simply through an increase in their size and the obliteration of their adhesive glands. If all pedunculated cirripedes had become extinct, and they have already suffered far more extinction than have sessile cirripedes, who would ever have imagined that the branchiae in this latter family had originally existed as organs for preventing the ova from being washed out of the sack?

(bold added)
Thanks, nic

Date: 2002/06/11 05:07:37, Link
Author: niiicholas
Now, to show that cooption is not only well-known to the old and grey (or dead), but is very much a concept in modern use:

Consider this article:



Trends Genet 2001 Mar;17(3):120-3
Were protein internal repeats formed by "bricolage"?

Lavorgna G, Patthy L, Boncinelli E.

DIBIT, Istituto Scientifico H. S. Raffaele, Via Olgettina 60, 20132 Milan, Italy.

Is evolution an engineer, or is it a tinkerer--a "bricoleur"--building up complex molecules in organisms by increasing and adapting the materials at hand? An analysis of completely sequenced genomes suggests the latter, showing that increasing repetition of modules within the proteins encoded by these genomes is correlated with increasing complexity of the organism.

The introduction reveals just how far the IDists are from the biologists on understanding the origins of new genetic information and new functions:


Evolution has brought about the formation of organisms of increasing complexity. This process involved mechanisms, such as exon-shuffling [1] and gene duplication, [2] that increased intermolecular duplications of the more sophisticated proteomes. For example, gene duplication contributed to the origin and evolution of vertebrates, which appear to possess several copies of an ancestral set of genes. [3] A single gene in flies usually has three or four paralogous genes in mammals, and this spare genetic capacity has permitted new possibilities, allowing the acquisition of new biochemical functions and expression capabilities. [4]

More than two decades ago, when only a handful of eukaryotic genes were cloned, Francois Jacob had already envisioned some of these basic evolutionary mechanisms. [5] In fact, he argued that evolution could work as a tinkerer, rather than an engineer, implying that evolutionary processes construct things with the materials at hand and the outcome bears the constraints imposed by those materials. [6] Translated into molecular terms, the raw materials are the existing set of genes, which can be, in part or entirely, elaborated again and redeployed to a new function during evolution. Extending to Jacob's view of `recyclement' of biological material, we investigated systematically the possibility that, besides the increase of inter-molecular duplications, an increase of intra-molecular duplications accompanied the evolution of proteins.

We decided to look for repeated protein modules, as opposed to short, low-complexity sequence repeats (i.e. runs of Qs, STSTSTSTS, etc) because, in several instances, modules of proteins are used to build the function of many multidomain proteins. As a result, we found, with a few exceptions, that:

1. There is a correlation between the complexity of functions controlled by the proteome of a given organism and its degree of internal repetitiveness.

2. The above correlation is often observed both for interdomain comparisons (e.g. archaeal proteins have, on average, more internal repeats than bacterial ones) and intradomain comparisons (e.g. human proteins have more internal repeats than those belonging to Drosophila melanogaster).

3. We also detected a decrease in the number of internal repeats following `reductive' evolution, in which the biological complexity of an organism is lower than that of its ancestor (occurring in, for example, endosymbiotic organisms).

A previous paper by Marcotte et al [7]., reported an analysis of 16 completely sequenced genomes (11 bacterial, four archaeal and one eukaryal), in which eukaryotic proteins displayed significantly more repeats than procaryotic ones. This study, which considered repeats containing both low-complexity and high-complexity sequences, was somewhat hindered by the availability of completely sequenced genomes ¯ then relatively scarce. In fact, some of the conclusions we reached are fairly subtle. For example, the increase of the protein repetitiveness from Bacteria to Archaea involves only small percentage changes, possibly because the trend was coupled with the massive gene exchange that occurred later in the microbial world. [8] A sufficiently high number of sequences needed to be analyzed to make our observations significant.

[& towards the end]

5. Mechanisms involved in intramolecular duplication
What mechanisms could have caused or favored the phenomenon of the increase of intramolecular duplications during evolution? There is a strong evidence for the involvement of intronic recombination and exon shuffling in the occurrence of gene insertions. [19] Intriguingly, we found the highest level of intramolecular duplications within high eukaryotic genomes, like C. elegans, D. melanogaster and Homo sapiens, whose genes are characterized by the presence of large numbers of exons and introns. [19] The invention of modular proteins could have been the mysterious force driving the acceleration of evolution and leading to a spectacular burst of evolutionary creativity ¯ the `Big Bang' of metazoan evolution ¯ that caused the sudden appearance of several phyla of animals with different body plans during the Cambrian period. [19]

Archaeal proteins, although belonging to intronless organisms, were found to possess, on average, a higher repetitiveness than the relatively less-evolved bacterial ones. Studies on the evolution of multidomain prokaryotic proteins have given insights on how they may be constructed without the assistance of introns. For example, a modular protein of Peptostreptococcus magnus is the product of a recent intergenic recombination of two different types of streptococcal surface protein. [20] Also, gene rearrangements can be facilitated by the presence of special recombinogenic DNA sequences in intermodule linker regions. [21] It has been proposed that an evolutionary bottleneck, such as the increased selective pressure given by the presence of antibiotics, could favor the creation of these advantageous chimeras. [21] A similar or identical environmental challenge could have been the stimulus directing the rapid evolution of new bacterial proteins and leading to the formation of the archaeal domain.

6. Conclusion
The data reported here, although suggestive, need to be extended. This will be possible when some more of the several genome sequencing projects currently underway are completed. However our results provide another indication that biological evolution works like a tinkerer, "who does not know exactly what he is going to produce, but uses whatever he finds around him whether it be pieces of string, fragments of wood, or old cardboards; in short, it works like a `bricoleur' who uses everything at his disposal to produce some kind of workable object". [5]


5. F. Jacob, Evolution and tinkering. Science 196 (1977), pp. 1161¯1166.

6. F. Jacob, Molecular tinkering in evolution. In: D. Bendall, Editor, Evolution from Molecules to Man, Cambridge University Press (1983), pp. 131¯144.

Date: 2002/06/11 05:41:00, Link
Author: niiicholas
Following the tangent of the evolution of repeats *within* protein sequences:


Protein Repeats: Structures, Functions, and Evolution  

pp. 117-131 (doi:10.1006/jsbi.2001.4392)  

Miguel A. Andrade*, ,  Carolina Perez-Iratxeta*, ,  Chris P. Ponting  

Internal repetition within proteins has been a successful strategem on multiple separate occasions throughout evolution. Such protein repeats possess regular secondary structures and form multirepeat assemblies in three dimensions of diverse sizes and functions. In general, however, internal repetition affords a protein enhanced evolutionary prospects due to an enlargement of its available binding surface area. Constraints on sequence conservation appear to be relatively lax, due to binding functions ensuing from multiple, rather than, single repeats. Considerable sequence divergence as well as the short lengths of sequence repeats mean that repeat detection can be a particularly arduous task. We also consider the conundrum of how multiple repeats, which show strong structural and functional interdependencies, ever evolved from a single repeat ancestor. In this review, we illustrate each of these points by referring to six prolific repeat types (repeats in -propellers and -trefoils and tetratricopeptide, ankyrin, armadillo/HEAT, and leucine-rich repeats) and in other less-prolific but nonetheless interesting repeats.


[...see especially the ribbon models in this paper]

Our survey of protein repeats has highlighted the multifunctionality of repeat types, their structural
differences, and their proliferations in different evo-lutionary
lineages. One likely reason for their evo-lutionary success is that repeat-containing proteins are relatively “cheap” to evolve. By this we mean that large and thermodynamically stable proteins may arise by the simple expedient of intragenic du-plications, rather than the more complex processes of de novo a-helix and b-sheet creation. This is sup-ported by the larger sizes of most repeat-containing
structures relative to compact domains (Fig. 4).

This does not, of course, present a complete an-swer
to their success since it addresses the question of how repeat-containing proteins arose, rather than why they have been selected for and fixed in evolu-tionary lineages on so many separate occasions. As suggested throughout this review, the reasons for the functional successes of repeat classes may be a proclivity of repeat assemblies to acquire different molecular functions, namely, the association with
different protein ligands. This, in turn, might be associated with the large solvent-accessible surface areas, presented by extended “open” assemblies, that are available for interactions with ligands. This is because burial of nonpolar residues at protein–protein interfaces is thought to be an important contributor to heterodimer stability (Tsai et al.,

In understanding the evolution of repeats, one major problem remains. Repeats are defined as oc-curring multiply, and all repeats in a family are homologous. This means that these repeats all evolved from a common ancestor, which necessarily must have contained only a single repeat. This is
apparently contradictory, since it is not expected that a single repeat could exist in isolation, as a single folded functional unit. Rescue is at hand if one suggests that the family’s common ancestor indeed represented a single repeat, but one that formed homooligomers. The homooligomeric structure of the ancestor might mirror that of the intrachain repet-itive structure of its modern homologue, except in its multichain character. This scenario has recently been suggested for the evolution of the b-trefoil fold (Ponting and Russell, 2000).

A problem with this proposal is that there are few, if any, known examples where homologous multire-peat assemblies are formed both from oligomers of single repeats and from a single chain of multiple repeats. However, this might not be too surprising since the highly cooperative process of folding a mul-tirepeat protein must be significantly more favor-able
than folding a homooligomeric protein from its constituent monomers. This is because the kinetic folding pathways of multirepeat protein structures may be nucleated at many positions. In this way ancient oligomeric single repeat proteins might have been driven to extinction by their monomeric multi-ple repeat-containing homologues.

There is an interesting analogy here to the "serial homology" concept in traditional organismal evolution -- e.g. the duplication and specialization of segments.  The same idea -- duplication and divergeence -- appears to occur on several different molecular levels, to wit:

- duplication of segments of a protein, followed by rapid divergence (the above paper)

- taking a homodimer, homotrimer, etc., duplicating the gene, and then specializing each gene in the e.g. heterodimer.  This is yet another way to produce IC by the way

- traditional gene duplication

- duplication of whole chromosomes/genomes -- many chunks will decay but some may get new functions.

All this could be treated in much more detail.  However, antievolutionists consistently fail to realize the importance of duplication, and write as if it didn't exist.  E.g., John Bracht's recent post to metanexus:


Knotty Pine and Corroding Coins: John Bracht


For concreteness, consider an example. Think of a man-made outboard motor. This system contains many of the same structures found in the bacterial flagellum: a motor (including stator, rotor, and acid-powered drive), drive shaft, u-joint, and propeller. Now, imagine starting with a basic rowboat and trying to evolve an outboard motor via the co-optation model. Perhaps, somehow, the metal outer skin of the boat peels up in the back and this forms a useful rack for a fishing pole, and is available to provide the internal support and external protective casing for the motor. Perhaps a support rod works loose from the hull and is available to be made into a drive shaft. But how do we move on from here to build up the motor, in functional steps, from existing parts? The problem is this: the various parts are already adapted to their old functions. To build an outboard motor, the old functions must be replaced by new functions. New functions require modifications of the old parts, and since the motor system doesn't work until all the parts are assembled, we inevitably need a large amount of coordinated change in various components before we can build the new system. For instance, the peeled-away metal on the back (previously adapted to form a watertight hull) will have to undergo extensive modification, including careful bending or shaping, and drilling holes in appropriate places to support motor components (all without letting the hull become leaky). The support rod from the hull, destined to become the drive shaft, will also need modification for attaching gears and the universal joint (and the removal of the support rod must not weaken the structural integrity of the boat). And so on.

IMO there is a clear assumption here that we are dealing with *one* copy of everything, that the old function is lost as the new function is gained.  But just ain't so...


Date: 2002/09/21 13:06:12, Link
Author: niiicholas
This thread is for accumulating

(1) Assertions
(2) Links to articles
(3) Facts

...regarding the question "where do peppered moths rest during the day".  The importance of this topic lies in that many have argued that peppered moths don't rest where Kettlewell thought they did, and that therefore his experiments were invalid, and that therefore the entire peppered moth bird-predation-theory is without support.  Or something.

Another avenue taken by Jonathan Wells in particular is the "this means that textbook photos of moths are fake and a fraud has been committed on students" avenue.  I suggest that we collect pictures that we can find on the web, with comments on the source (if we can find 'em), whether or not they are staged (if known), with a goal of getting a sense of whether or not textbook pictures are misleading.


Date: 2002/09/21 13:15:43, Link
Author: niiicholas
An initial list of Wells utterances on moths and tree trunks:

...peppered moths don't even rest on tree trunks
[Jonathan Wells,  Icons of Evoluton, p.140]

Peppered moths don't rest on tree trunks
[Icons of Evoluton, p. 148 (section heading)]

...peppered moths do not normally rest on tree trunks
[Icons of Evoluton, p. 149]

the fact that peppered moths do not rest on tree trunks...
[Icons of Evoluton, p. 153]

Peppered moths do not rest on tree trunks in the wild.
[Icons of Evoluton, p 260 (suggested textbook warning label)]

4) In the 1980's, several researchers showed independently that peppered moths do not rest on tree trunks in the wild.
[Jonathan Wells, ]

[Calvin debate, ]

(courtsey KC)

Date: 2002/09/21 13:26:13, Link
Author: niiicholas
This thread is for accumulating links on Judith Hooper's recent book Of Moths and Men.

We might as well start with the link to the book:

Of Moths and Men at

Most reviews of the book are positive, but my is not.  Mine, posted at

Hooper gets the science wrong, August 27, 2002

Reviewer: ntamzek (see more about me) from Santa Barbara, CA United States

The fundamental rule of science journalism should be "first, get the science right". Unfortunately, Hooper's book is marred by One Big Mistake: namely, Hooper misrepresents the state of the scientific question on Kettlewell's explanation for industrial melanism in the peppered moth, namely differential predation by birds against moth morphs more or less cryptic in polluted woodlands. Reading Hooper's book, one would think that this thesis, what I call the "Bird Predation Theory" (BPT), was on the rocks. But this just ain't so -- if we read peppered moth researcher Michael Majerus' (2002) book Moths, we find him writing on page 252,

[E]very scientist I know who has worked on melanism in the Peppered moth in the field still regards differential predation of the morphs in different habitats as of prime importance in the case. The critics of work on this case and those who cast doubt on its validity are, without exception, persons who have, as far as I know, never bred the moth and never conducted an experiment on it. In most cases they have probably never seen a live Peppered moth in the wild. Perhaps those who have the most intimate knowledge of this moth are the scientists who have bred it, watched it and studied it, in both the laboratory and the wild. These include, among others, the late Sir Cyril Clarke, Professors Paul Brakefield, Laurence Cook, Bruce Grant, K. Mikkola, Drs Rory Howlett, Carys Jones, David Lees, John Muggleton and myself. I believe that, without exception, it is our view that the case of melanism in the Peppered moth still stands as one of the best examples of evolution, by natural selection, in action.

Hooper, however, presents the peppered moth case as if it were falling apart, a story which of course the press reviews have uncritically repeated.

Hooper's hero in the book is the one critic of the bird predation thesis who is actually a moth expert, Ted Sargent, although even here Sargent is actually an expert on an entirely different family of moths (the Underwings, e.g. Catocala) and has done almost no work on peppered moths. Hooper, however, gives Sargent a huge platform and gives his numerous critics, and their published rebuttals to Sargent, very short shrift. Hooper portrays Sargent as a lone rebellious American taking on the dogmatic British establishment, but of course American peppered moth researcher Bruce Grant, who supports the BPT and has done numerous studies on peppered moths specifically, is not given the same chance to make his case.

As for Sargent's actual arguments against the bird predation thesis, both Bruce Grant and Laurence Cook wrote articles rebutting Sargent's critique, but Hooper gives Cook's article merely a brief brush-off in a paragraph, completely ignoring, for example, Cook's statistical analysis of all the previous peppered moth experiments, proving a correlation between moth fitness and morph frequency with a >99% confidence. This was a direct rebuttal to Sargent's most important argument, that the statistical support for the bird predation thesis was weak, but Hooper doesn't deal with it directly like she should if she is going to advocate an alternative view.

Hooper does come up with a few arguments that not even the creationists have proposed -- most importantly, that Kettlewell faked his results, or almost as bad, unconsciously mislead himself. This is despite the fact that the predation and mark-release-recapture experiments have been repeated by other researchers and have in the main confirmed his results (see the articles by Cook, Grant, and the books by Majerus 1998 and 2002 for detailed reviews). The most astounding passage in Of Moths and Men occurs when Hooper spends a paragraph "squinting" at the tables in Kettlewell's paper, and she notes that Kettlewell's moth recapture numbers increase suddenly on July 1, 1953. The implication is that Kettlewell fudged things somewhere.

But a modicum of investigation shreds Hooper's fraud hypothesis. What Hooper fails to look at seriously was that when Kettlewell released more moths, he recaptured more. Kettlewell started releasing far more moths on June 30th, and started catching far more moths on the morning of July 1st. In fact, when one does a linear regression, one discovers that "number of moths released" explains 80% of the variance in "number of moths recaptured". This is a nice strong linear relationship. Fraud is not a necessary explanation. Why didn't Hooper realize the obvious answer? Later in the book, Sargent keys off the same change in numbers, and he too mysteriously ignores the obvious explanation -- as in most of the book, Sargent's word is taken as gospel and is substituted for rigorous scientific evaluation.

In addition to the major issues discussed above, Hooper's book is peppered with small but disturbing mistakes of logic and science; there is a particularly nasty one about genetics that shows up Hooper's amateurishness (and frankly, that of her editors and glowing reviewers) rather blatantly. I will, however, leave these as exercises for future reviewers to acknowledge or not, so that readers of the reviews may distinguish the critical thinkers from the whatever-a-science-journalist-says-must-be-true types.

The peppered moth story is an awfully good story; but just as this doesn't make it true, it doesn't make it too good to be true either. Hooper's story, the story of a rebel (Sargent) overturning an oppressive orthodoxy is a "good story" also. As Hooper should know, the only way to tell if a "good story" is a true one is by a careful, balanced and weighted review of the evidence. The peppered moth researchers have and are doing this repeatedly, as every bit of new evidence comes in; this is their job as scientists; and their scientific conclusion is that Kettlewell's central finding, that bird predation is the agent of selection, remains firm. Hooper, however, chooses sensationalism, psychoanalysis, and a very selective review of authorities and evidence to reach her conclusion that the bird predation thesis is unsupported; this is the central flaw of her book.

Reader beware.

(9 of 19 people found this review helpful!;)

Date: 2002/09/22 14:40:18, Link
Author: niiicholas
Wells has an unusual talent for mixing several obfuscations together into a story that looks convincing to anyone who hasn't done some reading of the actual moth experts.

Some things to watch out for:

Obfuscation between "moths don't rest on exposed positions on tree trunks" and "moths don't rest on tree trunks".  Wells' quotes usually say the former, but Wells will argue the latter.

Obfuscation about what "'normal' resting position" means to the experts Wells cites.

Audience-dependent obfuscation about whether or not to mention Majerus' data on the natural resting positions of moths.  Wells has been bashed about the head so many times with this that in his most recent writing (reviewing Hooper's book for Christianity Today, here) he has finally brought the data forth rather than having a skeptic do it.  However, reports indicate that his normal strategy in front of friendly audiences is to not mention this inconvient data at all and instead talk about "fraudulent photos" in textbooks (but if peppered moths do rest on tree trunks at least sometimes, then any objection to the photos has become moot).

In every Wells debate on peppered moths that I've read, his ultimate last-ditch position on peppered moths is to talk about how small those observed numbers are in proportion to the thousands of moths observed over the years.  E.g., here:


Nevertheless, many defenders of Darwinian evolution rush to protect the peppered moth icon as though their religion depended on it. In 2000, I wrote a book pointing out that the peppered moth story—though of limited significance in itself—is part of a larger pattern of systematic misrepresentation serving to prop up Darwin's theory. Kevin Padian, a Berkeley professor and president of the National Center for Science Education, a militantly pro-Darwin advocacy group, responded by likening me to the sociopathic antihero of the film The Talented Mr. Ripley. According to Padian, "a particularly egregious example of Mr. Wells's talents is his treatment of the peppered moth." Padian then went on to defend the classic story by claiming that peppered moths "rest on tree trunks 26% of the time" (The Quarterly Review of Biology, March 2002).

Padian bases his astonishing claim (which contradicts the published scientific literature) on the fact that 47 moths were found resting in the wild between 1964 and 1996, and that one quarter of these were on tree trunks. During the same period, however, many thousands of moths were caught in nighttime traps, so the 47 found in natural resting positions were less than 1 percent of the moths studied, and much less than 1 percent of all peppered moths living in the wild. Padian might as well claim that a quarter of all ocean fish are visible to predatory birds because he did statistics on the few that can be spotted from a boat.

Character assassination supported by transparently bogus statistics—how does a highly placed scientist end up indulging in such tactics? Obviously, the peppered moth story involves more than objective science.

'Course, Wells doesn't mention that the "many thousands of moths" caught in traps were caught in traps that attract moths with light or pheromones and which are therefore utterly irrelevant to determining natural resting positions.  All this was pointed out to Wells in the very first moth debate on the Calvin listserv:

(URLs reviewed here: )

Fracks response to the traps claim:


[Frack, "RE: My last word": ]

I have only one comment on Wells's "last word". He wrote:

> 1. Since 1988, it has been well known to everyone who studies peppered
> moths that tree trunks are not their normal resting places. Michael
> Majerus lists six moths on exposed tree trunks over a forty year period,
> but this is an insignificant proportion of the tens of thousands that were
> observed during the same period. There simply is no question about it:
> peppered moths do not normally rest on tree trunks in the wild.

I have already been contacted by a list member asking me about the "tens of thousands" of moths. Attentive readers will probably have noticed that we were talking about Majerus's sample of field collected moths from resting positions as 47, and Wells's incessant "one moth". Wells has found me out. You can now be told the truth that the normal resting position of peppered moths is in the bottom tray of light traps, for that is where these specimens were "observed."

...and yet, you will find Wells ending every debate on peppered moths (with Frack, Miller, Dave Thomas, and probably others) with this false Ace.

And, of course, tactically leaving out important pieces of information like this is exactly what the Matt Daemon character in "The Talented Mr. Ripley" did at the beginning of the movie (the part cited in the Padian review), and is indeed the major fault of all of Wells' antievolution polemics.


Date: 2002/09/22 23:37:02, Link
Author: niiicholas
Here is the only review of Hooper that has come out thus far by a Real Live Peppered Moth Researcher: Bruce Grant.  His take is notably different than the press commentary on Hooper.

Science 297, 940-941 (2002)

Sour Grapes of Wrath

A review by Bruce S. Grant


Of Moths and Men: Intrigue, Tragedy and the Peppered Moth
Judith Hooper
Fourth Estate, London, 2002. 397 pp. £15.99. ISBN 1-84115-392-3.

Of Moths and Men The Untold Story of Science and the Peppered Moth
Norton, New York, 2002. 397 pp. $26.95, C$38.99. ISBN 0-393-05121-8.

Mark Twain once quipped that reports of his death had been exaggerated. Recent reports exaggerate the death of industrial melanism as an exemplar of natural selection. The latest is Judith Hooper's Of Moths and Men, which promises "the untold story of science and the peppered  moth." What it delivers is a quasi-scientific assessment of the evidence for natural selection in the peppered moth (Biston betularia), much of which is cast in doubt by the author's relentless suspicion of fraud. This is unfortunate. Hooper is a gifted writer. In places, her prose is quite enjoyable, even brilliant. But, sadly, the book is marred by numerous factual errors and by misrepresentations of concepts and controversies.

The fundamental problem is Hooper's failure to clearly distinguish the evidence for natural selection and the mechanism of selection. A dead body with a knife in its back is evidence that a murder has been committed. An inability to establish beyond reasonable doubt the guilt of the leading suspect does not mean that the murder did not occur.

Population geneticists define evolution as a change in allele (gene) frequency. Adult peppered moths come in a range of shades from mottled gray (pale) to jet black (melanic). We know from extensive genetic analysis that these phenotypes result from combinations of multiple alleles at a single locus. Changes in the percentages of the phenotypes in wild populations are well documented. The changes continue and are observable even now. The steady trajectory and speed of changes in allele frequencies indicate that this evolution results primarily from natural selection. J. B. S. Haldane's original calculation of a selection coefficient was estimated  from the number of generations it took for the melanic phenotype to effectively replace the pale phenotype during the 19th century. More detailed records document recent changes. For example, near Liverpool, England, the melanic phenotype declined from 93 to 18% in 37 generations (one generation per year); this change is consistent with a 15% selective disadvantage to genotypes with the dominant (melanic) allele.

We have amassed enormous records of changes in allele frequency in peppered moth populations that cannot be explained in the absence of natural selection. But what is the mechanism of selection? Even the answer "we have no clue" would not invalidate the conclusion that selection has occurred. Fortunately, the circumstances have left clues.

Geographic and temporal variations in the incidence of  melanism correlate with atmospheric levels of SO2 and suspended particles. (The correlations are not perfect; gene flow by migration spreads alleles, even into populations where they are deleterious.) Light reflectance from tree bark declines as suspended particles increase. Across a range of  backgrounds, the pale and melanic phenotypes are differently conspicuous to the human eye. As early as 1896, J. W. Tutt suspected that birds were selectively eating conspicuous phenotypes in habitats variously modified by industrial fallout; H. B. D. Kettlewell first tested Tutt's idea in the 1950s.

It is on Kettlewell and his experiments that Hooper focuses her attention. In a biography more akin to character assassination than to objective disclosure, she portrays Kettlewell as an insecure misfit so driven to please his "boss," E. B. Ford, that he is suspected (by Hooper) of fudging his data. She bases her case on experimental design changes that Kettlewell himself described in his papers and on a sudden increase in the recapture rate of marked moths released in polluted woodlands. Several obvious things that Hooper left unexamined affect the size of moth catches, and her case is unconvincing. In addition, she presents it as if the very evidence for natural selection in peppered moths depends on the validity of Kettlewell's experiments. But even the evidence for bird predation does not depend on them.

Fortunately, science assesses the correctness of work by testing its repeatability. Kettlewell's conclusions have been considered in eight separate field studies, of various designs, performed between 1966 and 1987. Some of the design changes--such as reducing the density of moths, randomly
assigning moths to trees, altering locations on trees where moths were positioned, and positioning killed moths to control for differences in viability and dispersal--were made to correct deficiencies identified in his original experiments. L. M. Cook's regression analysis of fitness estimates from these experiments plotted against phenotype frequencies at their various locations shows the studies to be remarkably consistent (1).

Other mechanisms of selection have been proposed. An inherent physiological advantage of melanic over pale phenotypes is consistent with the rise and spread of melanism, but the widespread decline in melanism that  followed the Clean Air Acts obviates that interpretation. Although the possibility remains that physiological differences might be facultative (changing with conditions), so far no experimental work supports this idea. To date, only selective predation by birds is backed by experiment.

Hooper's book turns bizarre when she showcases American biologist T. D. Sargent as a wounded iconoclast whose career was stultified because Kettlewell dismissed his work. She argues that Sargent is now under attack because he questions the "classical explanation" for industrial melanism. Hooper garbles the controversy regarding background  selection by moths, and she entertains Sargent's protracted speculation about phenotypic induction. (He has offered no evidence that melanism is an induced character in adult peppered moths.) But most egregious is Sargent's assertion that studies in North America falsify the classical explanation. The history of melanism in American peppered moths--which are conspecific with Kettlewell's moths, not a separate species as Hooper indicates--closely parallels what has  occurred in Britain, and melanism is correlated in like manner with levels of atmospheric pollution (2). The American studies corroborate rather than contradict the classical explanation.

The case for natural selection in the evolution of melanism in peppered moths is actually much stronger today than it was during Kettlewell's time. Textbook accounts should be expanded to reflect this newer information, and they should not cite Of Moths and Men as a credible resource.


1.    L. M. Cook, Biol. J. Linn. Soc. 69, 431 (2000).
2.    B. S. Grant, L. L. Wiseman, J. Hered. 93, 86 (2002).
The author is in the Department of Biology, College of William and Mary, Williamsburg, VA 23187-8795, USA. E-mail:

Date: 2002/09/24 03:36:07, Link
Author: niiicholas
Another review (or rebuttal of positive Hooper reviews, actually) on Intelligent Design Update yahoogroup:

...quite good IMO, several points that haven't been made by anyone else yet...


Date: 2002/09/24 03:44:53, Link
Author: niiicholas
Quote (niiicholas @ Sep. 24 2002,03:36)

Online letters on the review of Hooper:

The Wells FAQ is referenced :-)

Date: 2002/09/24 04:48:34, Link
Author: niiicholas
This thread is for accumulating links and posts on the topic of predictions made by the modern theory of evolution, i.e. the theory that processes we observe or directly infer today (especially random mutation (broadly construed to include everything from point mutations to genome duplications) and natural selection, but also the well-known sidekicks such as genetic drift, neutral evolution, etc.), were also acting in the long-distant past and produced the biodiversity of today.

This was prompted by Jesse's excellent post at ARN on this topic, which we should quote somewhere:

ARN post


Date: 2002/09/26 00:13:06, Link
Author: niiicholas
Here is another Wells gaffe:


(4) In the 1980's, several researchers showed independently that peppered moths do not rest on tree trunks in the wild. The moths normally fly only at night, and before dawn they apparently take up positions high in the canopy, underneath horizontal branches. In 40 years of field work, only one peppered moth was found resting on a tree trunk in the wild. Although some uncertainty remains about where the moths actually do rest during the day, it is absolutely clear that they do not rest on vertical tree trunks.

[ ]

Michael Majerus took the trouble to respond to this himself:


4) This is just wrong. Dr Wells' who gives the impression in his response that he has read my book, obviously has not. If he had, he would have seen that in Tables 6.1 and 6.2 I myself have recorded 168 peppered moths on tree trunks or at trunk/branch joins. If Dr Wells' wishes his views to be taken seriously, he should ensure that his research is thorough.

[ ]


Date: 2002/10/01 13:47:50, Link
Author: niiicholas
This thread is for references to lit. on, or relevant to, the origins of F1F0 ATPase.  I just came across some and I know of some others, I will post them whenever I dig 'em up.


Subunit rotation of ATP synthase embedded in membranes: a or ß subunit rotation relative to the c subunit ring

Kazuaki Nishio *, Atsuko Iwamoto-Kihara *, Akitsugu Yamamoto , Yoh Wada *, and Masamitsu Futai *
*Division of Biological Sciences, Institute of Scientific and Industrial Research, Osaka University, Core Research for Evolutional Science and Technology (CREST) of the Japan Science and Technology Corporation, Osaka 567-0047, Japan; and Department of Physiology, Kansai Medical University, Moriguchi, Osaka 570-8506, Japan

Edited by Paul D. Boyer, University of California, Los Angeles, CA, and approved August 15, 2002 (received for review March 13, 2002)

ATP synthase FoF1 (3ß3ab2c10-14) couples an electrochemical proton gradient and a chemical reaction through the rotation of its subunit assembly. In this study, we engineered FoF1 to examine the rotation of the catalytic F1 ß or membrane sector Fo a subunit when the Fo c subunit ring was immobilized; a biotin-tag was introduced onto the ß or a subunit, and a His-tag onto the c subunit ring. Membrane fragments were obtained from Escherichia coli cells carrying the recombinant plasmid for the engineered FoF1 and were immobilized on a glass surface. An actin filament connected to the ß or a subunit rotated counterclockwise on the addition of ATP, and generated essentially the same torque as one connected to the c ring of FoF1 immobilized through a His-tag linked to the  or ß subunit. These results established that the c10-14 and 3ß3ab2 complexes are mechanical units of the membrane-embedded enzyme involved in rotational catalysis.

Some have argued that the ATPase may be descended from a pyrophophatase, so this is relevant:


Proc. Natl. Acad. Sci. USA, 10.1073/pnas.212410399

Pyrophosphate-producing protein dephosphorylation by HPr kinase/phosphorylase: A relic of early life?

In most Gram-positive bacteria, serine-46-phosphorylated HPr (P-Ser-HPr) controls the expression of numerous catabolic genes (10% of their genome) by acting as catabolite corepressor. HPr kinase/phosphorylase (HprK/P), the bifunctional sensor enzyme for catabolite repression, phosphorylates HPr, a phosphocarrier protein of the sugar-transporting phosphoenolpyruvate/glycose phosphotransferase system, in the presence of ATP and fructose-1,6-bisphosphate but dephosphorylates P-Ser-HPr when phosphate prevails over ATP and fructose-1,6-bisphosphate. We demonstrate here that P-Ser-HPr dephosphorylation leads to the formation of HPr and pyrophosphate. HprK/P, which binds phosphate at the same site as the ß phosphate of ATP, probably uses the inorganic phosphate to carry out a nucleophilic attack on the phosphoryl bond in P-Ser-HPr. HprK/P is the first enzyme known to catalyze P-protein dephosphorylation via this phospho-phosphorolysis mechanism. This reaction is reversible, and at elevated pyrophosphate concentrations, HprK/P can use pyrophosphate to phosphorylate HPr. Growth of Bacillus subtilis on glucose increased intracellular pyrophosphate to concentrations (6 mM), which in in vitro tests allowed efficient pyrophosphate-dependent HPr phosphorylation. To effectively dephosphorylate P-Ser-HPr when glucose is exhausted, the pyrophosphate concentration in the cells is lowered to 1 mM. In B. subtilis, this might be achieved by YvoE. This protein exhibits pyrophosphatase activity, and its gene is organized in an operon with hprK.

Date: 2002/10/01 14:02:37, Link
Author: niiicholas
Here's a different one:


Published online before print September 17, 2002
Proc. Natl. Acad. Sci. USA, 10.1073/pnas.152445399
Evolution of moth sex pheromones via ancestral genes

Wendell L. Roelofs *, Weitian Liu *, Guixia Hao *, Hongmei Jiao *, Alejandro P. Rooney , and Charles E. Linn Jr. *
*Department of Entomology, Cornell University, Geneva, NY 14456; and Department of Biological Sciences, Mississippi State University, Mississippi State, MS 39762

Contributed by Wendell L. Roelofs, July 28, 2002

Mate finding in most moth species involves long-distance signaling via female-emitted sex pheromones. There is a great diversity of pheromone structures used throughout the Lepidoptera, even among closely related species. The conundrum is how signal divergence has occurred. With strong normalizing selection pressure on blend composition and response preferences, it is improbable that shifts to pheromones of diverse structures occur through adaptive changes in small steps. Here, we present data supporting the hypothesis that a major shift in the pheromone of an Ostrinia species occurred by activation of a nonfunctional desaturase gene transcript present in the pheromone gland. We also demonstrate the existence of rare males that respond to the new pheromone blend. Their presence would allow for asymmetric tracking of male response to the new blend and, thus, evolution of an Ostrinia species with structurally different sex pheromone components.

Date: 2002/11/28 23:11:25, Link
Author: niiicholas
Similar to the prokaryotic flagella thread.

Introductory material:
(don't confuse eukaryotic cilia/flagella with prokaryotic flagella)

Here we have the interesting sideshow of Margulis' and fans' hypothesis that the cilium is derived from a spirochete.  For many critical comments on this see:

Cavalier-Smith T. Int J Syst Evol Microbiol 2002 Mar;52(Pt 2):297-354
The phagotrophic origin of eukaryotes and phylogenetic classification of Protozoa.

Date: 2002/12/01 20:38:22, Link
Author: niiicholas
Might as well add these as I'm discussing them over at EvC:

On the evolution of PCP degradation:


Evolution of a metabolic pathway for degradation of a toxic xenobiotic: the patchwork approach.

Trends Biochem Sci 2000 Jun;25(6):261-5

Copley SD.

Dept of Chemistry and Biochemistry and Cooperative Institute for Research in Environmental Studies, University of Colorado at Boulder, Boulder, CO 80309, USA.

The pathway for degradation of the xenobiotic pesticide pentachlorophenol in Sphingomonas chlorophenolica probably evolved in the past few decades by the recruitment of enzymes from two other catabolic pathways. The first and third enzymes in the pathway, pentachlorophenol hydroxylase and 2,6-dichlorohydroquinone dioxygenase, may have originated from enzymes in a pathway for degradation of a naturally occurring chlorinated phenol. The second enzyme, a reductive dehalogenase, may have evolved from a maleylacetoacetate isomerase normally involved in degradation of tyrosine. This apparently recently assembled pathway does not function very well: pentachlorophenol hydroxylase is quite slow, and tetrachlorohydroquinone dehalogenase is subject to severe substrate inhibition.

[On the key step of the origin of PcpC, the central step in the origin of PCP degradation]

Recruitment of a double bond isomerase to serve as a reductive dehalogenase during biodegradation of pentachlorophenol.

Biochemistry 2000 May 9;39(18):5303-11

Anandarajah K, Kiefer PM Jr, Donohoe BS, Copley SD.

Department of Molecular, Cellular and Developmental Biology and Cooperative Institute for Research in Environmental Sciences, University of Colorado at Boulder, Campus Box 216, Boulder, Colorado 80309-0216, USA.

Tetrachlorohydroquinone dehalogenase catalyzes the replacement of chlorine atoms on tetrachlorohydroquinone and trichlorohydroquinone with hydrogen atoms during the biodegradation of pentachlorophenol by Sphingomonas chlorophenolica. The sequence of the active site region of tetrachlorohydroquinone dehalogenase is very similar to those of the corresponding regions of maleylacetoacetate isomerases, enzymes that catalyze the glutathione-dependent isomerization of a cis double bond in maleylacetoacetate to the trans configuration during the catabolism of phenylalanine and tyrosine. Furthermore, tetrachlorohydroquinone dehalogenase catalyzes the isomerization of maleylacetone (an analogue of maleylacetoacetate) at a rate nearly comparable to that of a bona fide bacterial maleylacetoacetate isomerase. Since maleylacetoacetate isomerase is involved in a common and presumably ancient pathway for catabolism of tyrosine, while tetrachlorohydroquinone dehalogenase catalyzes a more specialized reaction, it is likely that tetrachlorohydroquinone dehalogenase arose from a maleylacetoacetate isomerase. The substrates and overall transformations involved in the dehalogenation and isomerization reactions are strikingly different. This enzyme provides a remarkable example of Nature's ability to recruit an enzyme with a useful structural scaffold and elaborate upon its basic catalytic capabilities to generate a catalyst for a newly needed reaction.

[atrazine degradation, a similar case]
Melamine deaminase and atrazine chlorohydrolase: 98 percent identical but functionally different.

J Bacteriol 2001 Apr;183(8):2405-10

Seffernick JL, de Souza ML, Sadowsky MJ, Wackett LP.

Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, St. Paul, Minnesota 55108, USA.

The gene encoding melamine deaminase (TriA) from Pseudomonas sp. strain NRRL B-12227 was identified, cloned into Escherichia coli, sequenced, and expressed for in vitro study of enzyme activity. Melamine deaminase displaced two of the three amino groups from melamine, producing ammeline and ammelide as sequential products. The first deamination reaction occurred more than 10 times faster than the second. Ammelide did not inhibit the first or second deamination reaction, suggesting that the lower rate of ammeline hydrolysis was due to differential substrate turnover rather than product inhibition. Remarkably, melamine deaminase is 98% identical to the enzyme atrazine chlorohydrolase (AtzA) from Pseudomonas sp. strain ADP. Each enzyme consists of 475 amino acids and differs by only 9 amino acids. AtzA was shown to exclusively catalyze dehalogenation of halo-substituted triazine ring compounds and had no activity with melamine and ammeline. Similarly, melamine deaminase had no detectable activity with the halo-triazine substrates. Melamine deaminase was active in deamination of a substrate that was structurally identical to atrazine, except for the substitution of an amino group for the chlorine atom. Moreover, melamine deaminase and AtzA are found in bacteria that grow on melamine and atrazine compounds, respectively. These data strongly suggest that the 9 amino acid differences between melamine deaminase and AtzA represent a short evolutionary pathway connecting enzymes catalyzing physiologically relevant deamination and dehalogenation reactions, respectively.

Date: 2002/12/02 18:55:21, Link
Author: niiicholas
This is a "data accumulation" thread for me (and anyone else interested in Croizat) to learn the basics.

To start off:


León Croizat and the panbiogeography, never a serious scientist

Morrone JJ. 2000. Between the taunt and the eulogy: Leon Croizat and the panbiogeography. INTERCIENCIA 25: (1) 41-47.
The Italian botanist Leon Croizat (1894-1982) is a controversial figure in the most recent history of biogeography. Based on the metaphor that "life and earth evolve together" -which means that geographic barriers and biotas coevolve- Croizat developed a new biogeographic methodology, which he named 'panbiogeography '. This method was basically to plot distributions of organisms on maps and connect the disjunct distribution areas or collection localities together with lines called tracks. Croizat found that individual tracks for unrelated groups of organisms were repetitive, and considered the resulting summary lines as generalized tracks which indicated the preexistence of ancestral biotas, subsequently fragmented by tectonic and/or climatic changes. Some authors, mainly those belonging to the dispersalist establishment, have dismissed Croizat's contributions, considering him as idiosyncratic, or a member of a lunatic fringe. Others have considered Croizat as one of the most original thinkers of modern comparative biology, whose contributions advanced the foundations of a new synthesis between earth and life sciences. Following its synthesis with phylogenetic systematics, Croizat's panbiogeography has emerged as being central to vicariance or cladistic biogeography. In spite of this synthesis, some authors currently agree in the distinction between Croizat's panbiogeography and cladistic biogeography.

So, perhaps both a loon and brilliant in his way.

Lotsa info here, including some vituperative anti-Darwin, and anti-Mayr stuff from late Croizat:

Date: 2002/12/02 19:12:32, Link
Author: niiicholas


HALLAM, Anthony, School of Earth Sciences, Univ of Birmingham, Edgbaston, Birmingham B15 2TT United Kingdom,

One of the strongest arguments that Wegener put forward to support his continental drift hypothesis derived from biogeography. The conventional interpretation of the close taxonomic relationships of Mesozoic terrestrial organisms between the southern continents was of land bridges that had subsequently foundered beneath the South Atlantic and Indian Oceans. Wegener cited this biogeographic evidence in support of his hypothesis, pointing out that neither the geological evidence (absence of granitic rocks) nor the geophysical evidence (high density of ocean floor) supported the idea of foundered continents, and that the only plausible alternative was that the Atlantic and Indian Oceans had opened in the fairly recent geological past. Later last century this notion led directly to the concept of vicariance biogeography, following the work of Croizat, which focussed on the spatiotemporal analysis of distribution patterns of organisms and is different from phenetic biogeography, which investigates similarities between biotas in terms of numbers of taxa in common. Croizat's so called generalised tracks indicated the distribution pattern of an ancient biota before it vicariated. The tracks for terrestrial organisms may cross oceans and hence could not be explained by present-day biogeography. With the general acceptance of plate tectonics by the early 1970s, Croizat's work was used to create a new school of vicariance biogeography. The early work was characterised by a polemical approach that virtually denied any validity to the alternative dispersalist school. Many have subsequently reacted against this excessive polarisation, and dismissive attitudes towards dispersalist mechanisms, but without question a new scientific rigour has been introduced, with more emphasis being placed on testing models and with ad hoc hypothesising being discouraged. An important difference quickly emerged, however, between Croizat and the other vicariance biogeographers, who supported cladistic methods of taxonomic analysis, whereas Croizat favoured conventional phenetic methods.

2002 Denver Annual Meeting (October 27-30, 2002)

Session No. 141
Paleobiogeography: Integrating Plate Tectonics and Evolution
Colorado Convention Center: A102/104/106
8:00 AM-12:00 PM, Tuesday, October 29, 2002

A good short summary of biogeography that puts Croizat in context:,%20method.html

Date: 2002/12/03 23:13:15, Link
Author: niiicholas
Another Miller article, presents his argument on cilia missing parts:

"Answering the Biochemical Argument from Design"

The ID movement pretends that its biochemical arguments against evolution are new, novel, and scientific. In fact, they are nothing of the sort.

Date: 2002/12/07 15:23:08, Link
Author: niiicholas

Date: 2002/12/08 00:10:21, Link
Author: niiicholas
Looks like this bit got nuked in the server crash.  The 1969 paper on Hagemann factor loss in whales has been cited, but there is an interesting 1998 paper:


Thromb Res 1998 Apr 1;90(1):31-7
Whale Hageman factor (factor XII): prevented production due to pseudogene conversion.

Semba U, Shibuya Y, Okabe H, Yamamoto T.

Department of Clinical Laboratory Medicine, School of Medicine, Kumamoto University, Honjo, Japan.

In Southern blot analysis of the Hind III-digested whale genomic DNA obtained from the livers of two individual whales, we detected a single band with a size of five kilobase pairs which hybridized to full length guinea pig Hageman factor cDNA. We amplified two successive segments of the whale Hageman factor gene by polymerase chain reaction (PCR), and sequenced the PCR products with a combined total of 1367 base pairs. Although all of the exon-intron assemblies predicted were identical to those of the human Hageman factor gene, there were two nonsense mutations making stop codons and a single nucleotide insertion causing a reading frame shift. We could not detect any message of the Hageman factor gene expression by northern blot analysis or by reverse transcription-polymerase chain reaction (RT-PCR) analysis. These results suggest that in the whale, production of the Hageman factor protein is prevented due to conversion of its gene to a pseudogene. The deduced amino acid sequence of whale Hageman factor showed the highest homology with the bovine molecule among the land mammals analyzed so far.

...obvious implications concerning the origin of whales...

Date: 2002/12/08 00:57:42, Link
Author: niiicholas
Here's a good example of a debate that rapidly focused on the ambiguities in the defn of IC:

...other examples welcome.

Also, cites of IDists using/defining IC, SC, etc. in conflicting ways.

Date: 2002/12/08 14:34:57, Link
Author: niiicholas
Quote (Bebbo @ Dec. 08 2002,08:46)
While on the subject of ISCID, does anyone else find it strange that discussion of purpose of design is shyed away from even though the ISCID home page says something like "retraining the scientific mind to see purpose in nature"?


That is funny, isn't it.

"Look, there's purpose in biology!"

"But what's the purpose?"

"Sorry, can't talk about that!"

Date: 2002/12/12 20:58:50, Link
Author: niiicholas
Interesting.  Here's another one by the same folks:


A cytochrome b origin of photosynthetic reaction centers: an evolutionary link between respiration and photosynthesis

J Mol Biol 2002 Oct 4;322(5):1025-37
Xiong J, Bauer CE.

Department of Biology, Texas A&M University, College Station, TX 77843, USA.

The evolutionary origin of photosynthetic reaction centers has long remained elusive. Here, we use sequence and structural analysis to demonstrate an evolutionary link between the cytochrome b subunit of the cytochrome bc(1) complex and the core polypeptides of the photosynthetic bacterial reaction center. In particular, we have identified an area of significant sequence similarity between a three contiguous membrane-spanning domain of cytochrome b, which contains binding sites for two hemes, and a three contiguous membrane-spanning domain in the photosynthetic reaction center core subunits, which contains binding sites for cofactors such as (bacterio)chlorophylls, (bacterio)pheophytin and a non-heme iron. Three of the four heme ligands in cytochrome b are found to be conserved with the cofactor ligands in the reaction center polypeptides. Since cytochrome b and reaction center polypeptides both bind tetrapyrroles and quinones for electron transfer, the observed sequence, functional and structural similarities can best be explained with the assumption of a common evolutionary origin. Statistical analysis further supports a distant but significant homologous relationship. On the basis of previous evolutionary analyses that established a scenario that respiration evolved prior to photosynthesis, we consider it likely that cytochrome b is the evolutionary precursor for type II reaction center apoproteins. With a structural analysis confirming a common evolutionary origin of both type I and type II reaction centers, we further propose a novel "reaction center apoprotein early" hypothesis to account for the development of photosynthetic reaction center holoproteins.

Did I mention that I really like accumulating the refs and links on topics like this in topic-specific UBB threads?  Quite a useful thing to have around IMO...

Date: 2002/12/12 21:02:38, Link
Author: niiicholas
Philosopher/Historian of science, who has authored a PhD and several articles on Kettlewell's work, has weighed in against Jonathan Wells:


Cryptic designs on the peppered moth.

Rev Biol Trop 2002 Mar;50(1):1-7
Rudge DW.

Department of Biological Sciences, Institute for Science Education, Western Michigan University, 3134 Wood Hall, Kalamazoo, MI 49008-5410, USA.

In a provocative recent book, Jonathan Wells (2000) decries what he discerns as a systematic pattern in how introductory biology textbooks "blatantly misrepresent" ten routinely cited examples offered as evidence for evolution. Each of these examples, according to Wells, is fraught with interpretive problems and, as such, textbooks that continue to use them should at the very least be accompanied by warning labels. The following essay critiques his reasoning with reference to one of these examples, the phenomenon of industrial melanism. After criticizing Wells's specific argument, the essay draws several conclusions about the nature of science lost in his account.

Rudge's webpage is here:

One of Rudge's articles is online:
(another version of this was published in something like the Journal of Biological Education

"Does being wrong make Kettlewell wrong for science teaching?"

from here:

Rudge's current and upcoming articles are listed here:

Date: 2002/12/12 21:44:25, Link
Author: niiicholas
Other Biston researcher webpages:

Bruce Grant

Michael Majerus

Books by Majerus: link

Date: 2002/12/13 01:13:29, Link
Author: niiicholas
And in the "duplicated genes aren't necessarily selectively neutral, dammit" category:

(bold added)

Genome Biol 2002;3(2):RESEARCH0008
Selection in the evolution of gene duplications.

free online at pubmed central

Kondrashov FA, Rogozin IB, Wolf YI, Koonin EV.

National Center for Biotechnology Information, National Institutes of Health, Bethesda, MD 20894, USA.

BACKGROUND: Gene duplications have a major role in the evolution of new biological functions. Theoretical studies often assume that a duplication per se is selectively neutral and that, following a duplication, one of the gene copies is freed from purifying (stabilizing) selection, which creates the potential for evolution of a new function. RESULTS: In search of systematic evidence of accelerated evolution after duplication, we used data from 26 bacterial, six archaeal, and seven eukaryotic genomes to compare the mode and strength of selection acting on recently duplicated genes (paralogs) and on similarly diverged, unduplicated orthologous genes in different species. We find that the ratio of nonsynonymous to synonymous substitutions (Kn/Ks) in most paralogous pairs is <<1 and that paralogs typically evolve at similar rates, without significant asymmetry, indicating that both paralogs produced by a duplication are subject to purifying selection. This selection is, however, substantially weaker than the purifying selection affecting unduplicated orthologs that have diverged to the same extent as the analyzed paralogs. Most of the recently duplicated genes appear to be involved in various forms of environmental response; in particular, many of them encode membrane and secreted proteins. CONCLUSIONS: The results of this analysis indicate that recently duplicated paralogs evolve faster than orthologs with the same level of divergence and similar functions, but apparently do not experience a phase of neutral evolution. We hypothesize that gene duplications that persist in an evolving lineage are beneficial from the time of their origin, due primarily to a protein dosage effect in response to variable environmental conditions; duplications are likely to give rise to new functions at a later phase of their evolution once a higher level of divergence is reached.



Thus, the observation that purifying selection appears to act on all recent duplicates and examination of the functions of recently duplicated genes do not support the notion that gene duplication results in true functional redundancy and duplications may achieve fixation despite being redundant [26]. The alternative hypothesis - that gene duplications are fixed in a population by positive selection in all organisms - is supported by a combination of evidence of adaptive duplications from many types of living organisms: prokaryotes [31,33,45,46,48,50,55,56], protists [35,58,59], plants [39,44], fungi [43,49], invertebrates [40,41,51,52,53], non-mammalian vertebrates [54], as well as mammalian somatic tissues [34,36,37,38]. Combining these observations with the suggestion that gene duplication may be a general mechanism of adaptation to various conditions of environmental stress [32,33,46,48,49,50,52,53,55,60], we suggest that, in both prokaryotes and eukaryotes, most paralogs that are fixed in a population have a direct effect on fitness from the moment of duplication, and aid in the adaptation to various environmental conditions, primarily through a protein dosage effect.

That the short-term benefit of a gene duplication is a direct effect on protein dosage also stems from a variety of experimental observations in a number of organisms, prokaryotic and eukaryotic. Gene duplication may be a temporary mechanism to increase protein or RNA dosage, as in the case of rRNA genes in amphibian oocytes and ciliate macronuclei, the chorion genes in some dipterans, actin genes in chicken as well as drug transporters in somatic tissues (see [34,37] for reviews). Protein dosage effects have also been demonstrated in a number of other studies of inheritable adaptive gene duplications [32,34,35,43,44,46,49,51,53,61]. Furthermore, there is evidence from the analysis of the yeast genome that duplicated genes tend to be from those sets of functions that are more highly expressed [62], supporting a general role for selection on protein dosage in duplicated genes.
The present observation that duplicated genes experience a substantial relaxation of selection compared to unduplicated genes is compatible with the traditional view that gene duplications make a major contribution to the evolution of new gene functions. Additionally, the repertoire of protein functions among recent duplicates suggests that many gene duplications contribute to adaptation of the organism to various forms of environmental stress. The results of the present analysis of recent duplications suggest a two-stage evolutionary model of gene duplication: in the first stage, immediately after duplication and during the early phase of their evolution, paralogs are retained and are subject to purifying selection because of the short-term advantage of protein dosage regulation; at a later stage in their evolution, gene duplications are likely to provide a long-term advantage by enabling the creation of new functions.

What would be interesting to know would be the relative roles of regulation mutations vs. gene duplications in effecting adaptation (via amount of proteins produced) to changing conditions as discussed above.  One would think that regulatory changes would be the more "elegant" or "efficient" way to adapt, but apparently evolution doesn't know or care, at least sometimes...

(it may be that regulatory changes have a "limit" that could only be exceeded by duplicating the gene...but now I'm at the limits of my knowledge...)


(PS: The assumption that duplicating a gene doubles the level of a particular protein may not be a good one, particularly if the expression of the gene is regulated by some kind of feedback mechanism...just something to keep in mind)

Date: 2002/12/13 01:25:37, Link
Author: niiicholas
This thread is for links, refs, etc. on transitional fossils.

The big momma of 'net resources is:

Kathleen Hunt's Transitional Vertebrate Fossils MegaFAQ

...however, it was mostly written in 1995 or so, and an awful lot has been discovered since then.  But with Hunt's FAQ can as a starting point, I suggest we use this thread to "enhance" the material there with:

1) Online pictures we discover

2) Refs and pics of new discoveries (let's see, since 1995 there've been more transitionals discovered for whales, manatees, birds, ...and of course humans).

3) Online discussions of the topic

4) Review articles etc.

...all with the primary focus of rebutting the "there ain't no transitional fossils" claim.

Here is my favorite:

AMNH page on a feathered dromeosaur

Date: 2002/12/13 01:53:48, Link
Author: niiicholas
Post your favorite Internet resources for searching for accurate (peer-reviewed lit., high-quality science journalism, educational websites not directly evo/creo related, sequence or fossil data, etc.) scientific information on evolution.

Related hints and tips should also be added as appropriate, perhaps this would have potential as a FAQ at some point.

When posting links to journals, please make a note regarding access.



This is the National Library of Medicine's free search engine for "biomedical" literature, but in practice it includes all major general science journals, anything related to molecular biology, many more general biology journals (weaker on ecology etc.), and in general gobbs of evolution stuff on your topic of interest.

For an author search, do "lastname firstinitials" without commas or periods.  Separate multiple authors with commas.

For example, Thornhill and Ussery wrote an article outlining the various ways that "irreducibly complexity" can evolve.  Search PubMed on "ussery d, thornhill" and you get:

A classification of possible routes of Darwinian evolution

Searching on keywords or authors will never get you everything interesting on the first shot.  A key feature is the "Related Articles" link to the upper-right of each reference.

For example, here is an article on changes-of-function in evolutionary history:


Bioessays 1999 May;21(5):432-9
Generation of evolutionary novelty by functional shift.

Ganfornina MD, Sanchez D.

Biology Department, University of Utah, Salt Lake City 84112, USA.

That biological features may change their function during evolution has long been recognized. Particularly, the acquisition of new functions by molecules involved in developmental pathways is suspected to cause important morphologic novelties. However, the current terminology describing functional changes during evolution (co-option or recruitment) fails to recognize important biologic distinctions between diverse evolutionary routes involving functional shifts. The main goal of our work is to stress the importance of an apparently trivial distinction: Whether or not the element that adopts a new function (anything from a morphologic structure to a protein domain) is a single or a duplicated element. We propose that natural selection must act in a radically different way, depending on the historic succession of co-option and duplication events; that is, co-option may provide the selective pressure for a subsequent gene duplication or could be a stabilizing factor that helps maintain redundancy after gene duplication. We review the evidence available on functional changes, focusing whenever possible on developmental molecules, and we propose a conceptual framework for the study of functional shifts during evolution with a level of resolution appropriate to the power of our current methodologies.

But what else exists out there on this topic?  Trying different keywords is a possibility, e.g. "cooption", "co-option", "co-optation", "change in function", "functional shift", etc., but this is tedious.  Instead, once you've found one good article, click on "Related articles":

Articles related to Ganfornina and Sanchez 1999

...and you get a pile:


1:  Ganfornina MD, Sanchez D. Related Articles, Links  

Generation of evolutionary novelty by functional shift.
Bioessays. 1999 May;21(5):432-9. Review.
PMID: 10376014 [PubMed - indexed for MEDLINE]

2:  True JR, Carroll SB. Related Articles, Links  

Gene co-option in physiological and morphological evolution.
Annu Rev Cell Dev Biol. 2002;18:53-80.
PMID: 12142278 [PubMed - in process]

3:  Van de Peer Y, Taylor JS, Braasch I, Meyer A. Related Articles, Links  

The ghost of selection past: rates of evolution and functional divergence of anciently duplicated genes.
J Mol Evol. 2001 Oct-Nov;53(4-5):436-46.
PMID: 11675603 [PubMed - indexed for MEDLINE]

4:  Eizinger A, Jungblut B, Sommer RJ. Related Articles, Links  

Evolutionary change in the functional specificity of genes.
Trends Genet. 1999 May;15(5):197-202. Review.
PMID: 10322487 [PubMed - indexed for MEDLINE]

5:  Taylor JS, Van de Peer Y, Meyer A. Related Articles, Links  

Genome duplication, divergent resolution and speciation.
Trends Genet. 2001 Jun;17(6):299-301. Review.
PMID: 11377777 [PubMed - indexed for MEDLINE]

6:  Thornton JW, DeSalle R. Related Articles, Links  

Gene family evolution and homology: genomics meets phylogenetics.
Annu Rev Genomics Hum Genet. 2000;1:41-73. Review.
PMID: 11701624 [PubMed - indexed for MEDLINE]

7:  Otto SP, Yong P. Related Articles, Links  

The evolution of gene duplicates.
Adv Genet. 2002;46:451-83. Review.
PMID: 11931235 [PubMed - indexed for MEDLINE]

8:  Krakauer DC, Nowak MA. Related Articles, Links  

Evolutionary preservation of redundant duplicated genes.
Semin Cell Dev Biol. 1999 Oct;10(5):555-9. Review.
PMID: 10597640 [PubMed - indexed for MEDLINE]

9:  Kondrashov FA, Rogozin IB, Wolf YI, Koonin EV. Related Articles, Links  

Selection in the evolution of gene duplications.
Genome Biol. 2002;3(2):RESEARCH0008.
PMID: 11864370 [PubMed - indexed for MEDLINE]


Also, be sure to try the "Sort by" window and selected "Pub Date" to bring up the most recent articles.  Doing this on the above article brought up:


1:  Woolhouse ME, Webster JP, Domingo E, Charlesworth B, Levin BR. Related Articles, Links  

Biological and biomedical implications of the co-evolution of pathogens and their hosts.
Nat Genet. 2002 Dec;32(4):569-77.
PMID: 12457190 [PubMed - in process]

2:  Manley GA. Related Articles, Links  

Evolution of structure and function of the hearing organ of lizards.
J Neurobiol. 2002 Nov 5;53(2):202-11. Review.
PMID: 12382276 [PubMed - in process]

3:  Prince VE, Pickett FB. Related Articles, Links  

Splitting pairs: the diverging fates of duplicated genes.
Nat Rev Genet. 2002 Nov;3(11):827-37.
PMID: 12415313 [PubMed - in process]

4:  Karev GP, Wolf YI, Rzhetsky AY, Berezovskaya FS, Koonin EV. Related Articles, Links  

Birth and death of protein domains: A simple model of evolution explains power law behavior.
BMC Evol Biol. 2002 Oct 14 [epub ahead of print]
PMID: 12379152 [PubMed - as supplied by publisher]


Date: 2002/12/13 02:14:51, Link
Author: niiicholas
PubMed Central: a central archive of scientific literature that is freely available to the public without subscription.  Sometimes the whole journal is free, sometimes the material is made freely available after 6 months.

Oftentimes you will have to complete a free registration to access free content.

I believe this is the current list of journals with free online content:

Top journals from this list for evolution-related stuff:

Genome Biology

Proceedings of the National Academy of Sciences of the United States of America
(also at )

Journal of Biology

A free article from the last one, advocating open access to scientific lit -- a logical position, considering how most of this research is taxpayer-funded:
Open access to the scientific journal literature
Peter Suber
J Biol. 2002; 1(1): 3

A list of journals with full-text access for subscribers (the subscribers are usually university libraries, generally they are available to anyone within the University's edu domain) tied into the PubMed search engine is here:


PS: Another important journal:

Archives back to 1996:

From 2000 on:

Current issue:

Several critques of ID have been published in Evolution:  link to search results

Date: 2002/12/13 03:35:04, Link
Author: niiicholas
History of mousetraps:


"Build a better mousetrap, and the world will beat a path to your door," Emerson supposedly wrote. But writer Jack Hope finds what Emerson really wrote: "If a man has good corn, or wood, or boards, or pigs, to sell ... you will find a broad hard-beaten road to his house." [1] Nothing there about mousetraps. In 1889, seven years after Emerson died, someone quoted him as having said, "If a man can write a better book, preach a better sermon, or make a better mousetrap than his neighbor ..." and so on.

Emerson meant that quality prevails in the marketplace, and that comes to light in an odd way with the history of mousetraps. We've made a vast investment of ingenuity in them. By now the Patent Office has issued over 4400 mousetrap patents. Yet only twenty or so of those patents have ever made any money.

Today some 400 people still apply for mousetrap patents each year. That leaves me to wonder whether mousetraps really promise a fast track to inventive success, or if they're simply born of some morbid fascination with killing mice.

Actually, the mousetrap problem was solved in 1899 by one John Mast of Lititz, Pennsylvania. Mast filed for a patent on his now-familiar snap-trap. A heavy spring-steel wire swings down and breaks the mouse's neck when he nibbles cheese on the trigger mechanism. That was only ten years after the mousetrap quotation became common currency. The inventive muse (or maybe the inventive mouse!;) keeps generating mousetrap patents, but none has yet beaten the snap-trap in the marketplace. No one has really built a better mousetrap.

Before (and after) Mast, inventors cooked up an unending series of gadgets for mashing, cutting, and maiming mice -- for drowning them -- for catching them alive. Early in the 20th century, people tried electrocution. The problem is, an electrocuted mouse continues to fry until someone smells the mess.

In the end, esthetics and mercy are twin factors that've strongly determined what the public will and will not use. In the 1980s, a superglue trap came out. It worked, but homeowners found themselves faced with a screaming mouse, still living, glued to a piece of sticky cardboard, dying of exhaustion. If mice have to be killed, most people can deal with a quickly broken neck. The more gruesome stuff won't sell in the long run.

And when snap-trap makers found most people throwing the trap out with the mouse, not even trying to disengage it, they followed the public's lead and began advertising snap-traps as "disposable."

So while the mousetrap has become an icon for inventive creativity, the public eventually stipulates what's acceptable and what is not -- in the grisly business of holding a competing species at bay.

I'm John Lienhard, at the University of Houston, where we're interested in the way inventive minds work.

(Theme music)

1. Hope, J., A Better Mousetrap. American Heritage, October 1996, pp. 90-97.
Here's a mousetrap for you! See the following website:


The Conventional Snap Trap

Date: 2002/12/13 03:41:18, Link
Author: niiicholas
The History of the Mousetrap

Some patented mousetraps:

Date: 2002/12/17 15:28:17, Link
Author: niiicholas

I'd like to say that it's refreshing to hear an evolutionist saying the opposite of what the majority on their side claim.  I personally perceive that the main reason you see ID'ers staying away from identifying the Designer is a reaction to evolutionists who insist that any inquiry which gives even a semblance of similarity to creation ideas needs to be quashed pronto.

Most of the reactions that I see on the internet by evolutionists involve them stating that religion has absolutely no place in any scientific investigation.  Naturally, if an ID'er should mention a Deity, he/she would immediately be branded as a scientific heretic for allowing religion in the investigation.

The problem, of course, with supernatural explanations is that are usually unconstrained -- anything can be explained, so nothing is explained.  Such explanations -- and here I think that "superadvanced aliens" and "unspecified designer" are also in the same epistemic category -- deserve to be excluded.

However, if the designer hypothesis is constrained enough, so that certain things are expected and other things are not, then it is at least potentially testable and hence potentially scientific.  E.g. "stone age humans did that" is a perfectly testable hypothesis for Stonehenge, even if the reasons aren't completely known.

Date: 2002/12/17 20:27:28, Link
Author: niiicholas
I would just like to say that I think the name Ciona intestinalis sounds like a disease rather than a tunicate.

(or, maybe, the scientist who named it thought it resembled a bit of intestine)

Ciona genome homepage

Date: 2002/12/17 20:39:37, Link
Author: niiicholas
Some articles on virulence functions for:

(1) Type III secretion systems
Cornelis GR, and Frédérique Van Gijsegem. Assembly and function of Type III secretory systems. Annual Reviews Microbiology. 2000. 54:735-774.

In the "T3SS are not good for you" theme:


For a rather long period, it was assumed that gram-negative bacteria do not "secrete" proteins into their environment but only export proteins in their strategic periplasm. However, research in the last two decades has revealed that gram-negative bacteria do indeed transfer proteins across their sophisticated outer membrane, and they do this by a variety of systems that are now classified into four major types and several minor ones. Type I, exemplified by the hemolysin secretion system of Escherichia coli, is a rather simple exporter that is based on only three proteins, one of which belongs to the ABC transporters. Type II is a very complex apparatus that extends the general secretory pathway and transfers fully folded enzymes or toxins from the periplasm to the extracellular medium, across the outer membrane. Type IV, another complex system that transfers pertussis toxin among others, is related to the apparatus of Agrobacterium spp. that transfers DNA to plant cells. Finally, type III, the subject of this review, is a sophisticated apparatus that couples secretion with pathogenesis.

In bacteria that are pathogenic for animals, type III secretion systems allow extracellular bacteria adhering to the surface of a host cell to inject specialized proteins across the plasma membrane. This system probably also allows bacteria residing in vacuoles to inject proteins across the vacuolar membrane. The injected proteins subvert the functioning of the aggressed cell or destroy its communications, favoring the entry or survival of the invading bacteria. Type III is thus not a secretion apparatus in the strict sense of the term but rather a complex weapon for close combat. It contributes to a number of totally different animal diseases with a variety of symptoms and severities, from fatal septicemia to mild diarrhea and from fulgurant diarrhea to chronic infection of the lung. Type III secretion has been extensively studied in Yersinia spp. (reviewed in 25), in Salmonella spp. (reviewed in 47), in Shigella spp. (reviewed in 138), and in enteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli (EHEC) (40, 50, 72). It has also been described in Pseudomonas aeruginosa (TL Yahr & DW Frank, Genbank PAU56077), Chlamydia trachomatis and Chlamydia pneumoniae (73A), Bordetella bronchiseptica (MH Yuk, ET Harvill, JF Miller, Genbank AFO49488), Bordetella pertussis (78A) and in Burkholderia pseudomallei (The Sanger Center, Cambridge, UK). It is surprising that Salmonella typhimurium and Yersinia spp. have not only one type III system but two (61, 104; S Carlson & DE Pierson, Genbank AFO055744; The Sanger Center, Cambridge, UK), presumably playing their role at different stages of the infection (Figure 1).

Type III systems in animal pathogens. Illustrated are the various bacterial pathogens endowed with type III secretion, injecting effectors into the cytosol of a eukaryotic target cell. See Table 3 for references.

(bold added)

(2) In the "Flagella aren't necessarily good for you either" category:

Giron JA, Torres AG, Freer E, Kaper JB. The flagella of enteropathogenic Escherichia coli mediate adherence to epithelial cells. Molecular Microbiology 2002 Apr;44(2):361-79

Date: 2002/12/17 21:06:24, Link
Author: niiicholas
In the "nonmotile appendages can have a dispersal-related function despite being nonmotile" category:


Knutton S, Shaw RK, Anantha RP, Donnenberg MS, Zorgani AA. The type IV bundle-forming pilus of enteropathogenic Escherichia coli undergoes dramatic alterations in structure associated with bacterial adherence, aggregation and dispersal.  Mol Microbiol 1999 Aug;33(3):499-509
BFP, a plasmid-encoded type IV bundle-forming pilus produced by enteropathogenic Escherichia coli (EPEC), has recently been shown to be associated with the aggregation of bacteria and dispersal of bacteria from bacterial microcolonies. In standard 3 h HEp-2 cell assays, EPEC adhere in localized microcolonies; after 6 h, bacterial microcolonies are no longer present, indicating that bacterial aggregation and dispersal occurs in vitro during EPEC adhesion to cultured epithelial cells. To examine the role of BFP in EPEC aggregation and dispersal, we examined HEp-2 cell adhesion of strain E2348/69 and defined E2348/69 mutants by immunofluorescence and immunoelectron microscopy. BFP was expressed initially as approximately 40 nm diameter pilus bundles that promoted bacteria-bacteria interaction and microcolony formation. BFP subsequently underwent a striking alteration in structural organization with the formation of much longer and thicker ( approximately 100 nm diameter) pilus bundles, which frequently aggregated laterally to form even thicker bundles often arranged in a loose three-dimensional network; EPEC dispersal from bacterial microcolonies was associated with this transformation of BFP from thin to thick bundles. Bacterial dispersal and transformation of BFP from thin to thick bundles did not occur with a bfpF mutant of strain E2348/69. It is concluded that BFP promotes both the formation and the dispersal of EPEC microcolonies, that the dispersal phase requires BfpF and that dispersal is associated with dramatic alterations in the structure of BFP bundles.


As dispersal of bacteria from microcolonies occurred between 3 h and 6 h, we examined cells at intermediate times in order to follow the dispersal process and any associated change in BFP morphology. At 4 h, by both immunofluorescence (Fig. 6A, arrow) and scanning electron microscopy (Fig. 7A, arrows), one could start to see the formation of thick BFP bundles within some bacterial microcolonies and, by scanning electron microscopy, bacteria appeared to have been lost from regions of the microcolony in which thick BFP bundles had formed (Fig. 7A). At 5 h, significant dispersal of bacteria from many microcolonies had occurred, although this varied from colony to colony.

Fig. 7. Scanning electron micrographs of HEp-2 cells infected with EPEC strain CVD206 for 4 h (A), 5 h (B) and 6 h © showing stages in bacterial dispersal. After 4 h, thick BFP bundles are forming within this bacterial microcolony, and bacteria look as though they may have been lost from these regions of the microcolony (A, arrows). After 5 h, dispersal of bacteria from some microcolonies is almost complete, and only a few small bacterial aggregates remain attached to thick BFP bundles (B, arrows); in contrast, there is no evidence of BFP transformation or bacterial dispersal in the microcolony seen on the right (B, asterisk). After 6 h, bacterial dispersal is virtually complete; one of the few remaining bacteria from this microcolony is anchored to the thick BFP bundles by thin bundles (C, arrows). Scale bars: A, 1 m; B, 2 m; C, 0.5 m.


BfpF and bacterial dispersal

BfpF has been shown to be required for the dispersal of EPEC from bacterial microcolonies (Bieber et al., 1998). We therefore examined a bfpF mutant of E2348/69 in order to determine whether the observed morphological transformation of BFP was affected by this component of the BFP operon. In 3 h assays, we confirmed previous observations that a mutation in bfpF resulted in increased localized adhesion and that bfpF mutants are hyperpiliated compared with the wild-type strain. Furthermore, the mutation did not affect the ability of this strain to produce A/E lesions. Other than the size of microcolonies, this phenotype showed no alteration after 6 h (Fig. 8); bacteria remained hyperpiliated (Fig. 8A), adherent bacteria produced A/E lesions (Fig. 8C and D), but there was no transformation of thin BFP bundles to thick bundles (Fig. 8A and B) and no dispersal of bacteria from microcolonies (Fig. 8A, B and D).

The original description of BFP defined a role in bacteria-bacteria interaction and microcolony formation (Girón et al., 1991); recently, it has been shown that BFP also promotes dispersal of bacteria from aggregates (Bieber et al., 1998). Bieber et al. (1998) ended their paper by suggesting that 'to dissociate from the aggregate, bacteria would need to shed or distangle their pilus filaments from each other, a process that may require BfpF-mediated, energy dependent pilus retraction or a conformational change in the pilus quaternary structure'. This study, which has now demonstrated that EPEC aggregation and dispersal occurs in vitro during infection of cultured epithelial cells, suggests that the latter may be the case and that BFP undergoes a dramatic BfpF-dependent change in quaternary structure, the consequences of which are (i) a change from a thin to a thicker BFP bundle structure; (ii) disruption of bacteria-bacteria interactions; and (iii) dispersal of EPEC from bacterial microcolonies. The advantage to the organism of such a mechanism is that dispersal of bacteria primed to produce A/E lesions would be expected to lead to infection of new epithelial sites within the small bowel and, therefore, to a more efficient colonization of the gut. It has been known for some time that EAF plasmids are important in EPEC pathogenicity; BFP, by promoting more efficient colonization, is one likely reason why typical EPEC, which possess EAF plasmids, are more virulent than atypical EPEC, which lack EAF plasmids (Levine et al., 1985), and also more virulent than EPEC BfpF mutants, which lack the ability to disperse from microcolonies (Bieber et al., 1998).

Although we suggest a causal relationship between BfpF function, transformation of BFP morphology and bacterial dispersal, the data do not, in fact, demonstrate such a relationship, and so we cannot rule out the possibility that the converse is true, namely that BfpF is involved in other events that promote dispersal of bacteria from microcolonies, which leads, in turn, to the formation of the thick BFP bundles. BFP are very hydrophobic pili and, as bacteria disperse from an aggregate, it could be that the thin BFP filaments become more accessible to each other and are able to associate to form the thick BFP bundles.

In addition to playing a role in bacterial dispersal, an adhesive role for BFP has also been suggested (Girón et al., 1991). While the aim of this study was to examine the role of BFP in bacterial aggregation and dispersal, some of the observations have relevance to the possible role of BFP in cell adhesion. For example, the data suggest that BFP may be involved in initial EPEC adhesion, but that intimin-mediated intimate attachment is required for subsequent adhesive events. Also, the presence of cell-associated BFP after dispersal of all CVD206 bacteria after 6 h demonstrates that this form of BFP can adhere to the surface of HEp-2 cells. However, the role of BFP in EPEC adhesion to cultured and intestinal epithelial cells is the subject of a separate study to be published elsewhere (S. Knutton et al., manuscript in preparation).

[well, "nonmotility" is debatable, but this doesn't appear to be directional movement, i.e. swimming or crawling]

This study confirmed a role for BfpF in microcolony dispersal (Bieber et al., 1998) and showed that this protein, while not required for thin BFP bundle assembly, is involved either directly or indirectly in transformation from thin to thick BFP bundles. Based on the similarity between BfpF and PilT, the putative nucleotide-binding protein of P. aeruginosa, it has been proposed that BFP may play an analogous role to that proposed for PilT in type IV pilus function, namely as an energy source for the retraction of BFP (Anantha et al., 1998). The proposed function of PilT is based on electron microscopic studies of the distribution of antibody and bacteriophage binding to pili from wild-type and mutant P. aeruginosa strains (Bradley, 1974). The mutant used for these studies was subsequently found to have a mutation in pilT, which is also required for twitching motility (Whitchurch et al., 1991). As proteins in the PilT family are proposed to reside in the cytoplasm, our finding that BfpF appears to have a profound effect on the quaternary structure of BFP outside of the bacteria is surprising. However, as BFP has a marked propensity to intertwine in rope-like bundles, it is possible that retraction of individual pili within a bundle mediated by BfpF leads to thickening of the bundle in much the same way as pulling on an individual fibre leads to thickening of a twine. Thus, our study provides additional evidence that type IV pili such as BFP are not fixed structures, but are capable of dynamic alterations that influence bacterial adherence and pathogenesis.

Date: 2002/12/18 12:20:34, Link
Author: niiicholas
Here is a masterful bit of propaganda from the DI's John West (he is a political scientist, literally). Particularly annoying is the "truth is established by endless repetition" tactic used by demagogues in the media, and by IDists regarding Icons of Evolution.

This guy oughta read the Icons FAQs:

If there was ever a bit of propaganda that deserved a refutation, it is below, so if you can't resist spending some time debunking this, CC your replies here.


December 17, 2002, 9:20 a.m.
Darwin in the Classroom
Ohio allows alternatives.

By John G. West Jr.

After months of debate, the Ohio State Board of Education unanimously adopted science standards on Dec. 10 that require Ohio students to know "how scientists continue to investigate and critically analyze aspects of evolutionary theory."

Ohio thus becomes the first state to mandate that students learn not only scientific evidence that supports Darwin's theory but also scientific evidence critical of it. While the new science standards do not compel Ohio's school districts to offer a specific curriculum, Ohio students will need to know about scientific criticisms of Darwin's theory in order to pass graduation tests required for a high-school diploma.

Ohio is not the only place where public officials are broadening the curriculum to include scientific criticisms of evolution. In September the Cobb County School District in Georgia, one of the largest suburban school districts in the nation, adopted a policy encouraging teachers to discuss "disputed views" about evolution as part of a "balanced education." And last year, Congress in the conference report to the landmark No Child Left Behind Act urged schools to inform students of "the full range of scientific views" when covering controversial scientific topics "such as biological evolution."

After years of being marginalized, critics of Darwin's theory seem to be gaining ground. What is going on? And why now?

Two developments have been paramount.

First, there has been growing public recognition of the shoddy way evolution is actually taught in many schools. Thanks to the book Icons of Evolution by biologist Jonathan Wells, more people know about how biology textbooks perpetuate discredited "icons" of evolution that many biologists no longer accept as good science. Embryo drawings purporting to prove Darwin's theory of common ancestry continue to appear in many textbooks despite the embarrassing fact that they have been exposed as fakes originally concocted by 19th-century German Darwinist Ernst Haeckel. Textbooks likewise continue to showcase microevolution in peppered moths as evidence for Darwin's mechanism of natural selection even though the underlying research is now questioned by many biologists.

When not offering students bogus science, the textbooks ignore real and often heated scientific disagreements over evolutionary theory. Few students ever learn, for example, about vigorous debates generated by the Cambrian Explosion, a huge burst in the complexity of living things more than 500 million years ago that seems to outstrip the known capacity of natural selection to produce biological change.

Teachers who do inform students about some of Darwinism's unresolved problems often face persecution by what can only be termed the Darwinian thought police. In Washington state, a well-respected biology teacher who wanted to tell students about scientific debates over things like Haeckel's embryos and the peppered moth was ultimately driven from his school district by local Darwinists.

Science is supposed to prize open minds and critical thinking. Yet the theory of evolution is typically presented today completely uncritically, as a dogma to be accepted rather than as a theory to be explored and questioned. Is it any wonder that policymakers and the public are growing skeptical of such a one-sided approach?

A second development fueling recent gains by Darwin's critics has been the demise of an old stereotype.

For years, Darwinists successfully shut down any public discussion of Darwinian evolution by stigmatizing every critic of Darwin as a Biblical literalist intent on injecting Genesis into biology class. While Darwinists still try that tactic, their charge is becoming increasingly implausible, even ludicrous. Far from being uneducated Bible-thumpers, the new critics of evolution hold doctorates in biology, biochemistry, mathematics and related disciplines from secular universities, and many of them teach or do research at American universities. They are scientists like Lehigh University biochemist Michael Behe, University of Idaho microbiologist Scott Minnich, and Baylor University philosopher and mathematician William Dembski.

The ranks of these academic critics of Darwin are growing. During the past year, more than 150 scientists — including faculty and researchers at such institutions as Yale, Princeton, MIT, and the Smithsonian — adopted a statement expressing skepticism of neo-Darwinism's central claim that "random mutation and natural selection account for the complexity of life."

Deprived of the stock response that all critics of Darwin must be stupid fundamentalists, some of Darwin's public defenders have taken a page from the playbook of power politics: If you can't dismiss your opponents, demonize them.

In Ohio critics of Darwinism were compared to the Taliban, and Ohioans were warned that the effort to allow students to learn about scientific criticisms of Darwin was part of a vast conspiracy to impose nothing less than a theocracy. Happily for good science education (and free inquiry), the Ohio Board of Education saw through such overheated rhetoric. So did 52 Ohio scientists (many on the faculties of Ohio universities) who publicly urged the Ohio Board to require students to learn about scientific criticisms of Darwin's theory.

The renewed debate over how to teach evolution is not likely to stop with Ohio.

Under the No Child Left Behind Act, every state must enact statewide science assessments within five years. As other states prepare to fulfill this new federal mandate, one of the looming questions will be what students should learn about evolution. Will they learn only the scientific evidence that favors the theory, or will they be exposed to its scientific criticisms as well?

Ohio has set a standard other states would do well to follow.

— John West is a senior fellow of the Seattle-based Discovery Institute and chair of the department of political science at Seattle Pacific University.

Date: 2002/12/18 13:00:29, Link
Author: niiicholas
Here it is, I hadn't seen it before

The Wedge: A Christian Plan to Overthrow Modern Science?
Doubting Thomas, Feature Story, No. 6, April/May 1999. By Keith Lankford

Some minor inaccuracies and now a little out of date, but it features:

- a cogent comparison of ID to the 1950's Velikovskian movement

- a fair amount of material about Ed Larson, author of Summer of the Gods, and his conflict with the DI over his book being cited as part of the "Wedge" strategy.

Date: 2002/12/18 15:40:56, Link
Author: niiicholas
Atrazine degradation pathways appear to have arisen recently:

This lab studies 'em:

...Some of their papers are free online:

DeSouza, M. L., J. Seffernick, B. Martinez, and M. J. Sadowsky, L. P. Wackett (1998) Atrazine catabolism genes atzABC are widespread and highly conserved J. Bacteriol. 180(1):1951-1954.

De Souza, M. L., L. P. Wackett, and M. J. Sadowsky (1998) The atzABC genes encoding atrazine catabolism are located on a self-transmissible plasmid in Pseudomonas sp. strain ADP. Appl. Envir. Microbiol. 64(6): 2323-2326.

M.L. deSouza, D. Newcombe, S. Alvey, Crowley, D.E., A. Hay, M.J. Sadowsky, and L.P. Wackett (1998) Molecular basis of a bacterial consortium: Interspecies catabolism of atrazine. Appl. Environ. Microbiol. 64(1):178-184.

In the latter paper, it looks as if three different enzymes found in different bacteria were first combine in multispecies consortia that could metabolize atrazine, and that eventually the 3 genes were combined on a plasmid which then spread around the world in an evolutionary eyeblink.  If this is basically what happened it is yet another method of producing IC (as well as new information).


Atrazine is the most widely used s-triazine herbicide; it is utilized globally to control broadleaf weeds. Atrazine has been deployed only over the last 40 years and was previously considered to be nonmetabolizable by the majority of soil bacteria. During the first 35 years of its use, bacterial atrazine catabolism was proposed to occur largely via N-dealkylation reactions, resulting in the accumulation of aminotriazine compounds in both soils and laboratory media (3-5, 11, 20, 21). More recently, pure cultures of bacteria that catabolize atrazine to CO2 have been described (8, 26, 27, 30, 37).

The nearly simultaneous reports of atrazine-mineralizing pure cultures by five research groups (8, 26, 27, 30, 37) after years of unsuccessful efforts suggested a recent evolutionary origin and distribution of atrazine degradation genes. Consistent with this, all of the recently identified atrazine-degrading bacteria, isolated from around the world, have been shown to contain similar genes that encode enzymes which catabolize atrazine to cyanuric acid (16) (see Fig. 1). Cyanuric acid can be used by many soil bacteria as the sole nitrogen source (10-12, 19, 23). The enzymes for atrazine catabolism to cyanuric acid are encoded by the atzABC genes, which are found on a self-transmissible plasmid in Pseudomonas sp. strain ADP, the best characterized atrazine-metabolizing bacterium studied at the molecular level (7, 16, 17, 26, 32). Moreover, multiple insertion sequence-like elements have been identified in DNA flanking the atz genes. These studies are beginning to yield insights into atrazine gene evolution and dispersion.

These data also provide the tools for investigating bacterial atrazine genes in situ or in microbial consortia cultured in the laboratory on atrazine. For example, an atrazine-catabolizing consortium was reported in 1994 (3), but that predated the identification of catabolic genes and pure cultures which metabolize atrazine to carbon dioxide. More recently, a stable aerobic consortium was obtained from an agricultural soil and characterized with respect to its ability to catabolize atrazine (1, 2).

The present study was conducted to determine whether the genes and metabolism of the consortium (1, 2) resembled those found in recently described atrazine-metabolizing pure cultures. Our results show that different consortium members separately contained the atzA, -B, and -C genes. Coupled with biochemical studies, this revealed the interspecies metabolic interactions relevant to atrazine catabolism by the consortium. Our findings begin to provide a framework for understanding how catabolic pathways may evolve and the different conditions under which pure-culture or consortial metabolism may be selected for during the global recycling of organic matter.


The present study extends previous work by demonstrating the individual metabolic and genetic contributions of consortium members that use a proposed recently evolved catabolic pathway (16). Atrazine and related s-triazine herbicides have been in commercial use for approximately 40 years. The wide use of s-triazine herbicides has led to their detection as contaminants in groundwater (6, 28, 29) and to point source soil contamination problems where these herbicides have been spilled. Previously, many isolates and mixed cultures that partially degrade atrazine have been found (3, 10); more recently, several bacterial pure cultures which can completely mineralize atrazine and other s-triazines have been isolated (8, 26, 27, 30, 37). In 1995, Mandelbaum et al. (26) isolated a single atrazine-mineralizing bacterium from a mixture of bacteria originally reported to be a consortium (24, 25), which suggested that the isolate arose from gene transfer which occurred in the mixed culture. The possibility of this has been heightened by our observation that the atzABC genes are located on a 96-kb plasmid, with at least two genes having flanking regions with high homologies to known insertion sequence elements (16). Thus, the present study may offer a window to the evolution of a catabolic pathway by beginning to reveal how genes move from a consortium to individual strains and how mixed cultures containing metabolically cooperating genes may be stably maintained.

Date: 2002/12/18 18:24:58, Link
Author: niiicholas
Over at ARN, Mike Gene is again claiming that the question "What should make one suspect ID?" has not/cannot be sufficiently answered by ID skeptics.  The implication is basically that ID skeptics are close-minded and unable to consider the matter in a neutral, open, explorative way.;f=13;t=000536

But there are lots of things that would make me suspect ID.  Note that these things are not the same things that would prove it beyond a reasonable doubt, although a lot of these "evidences for suspicion" put together might fit that bill.

MG specifically put forward the flagellum as an example, conveniently a particularly ancient system for which the kinds of evidence available for e.g. the immune system are much more difficult to come by.


Tell me what would cause you to suspect the flagellum as designed. Thus far, not one ID critic has shared a useful criterion.

As JP has noted in the thread, many answers to the "suspect" question have already been provided, it's just that Mike Gene doesn't like them because design does not entail that these things exist.  That's pretty much the problem with Mike-Gene-design, it doesn't appear to entail anything in particular at all.  Even IC systems are apparently accessible to evolution under MG-ID, so if the tremendously complicated immune system is shown to have plenty of evidence of gradual natural origins, he can just shrug it off and say that ID designed something more remote, like the flagellum.

Still, an observation does not have to be *entailed* by design in order to be an observation that would legitimately raise suspicion.  Evolution does not predict that any particular transitional fossil will be found, just that some will be found somehwere, and these legitimately raise suspicion.  Presumably even a rarified design hypothesis predicts that some kind of positive evidence will be found somewhere.

I would suspect (not conclude) design for the flagellum if there were evidence for any of the following:

1) A purpose other than maximizing the reproduction of the genes of the bacterium in question, that fits with some hypothesized designer.  E.g., mousetraps are designed for trapping mice that are annoying humans.  Note that in contrast, evolutionary theory predicts this for all complex "designed" systems.  Find a counterexample and you've disproved evolution.  Find a counterexample with a purpose that fits some specific designer hypothesis and you've got reason to suspect that designer hypothesis.

2) True IC, i.e. if the parts of the flagellum really did not have any function apart from contributing to flagellar function, i.e. that any subset of flagellar parts really was "by definition nonfunctional".  This was Behe's original attempted argument, and if it had held up under the weight of evidence then he would have had something.

3) Biologically impossible transplants of the complex "design" across phylogenetic lines.  This is seen *in spades* in human design systems.  However, in biological systems, such transplants appear to be limited in numerous ways:

a) Basically limited to single-celled critters without protected germ-line cells
b) Most commonly there to prokaryotes that are *known* to do all kinds of conjugation, DNA uptake, etc.
b.5) In eukaryotes, the most impressive cases lateral transfer are the cases of symbiosis, in which the genomes of the host and symbiont are in close association for millions of years and transfers can occur bit-by-bit while maintaining function
c) Suspicions of transplants are often confirmed by finding plasmids, insertion remnants, and evidence of other known lateral transfer mechanisms
d) Transplants are most common between prokaryotes (a) closely related or (b) living in close proximity
e) Apparently limited to relatively simple systems (single operon?), and the more complex the system, the more closely related must be the donor/acceptor.  The most complex system transferred that I can think of is Type III virulence systems, and (IIRC) these are all restricted to a relatively narrow group.

As an example of the contrast seen in human designs, the following highly complex systems originated locally and were rapidly transplanted into any manner of larger devices (cars, planes, boats, etc.) without any regard for the kinds of biological, ecological, and phlyogenetic patterns described above:

- computers
- GPSs
- satellite phones
- emergency transponders

4) It occurs to me suddenly that the pattern that all of these designed transplants follow is that they are useful *to the designer*, i.e. safety, navigation, etc.  So, even in a case where the lateral transfers were biologically possible, if the pattern of transfer fit the purposes of a hypothesized designer(s), I would suspect design.

5) Evidence of "front-loading", e.g. if many bacteria had buried instructions for flagella, protected somehow from degradative mutations (not a tough burden for your average superadvanced designer), that were waiting to be "turned on" at some point in the future for some purpose of a hypothesized designer (this is a modified version of Behe's supercell idea)

6) A communication-to-intelligent-beings signal encoded in the flagellar genes.  E.g., a prime number sequence apparently cleverly encoded in the essential nucleotides or amino acids of the flagellum.  I say "apparently" because just the bare fact of a prime number sequence would not constitute proof, only suspicion (which is all MG wants anyway), unlike in astronomy it is just possible that there are ways for biological mechanisms to generate primes (although it is quite a stretch from 17-year cicadas to genome sequences).

I'm sure there's more...I won't, however, say the one that I think MG prefers, namely "it looks designed", because it's pretty clear that natural selection can produce complex "designed" adaptation when the adaptation benefits the genes of the organism.  Even Mike Gene concedes this, so IMO it appears that he is being inconsistent when he places the thus-far-unverified-in-biology ID hypothesis on the same footing as the well-verified-in-biology NS hypothesis.  Why not also include Lamarkian evolution and complexity theory on the same footing also?  I would say that each of these has at least a wee bit of positive evidence raising a little bit of suspicion, unlike ID.

Links to other threads and CCed posts on this topic would be worthwhile.

Date: 2002/12/19 00:04:03, Link
Author: niiicholas
This is a big enough topic to deserve a thread separate from the origin of information or the origin of particular systems.

Short version: there is lots of evidence that multiple-parts-required metabolic pathways have originated via known evolutionary processes, in human and even lab lifetimes.

Here is a synthesis article I just came across:


Curr Opin Struct Biol 2002 Jun;12(3):374-82
Pathway evolution, structurally speaking.

Rison SC, Thornton JM.

Department of Biochemistry and Molecular Biology, University College London, Darwin Building, Gower Street, London WC1E 6BT, UK.

Small-molecule metabolism forms the core of the metabolic processes of all living organisms. As early as 1945, possible mechanisms for the evolution of such a complex metabolic system were considered. The problem is to explain the appearance and development of a highly regulated complex network of interacting proteins and substrates from a limited structural and functional repertoire. By permitting the co-analysis of phylogeny and metabolism, the combined exploitation of pathway and structural databases, as well as the use of multiple-sequence alignment search algorithms, sheds light on this problem. Much of the current research suggests a chemistry-driven 'patchwork' model of pathway evolution, but other mechanisms may play a role. In the future, as metabolic structure and sequence space are further explored, it should become easier to trace the finer details of pathway development and understand how complexity has evolved.

Then of course we have:


Trends in Biochemical Sciences
Volume 25, Issue 6, 1 June 2000, Pages 261-265
Evolution of a metabolic pathway for degradation of a toxic xenobiotic: the patchwork approach

Shelley D. Copley

The pathway for degradation of the xenobiotic pesticide pentachlorophenol in Sphingomonas chlorophenolica probably evolved in the past few decades by the recruitment of enzymes from two other catabolic pathways. The first and third enzymes in the pathway, pentachlorophenol hydroxylase and 2,6-dichlorohydroquinone dioxygenase, may have originated from enzymes in a pathway for degradation of a naturally occurring chlorinated phenol. The second enzyme, a reductive dehalogenase, may have evolved from a maleylacetoacetate isomerase normally involved in degradation of tyrosine. This apparently recently assembled pathway does not function very well: pentachlorophenol hydroxylase is quite slow, and tetrachlorohydroquinone dehalogenase is subject to severe substrate inhibition.

An important update:


J Bacteriol 2003 Jan;185(1):302-10
A Previously Unrecognized Step in Pentachlorophenol Degradation in Sphingobium chlorophenolicum Is Catalyzed by Tetrachlorobenzoquinone Reductase (PcpD).

Dai M, Rogers JB, Warner JR, Copley SD.

The first step in the pentachlorophenol (PCP) degradation pathway in Sphingobium chlorophenolicum has been believed for more than a decade to be conversion of PCP to tetrachlorohydroquinone. We show here that PCP is actually converted to tetrachlorobenzoquinone, which is subsequently reduced to tetrachlorohydroquinone by PcpD, a protein that had previously been suggested to be a PCP hydroxylase reductase. pcpD is immediately downstream of pcpB, the gene encoding PCP hydroxylase (PCP monooxygenase). Expression of PcpD is induced in the presence of PCP. A mutant strain lacking functional PcpD has an impaired ability to remove PCP from the medium. In contrast, the mutant strain removes tetrachlorophenol from the medium at the same rate as does the wild-type strain. These data suggest that PcpD catalyzes a step necessary for degradation of PCP, but not for degradation of tetrachlorophenol. Based upon the known mechanisms of flavin monooxygenases such as PCP hydroxylase, hydroxylation of PCP should produce tetrachlorobenzoquinone, while hydroxylation of tetrachlorophenol should produce tetrachlorohydroquinone. Thus, we proposed and verified experimentally that PcpD is a tetrachlorobenzoquinone reductase that catalyzes the NADPH-dependent reduction of tetrachlorobenzoquinone to tetrachlorohydroquinone.


Pentachlorophenol (PCP) is a widely used and highly toxic wood preservative. It was first introduced as a pesticide in 1936 (7) and is not known to be a natural product. Despite its recent introduction into the environment and its high toxicity, several strains of Sphingobium chlorophenolicum (previously Sphingomonas chlorophenolica) (24) that can mineralize PCP have been identified. The best studied of these are strains ATCC 39723 (19), RA-2 (23), and UG30 (6). It appears that S. chlorophenolicum has assembled a new metabolic pathway capable of converting this anthropogenic compound into a recognizable metabolite. Our previous studies suggest that this pathway has been assembled by patching together enzymes from at least two different metabolic pathways (8). PCP hydroxylase (PCP monooxygenase; EC and 2,6-dichlorohydroquinone dioxygenase may have originated from enzymes that hydroxylated a naturally occurring chlorinated phenol and then cleaved the resulting hydroquinone. Tetrachlorohydroquinone (TCHQ) dehalogenase appears to have originated from a glutathione-dependent double bond isomerase such as maleylacetoacetate isomerase or maleylpyruvate isomerase (which are involved in degradation of tyrosine and benzoate, respectively) (2). If this pathway has evolved recently in response to the introduction of PCP into the environment, then it would not be expected to perform at the high level characteristic of pathways that have evolved over periods of millions or billions of years. Indeed, the PCP degradation pathway shows signs of immaturity in several respects. First, PCP hydroxylase, the first enzyme in the pathway, is very inefficient in vitro (P. M. Kiefer and S. D. Copley, unpublished data), and appears to severely limit the flux of PCP through the pathway in vivo (17). Second, TCHQ dehalogenase is profoundly inhibited by its aromatic substrate (K. Anandarajah, P. M. Kiefer, and S. D. Copley, unpublished data). Third, TCHQ dehalogenase expression is not regulated in tandem with the other known enzymes in the pathway but is apparently constitutive (21). All of these findings are consistent with the idea that the PCP degradation pathway has been patched together rather recently and has not been fine-tuned to perform as effectively as do most bacterial metabolic pathways.

The gene encoding PCP hydroxylase (pcpB) is immediately upstream of two additional genes. pcpR encodes a regulatory protein that responds to PCP (5). pcpD, which is immediately downstream of pcpB, resembles genes for the reductase components of two-component oxygenases, some of which hydroxylate aromatic compounds. Based upon this resemblance, it has been proposed that PcpD is a reductase that facilitates the hydroxylation of PCP by PCP hydroxylase (19), and the annotation of PcpD in GenBank states that it is PCP 4-monooxygenase reductase. We suspected that this assignment was incorrect because PCP hydroxylase is a flavin monooxygenase, and such enzymes do not generally require reductases. Consequently, we undertook studies to determine whether PcpD is required for degradation of PCP. We find that transcription of pcpD is induced by PCP, as previously reported for pcpA (29) and pcpB (20). A mutant strain in which PcpD has been knocked out is able to remove PCP from the medium when it is present at low concentrations, but not when it is present at high concentrations. In contrast, the knockout strain can remove tetrachlorophenol (TCP) from the medium as well as the wild-type strain, even at high concentrations. These results suggest that PcpD may catalyze a step that is critical for degradation of PCP but not TCP and therefore must involve the chlorine at the 4 position of PCP. Based upon the expected mechanism of the hydroxylase reaction, the sequence of PcpD, and our experimental results, we propose that PcpD is a tetrachlorobenzoquinone (TCBQ) reductase required for degradation of PCP but not TCP.

Date: 2002/12/20 01:06:29, Link
Author: niiicholas
I rediscovered the Breakpoint article, it has a list of links at the bottom:

The Moth Myth
BreakPoint with Charles Colson
July 25, 2002
Nothing Natural about This Selection

Date: 2002/12/20 01:10:56, Link
Author: niiicholas
Intelligent Design jargon explained!
By Casey Luskin

Lesse, by my count there were 3-4 terms discussed and none were significantly clarified...basically "trust me, ID is for real".

Date: 2002/12/20 02:11:24, Link
Author: niiicholas
This was posted on the DI website.  


Alan Gishlick and the NCSE: Full of Sound and Fury, Signifying Nothing New on the Icons of Evolution

Jonathan Wells
Discovery Institute
December 13, 2002

On November 22, 2002, the National Center for Science Education posted Alan D. Gishlick’s “Icons of Evolution?: Why much of what Jonathan Wells writes about evolution is wrong” on their website.

Gishlick’s piece is a long-winded version of a review of my book, Icons of Evolution: Why much of what we teach about evolution is wrong (Regnery, 2000), that he and NCSE President Kevin Padian published in March, 2002, in The Quarterly Review of Biology. Like their review, Gishlick’s new essay is primarily an attempt to defend the icons; and like the review, Gishlick’s essay is heavily seasoned with ad hominem attacks on me. But it adds nothing substantially new to the debate.

One point that Gishlick’s essay establishes beyond a shadow of a doubt, however, is that the icons of evolution are NOT simply textbook mistakes. In their March book review, Padian and Gishlick likened me to “kids who used to write to the letters page of Superman comics years ago” to complain about trivial typos. “Okay, kid,” they wrote, “mistakes happen, but did it really affect the story?” Apparently, Gishlick has decided that the icons of evolution are not simply mistakes that can be corrected or ignored; instead, they must be defended at all costs. Gishlick’s essay thereby reaffirms what I wrote in my response to published book reviews (including the one by him and Padian) a few months ago:

“If Darwinists could show that my criticisms of the icons of evolution were unwarranted, or if they would stop trying lamely to defend the icons and simply replace them with better evidence, I would drop my case. But Darwinists cannot defend the icons, and they cannot afford to abandon them, so they resort to insults and smears.”

Unfortunately for Gishlick, the cats are already out of the bag. When I lectured to biology students on a state university campus recently, their professors were incredulous when I told them that some people still defend the Miller-Urey experiment, Haeckel’s embryo drawings and the peppered myth. The NCSE’s desperate attempts to defend the indefensible are not fooling biologists in the field.

For more information, and for my previous responses to the sorts of things Gishlick rehashes in his essay, see my postings on the Discovery Institute website, especially the following:

“Critics Rave Over Icons of Evolution: A Response to Published Reviews” (June 12, 2002)

“Inherit the Spin: Darwinists Answer ‘Ten Questions’ with Evasions and Falsehoods” (January 15, 2002)

“Desperately Defending the Peppered Myth: A Response to Bruce Grant” (October 2, 2002)

“Moth-eaten Statistics: A Reply to Kenneth R. Miller” (April 16, 2002)

“There You Go Again: A Response to Kenneth R. Miller” (April 9, 2002)

Funny, Bruce Grant (lots of articles linked) was originally supposed to be one of the experts who had overturned the icon, but now the foremost American expert on the peppered moth has been relegated to being a non-authority by Wells.

Grant's most pointed comments are here:

Too bad Wells didn't take the opportunity to attempt to rebut a review that actually had the space to debunk his arguments in the detail they deserve.

Why much of what Jonathan Wells writes about evolution is wrong
by Alan D. Gishlick

Date: 2002/12/20 20:53:02, Link
Author: niiicholas
I probably made a mistake in mentioning a specific personality. Recommend we keep the focus on the topic rather than on personalities.

And having had my pseudonym "exposed" myself awhile ago, I strongly recommend against trying to figure out who pseudonyms are, people have a right to privacy whether or not they have a good reason. 'Net pseudonyms are the norm in discussion forums.  

Another thing that would make me suspect ID: if the various IC systems usually proposed to be the result of "interventions" (even this low level of detail is rarely reached) all showed some kind of common signature apart from adaptive complexity, this might be suspicious (depending on the signature).

Date: 2002/12/20 21:02:53, Link
Author: niiicholas
Over at the ID network's response to the AAAS resolution:

[url= 6 text]Here if the internal spaces don't muck it up[/url] is written:


6. The AAAS claim that a design inference is not testable is simply disingenuous. An inference of design is testable. Many scientific disciplines test for design every day, including routine testing of radio and light waves for alien intelligence by the SETI program.

   If ID is not testable and thus "non-scientific," then neither are several other disciplines currently held to be scientific. For example, in the SETI program, researchers are testing patterns in light and radio waves from outer space for non-human alien intelligence. ID and SETI both use the same design detection methodology. How could the SETI enterprise be considered scientific if its design detection methods are not scientifically valid? If design cannot be falsified, how can the AAAS consider it to be false? The AAAS claim that a design inference is not testable is refuted every day by countless design detection experts whose livelihood depends on design detection (e.g., forensic scientists, arson and crime investigators, cryptologists, archaeologists and SETI researchers).

   How does one "test" a design inference? A pattern or system that yields an inference of design must satisfy all of three criteria. If it cannot, then a design inference is not warranted (i.e., design is rejected as an explanation).

  • First, the pattern must exhibit apparent design - something that appears to be "specified." A specification is a pattern that has been configured for a purpose or that conveys some meaning or message that is independent of the significance of the individual events that make up the pattern. For example, the pattern "DESIGN" appears designed because it reflects meaning that is independent of the significance of each of the six letters that comprise it. DNA has the same characteristic.

  • Second, there must be no adequate natural explanation for the pattern. It cannot be a pattern that is required to appear by the operation of natural law. For example, a salt crystal and a river channel are regular patterns that can be explained by natural law (electromagnetism, gravity, erosion, moving water, the natural terrain). However, the precise sequence of the genetic symbols in "message bearing" DNA are not dictated by any known law.

  • Third, the pattern must be sufficiently complex that its arrangement by chance and law alone is statistically improbable. As mentioned above, the chance formation of the necessary DNA sequence for the first cell would appear to be statistically impossible.

       These general criteria are used in the analysis of patterns in all design detection sciences - archaeology, forensic sciences, cryptanalysis and the search for extraterrestrial intelligence. They are deemed adequate to test for design in those sciences. Why not in evolutionary biology? No scientific rational has been provided for accepting design detection methodologies in these other historical sciences and rejecting them in evolutionary biology.

    [italics original]

  • Point #2 looks like GOTG to me...

    There are lots of other problems here but this was particularly clear IMO.

    Date: 2002/12/20 21:49:41, Link
    Author: niiicholas
    This was just pointed out on an II thread:

    The Online Biology Textbook

    Lots of good graphics.  Although, they need a new horsey graphic:

    More like this:

    ...fortunately, Wells apparently prefers the older view of things, despite what you might think from the title of Icons of Evolution.  On page 199 he wrote,

    "The mere existence of extinct side-branches doesn't rule out the possibility that the evolution of modern horses was directed. A cattle drive has a planned destination, even though some steers might stray along the way."

    Discussed here:

    Another resource:

    Also the UC Museum of Paleontology Online:

    Teachers e-volution forum:

    Date: 2002/12/21 16:50:30, Link
    Author: niiicholas
    You're kidding.  I thought Chris Langan was the new ARN luminary, and a moderator himself to boot.

    I never could figure out what CTMU had to do with ID (or what it was at all), but then I didn't try very hard.

    Date: 2002/12/21 18:45:33, Link
    Author: niiicholas
    Over on this ARN thread,;f=13;t=000536;p=2

    ...Joy & Mike Gene are missing JP's point.  As explanatory hypotheses in science, an unconstrained supernatural designer and an unconstrained natural designer (or an unconstrained designer of unspecified supernaturalness or naturalness) have the same problem: they have no empirical implications.  

    (I am speaking of "constraint" in terms of "explanatory constraint" here -- an omnipotent designer or super-technological designer would be all-powerful but would still be a "constrained" explanation if his actions followed a pattern motivated by a specific goals.  But an unconstrained ID hypothesis is essentially what is often called "rarified design")

    Note that the point is not that we have to know these things about the IDer ahead of time, the point is that we have to hypothesize something with some empirical implications so that we have some idea of what kinds of evidence would strengthen or weaken our confidence in the hypothesis.

    Otherwise nothing is getting explained at all, even hypothetically.

    The two major explanatory constraints that can begin to elevate design hypotheses to something above the "IDdidit" level are, I think:

    1) Designer methods/capabilities
    2) Designer goals

    ...although there may be others.  Notably, for human-design hypotheses we have a lot of evidence informing both #1 and #2, even for prehistoric cases.

    For SETI, the scientists involved are quite clearly hypothesizing that alien designers will be like us in certain minimal but ways, namely:

    1) Designer methods/capabilities: radio
    2) Designer goals: interstellar communication (with us or others)

    If either of these hypotheses is wrong, then even if the universe is teeming with intelligent life, we will not discover it through SETI no matter how much money and time are put in.  This is not a weakness but a strength: the status of the hypothesis can be fairly rigorously evaluated at any point.  Currently it is:

  • Positive evidence: none
  • Negative evidence: a little bit (nothing found with current restricted detection limits)

    As for the general likelihood of intelligent life in the universe, this can begin to be assessed if we constrain our "existence of intelligent life" hypothesis to something like "basically like human life and formed by the same processes we think created us".

    If, on the other hand, our "existence of intelligent life" hypothesis is "intelligent life of unknown characteristics formed by unknown processes" then we have no basis on which to procede and the hypothesis is relegated to the shrugworthy category of "undetectable invisible pixies exist".

    As for ID, I think that IDists do specify constraints #1 and/or #2 fairly regularly, it's just that they usually do it in passing (or even in a semi-hidden fashion) rather than explicitly, they tend to deny such specifications in public, and when an ID skeptic thinks they detect a specific hypothesis and raises counterevidence that weakens it, the IDist tends to deny that such a specific hypothesis was ever proposed.  Such vagueness may be helpful in debates, but it stands no chance of moving the ID ball towards the goal line of science.
  • Date: 2002/12/23 23:39:22, Link
    Author: niiicholas
    I think that several considerations have to be added to Hunter's post before serious discussion can be had.  

    1) "Congruence" and "noncongruence" are not either/or entities, they a matter of degree.  Given N species being analyzed, there are something like (2n-3)!/(2n-2(n-2)!;) hypothetically possible ways of arranging them into a tree (Theobald 2002), and the (dis)similarity between two trees can be rigourously quanitified.

    This equation will differ slightly depending on whether the trees are rooted vs. unrooted, binary splits only, etc.  Regardless, the number of possible trees gets very big very fast: 4 species = 15 possible trees, 8 species = 135,135 possible trees.

    You can randomly generate tree diagrams at this cool page (Phylogeny and Reconstructing Phylogenetic Trees) and get the idea very quickly what the odds are of getting the same tree twice by random chance.

    So the question is not whether two phylogenies from different data sources/research labs are congruent or incongruent, full stop, the question is how congruent or incongruent are they?  Most of the examples touted as showing "incongruence" are actually quite minor phylogenetic disagreements.  E.g., the interrelationships of different groups of bats is a pretty trivial issue in the context of vertebrates or animalia.  If the microbats grouped most closely with anthropoid apes, and the macrobats with giraffes, then we'd have a significant disagreement.  This kind of thing does not happen in multicellular organisms with protected germ line cells, rather different datasets keep returning highly congruent phylogenies.

    So, just like any scientific measurement, there will be noise in input data.  The analogy here is to radiometric dating: if two measurement dates of a moon rock return ages of 4.6 and 4.5 billion years, this is very minor disagreement relative to the result (100 million years sounds like alot but is only a 2% disagreement).  If someone were to go around saying "geological measurements disagree by 100 million years and this is evidence against an old earth" they would be wrong. Similar minor disagreements, such as Teeling et al.'s 2002 bat study,  should not be cited as evidence for Hunter's proposition "there are also plenty of character/species sets that do not produce congruent phylogenies".  A real disagreement would occur if all of these different bat species did not group together and instead were randomly associated with the outgroup taxa, but as we can see this did not occur:


    The odds of all these bat species grouping together by chance are astronomical.

    2. Scale of the study and range of dataset

    As the age-of-the-moon example points out, what is important in considering disagreement in results is not the absolute measurement, but the size of the disagreement relative to the scale of the study.  100 million years sounds like alot but is peanuts in terms of the age of the earth.  Such a disagreement would be major, however, in a radiometric dating of dinosaur bones, and a data source with a smaller error would have to be used.  

    Radiometric datasets have ranges and scales over which they are useful, due essentially to their rate of decay.  You use uranium-lead to date the age of the moon, because it has a half-life of hundreds of millions of years, but it would be ridiculous to use it for dating an archeological artifact because the answer you would get (assuming the artifact was, say, something that had been forged by remelting the ore) would be "0 +/- millions of years".  Similarly, the half-life of C-14 is only ~5,000 years, so it is excellent for archeology but for anything older than 50,000 years it is useless (a result of "50,000 years old" for a carbon date essentially means "this sample is between 50,000 and infinite years old").  In the first case, the noise is much larger than the signal, and in the second case the signal is much smaller than the noise (these are slightly different, think about it for a sec.).

    With molecular sequences the same factors must be taken into account.  I don't currently have access to Hunter's cited Balter (1997), " Morphologists learn to live with molecular upstarts", but I would note that there is apparently a contrasting commentary (Mindell 1997) on that very article from the next month of Science, entitled ""Misleading" molecules?".  Probably the basic point is that the particular mtDNA sequences being used evolve too quickly (certain mtDNA sequences are, after all, used for tracing migration patterns within the human species), such that sequence similarity is low and therefore "noise" in the form of mutational biases is larger than the signal.  Certainly comparing chickens, amphibians, and fish is a long ways from what one normally sees mtDNA used for, e.g. species within a genus.  

    (Note in passing: not all mtDNA within a mitochondrion is the same.  It's possible that the above study used a very slowly evolving mtDNA sequence and similarity between e.g. birds and fish was high, e.g. >75%.  But I doubt it.  Let's get the Balter and Mindell articles and see what they say, shall we?)

    In summary, anytime one sees a cited "incongruence" they must consider the dataset is appropriate for the scale of the analysis.  If sequence similarity is approaching randomness then mutational biases are increasingly important to consider.

    3. Actual violation of lineal descent.  This is commonly the case for single-celled prokaryotes without protected germline DNA.  If you like, the tree hypothesis has been falsified, because it is known and has been observed in the lab that they can trade DNA laterally.  But this leaves the evidence for the common descent of e.g. all animals unquestioned.  Much more can be said here because LGT is itself a nonrandom process and certainly some things are harder to LGT than others, but this is another topic.  If we saw the kinds of disagreements in animals that we have in prokaryotes, as we have no mechanism for significant LGT in animals (viral transfers is about it I think), this would be a significant problem for the common descent theory.  But we don't.  "Disagreements" that I have seen cited for multicellular critters basically fall into the above categories.

    In summary, in answer to Hunter's question,


    My point is not to say explanatory mechanisms are out of bounds or that complicating factors should not be expected, but merely to raise the question: At what point does the use of these explanatory mechanisms become ad hoc and do we consider the Step 1 in the syllogism falsified?

    ...basically, these explanatory mechanisms are allowed when they themselves are well-supported by available data.  We can measure mtDNA rates of change and mutational biases.  We can observe and explain why LGT occurs in prokaryotes but not in mammals.  We can measure the degree of disagreement between trees and determine if the error is equivalent to 100 million years/4.6 billion years or not.

    There is a massive literature on all of this, which is why I'm surprised that Hunter thinks that biologists haven't thought about it.  The best introduction to it all is Theobald's FAQ at that talkorigins archive, referenced below. It references a lot of articles with titles like "Testing Common Descent" about the probabilities of hitting on congruent trees by chance.


    Theobald, Doug. 2002.  29 Evidences for Macroevolution

    Teeling, Emma C. et al. 2002 Microbat paraphyly and the convergent evolution of a key innovation in Old World rhinolophoid microbats Proc. Natl. Acad. Sci. USA, Vol. 99, Issue 3, 1431-1436.

    (bold added below)


    Molecular phylogenies challenge the view that bats belong to the superordinal group Archonta, which also includes primates, tree shrews, and flying lemurs. Some molecular studies also challenge microbat monophyly and instead support an alliance between megabats and representative rhinolophoid microbats from the families Rhinolophidae (horseshoe bats, Old World leaf-nosed bats) and Megadermatidae (false vampire bats). Another molecular study ostensibly contradicts these results and supports traditional microbat monophyly, inclusive of representative rhinolophoids from the family Nycteridae (slit-faced bats). Resolution of the microbat paraphyly/monophyly issue is essential for reconstructing the temporal sequence and deployment of morphological character state changes associated with flight and echolocation in bats. If microbats are paraphyletic, then laryngeal echolocation either evolved more than once in different microbats or was lost in megabats after evolving in the ancestor of all living bats. To examine these issues, we used a 7.1-kb nuclear data set for nine outgroups and twenty bats, including representatives of all rhinolophoid families. Phylogenetic analyses and statistical tests rejected both Archonta and microbat monophyly. Instead, bats are in the superorder Laurasiatheria and microbats are paraphyletic. Further, the superfamily Rhinolophoidea is polyphyletic. The rhinolophoid families Rhinolophidae and Megadermatidae belong to the suborder Yinpterochiroptera along with rhinopomatids and megabats. The rhinolophoid family Nycteridae belongs to the suborder Yangochiroptera along with vespertilionoids, noctilionoids, and emballonuroids. These results resolve the apparent conflict between previous molecular studies that sampled different rhinolophoid families. An important implication of rhinolophoid polyphyly is independent evolution of key anatomical innovations associated with the nasal-emission of echolocation pulses.

    Originally posted here:

    ICSID thread

    Date: 2002/12/24 02:32:17, Link
    Author: niiicholas
    Wow.  This just goes to show that everything is relative.

    Date: 2002/12/24 02:39:32, Link
    Author: niiicholas
    Quote (charlie d @ Dec. 20 2002,12:51)
    Yes, nice strategy.  
    According to Wells, if people ignore his arguments on the Icons, it's because they are not able to answer the arguments.
    If they answer the arguments, by showing that Wells is wrong, it's because they have to defend the Icons "at all costs".
    And if they change whatever there is to be changed about the Icons, it's because Wells' arguments were right in the first place.

    LOL, what a smoke seller!

    I noticed recently that the QRB has ended it's free-online-access startup policy (or whatever it was called) and that therefore the Padian and Gishlick review is no longer available to non-subscriber public types...making the various asundry links from Wells FAQs rather useless.

    Could this be remedied, or perhaps QRB will release their papers for free after a year or some such?

    Date: 2002/12/24 03:34:11, Link
    Author: niiicholas
    In the "yes, IDists have in fact argued that IC precludes the existence of precursors with other functions" category:


    There seem to be no obvious evolutionary forebears in nature, and certainly no fossil record, to explain how such a machine might have been selected for through a series of random mutations in some simpler flagellum-like structures.

    "If you don't have intermediate structures, it could mean one of two things, " Behe said. "Either we just haven't found them, or they are not there. It's a good bet, with these biochemical machines, that they aren't there."

    Nature's diversity beyond evolution
    Debate over 'intelligent design'

    Carl T. Hall, San Francisco Chronicle
    Sunday, March 17, 2002

    Date: 2002/12/26 02:19:56, Link
    Author: niiicholas
    A post from ICSID here:

    Perhaps the reason that Hunter finds the evidence for common descent weak is that he misunderstands crucial points.

    E.g., he has repeatedly alleged, without evidence, that designed objects will produce nested hierarchies.  But it just ain't so:



    Although it is trivial to classify anything subjectively in a hierarchical manner, only certain things can be classified objectively in a consistent nested hierarchy. The difference drawn here between "subjective" and "objective" is crucial and requires some elaboration, and it is best illustrated by example. Different models of cars certainly could be classified hierarchically - perhaps one could classify cars first by color, then within each color by number of wheels, then within each wheel number by manufacturer, etc. However, another individual may classify the same cars first by manufacturer, then by size, then by year, then by color, etc. The particular classification scheme chosen for the cars is subjective. In contrast, human languages, which have common ancestors and are derived by descent with modification, generally can be classified in objective nested hierarchies (Pei 1949; Ringe 1999). Nobody would reasonably argue that Spanish should be categorized with German instead of with Portugese. The difference between classifying cars and classifying languages lies in the fact that, with cars, certain characters (for example, color or manufacturer) must be considered more important than other characters in order for the classification to work. Which types of car characters are more important depends upon the personal preference of the individual who is performing the classification. In other words, certain types of characters must be weighted subjectively in order to classify cars in nested hierarchies; cars do not fall into natural, unique, objective nested hierarchies.

    Because of these facts, a cladistic analysis of cars will not produce a unique, consistent, well-supported tree that displays nested hierarchies. A cladistic analysis of cars (or, alternatively, a cladistic analysis of imaginary organisms with randomly assigned characters) will of course result in a phylogeny, but there will be a very large number of other phylogenies, many of them with very different topologies, that are as well-supported by the same data. In contrast, a cladistic analysis of organisms or languages will generally result in a well-supported nested hierarchy, without arbitrarily weighting certain characters (Ringe 1999). Cladistic analysis of a true genealogical process produces one or relatively few phylogenetic trees that are much more well-supported by the data than the other possible trees.

    The degree to which a given phylogeny displays a unique, well-supported, objective nested hierarchy can be rigorously quantified. Several different statistical tests have been developed for determining whether a phylogeny has a subjective or objective nested hierarchy, or whether a given nested hierarchy could have been generated by a chance process instead of a genealogical process (Swofford 1996, p. 504). These tests measure the degree of "cladistic hierarchical structure" (also known as the "phylogenetic signal") in a phylogeny, and phylogenies based upon true genealogical processes give high values of hierarchical structure, whereas subjective phylogenies that have only apparent hierarchical structure (like a phylogeny of cars, for example) give low values (Archie 1989; Faith and Cranston 1991; Farris 1989; Felsenstein 1985; Hillis 1991; Hillis and Huelsenbeck 1992; Huelsenbeck et al. 2001; Klassen et al. 1991).

    He also severely misunderstands convergence.  Convergence can only produce functionally-relevant similarities, because that is all that selection can "see".  Homologies, i.e. similarities between systems that are not necessary for functional similarity between systems, are what allows paleontologists to easily distinguish between these placental wolf and marsupial "wolf" skulls that cre8tionist posted in another thread:

    I invite readers to go to The Thylacine Museum and look at the side-by-side comparison of 'wolf' skulls (with cool magnifier lense).

    The caption reads:


    Portrayed here are side-by-side images demonstrating the anatomical differences between the skulls of the Grey wolf (Canis lupus) and the thylacine (Thylacinus cynocephalus).  In the dorsal view, note that the thylacine has a much broader forehead than the wolf, and there are differences in the design of the zygomatic arches and brain case.  Also, the rostrum (snout) of the thylacine is far narrower than that of the wolf, and the thylacine has proportionately larger eye sockets which are rather more square in shape.  In the ventral view, one can easily see the great differences in dentition that  readily distinguish the two species as being members of distinct mammal groups.  The dentition of both species will be represented in greater detail on the following page.  Also visible in the ventral view is the thylacine's maxillary palatal vacuity (the two parallel openings in the roof of the mouth).  This is a feature that the wolf and other placental mammals do not have.

    ...on the next page...


    Here I show some diagrams which I have prepared to illustrate the extreme difference in dental anatomy which exists between the thylacine and its placental counterpart, the wolf.  The images are portrayed at life size.  Although there are also a number of notable differences in post cranial skeletal structure between the thylacine and wolf, I felt that the dentition represented one of the most striking dissimilarities.  As you can easily see in the image of the maxilla, the thylacine has 8 top incisors, whereas the wolf has only 6.  In the mandible however, the thylacine and wolf have an equal number of incisors.  Another major difference is the presence of a specialized shearing tooth, the carnassial, in the wolf.  This tooth design is a trademark of the wolf and other members of the placental mammal family Carnivora.  Also make note that unlike the wolf, the thylacine lacks large grinding surfaces on its molars.  Altogether, the wolf has a complement of 42 teeth, and the thylacine 46.

    I can't post the images here because they are copyright protected, but the differences in the tooth-numbering are dramatic.

    All commonly-sighted cases of "uncanny convergence" in biology turn out, on investigation, to be externally impressive but superficial when you get down to details.  This is notably different from the kinds of things that have happened in aircraft design, e.g. the addition of (the same) transponders, GPS units, computers, TV screens, etc., to planes of widely different models.

    This has been pointed out many times over the years, so I'm not sure why these cases still get seriously cited.


    PS: There is also the interesting question of:

    If the hypothesized IDer decided that there needed to be some carnivorous canine-type critters in Australia, why bother with all the genetic engineering that would be required, when a simple aboriginal boat sufficed to bring dingos to Australia only ~15,000 years ago?

    Such ID puzzles are absolutely ubiquitous in biogeography.  To me they indicate strongly that whatever creativity made these wonderful adaptations was, for some odd reason, highly constrained so that "design information" could not be transmitted across deep water barriers and instead had to be re-invented from scratch each time the adaptation was "needed" in particular locations.  Strangely, such geographical constraints did not apply to flying birds, sea mammals, and other easily-dispersed organisms.

    If you can find an ID theory that can explain this (and "the designer's actions are  mysterious" is not an explanation), I'll eat my hat.  If on the other hand you give natural selection the credit for these instances of creativity, then I guess natural selection can "design" things after all, and quite skillfully too...

    Date: 2002/12/26 14:19:39, Link
    Author: niiicholas

    You argue that designed objects will not produce nested hierarchies. I already gave the aircraft example, let's consider the example a bit further. Consider all machines that use gasoline as a fuel. Within that set you have various subsets, such as those that move and do not move. Of those that move, some fly, others move along the surface of the earth. In the latter, you have various numbers of wheels, such as 2, 4, 6, 8, …, and a few outliers with odd number of wheels. Of those with 4 wheels, you have different ratios of interior volume to overall size (eg, vans have a higher ratio). Of those with lower ratios you have different carburetors (fuel injection for sports cars), and so forth. I am contriving this example off the top of my head, but perhaps you can explain why this cannot be a case of a nested hierarchy. In support of your claim you pasted a few paragraphs from a web document which does not support your claim. The web document is discussing the relationships, across designed objects, of characters which have no influence on performance or are constant over the entire set. What we have called in this thread "arbitrary design decisions."

    Did you even read the quote?  The very first sentence pointed out that anything can be subjectively classified into a nested hierarchy if you arbitrarily pick characters.  This is exactly what you do above.  The point is that your "tree" would not be produced by an analysis of other subsystems of gasoline-driven machines, e.g. tires, liscense plates, GPS units, radios, onboard computers, whatever.  On the other hand, in biology there are a large number of systems (genes, limbs, skulls, etc.) that produce highly-congruent nested trees.  Other fairly similar examples are things like languages and scribe-copied documents, both of which are produced by a process of copying and gradual modification (although in these cases the possibility of lateral transfer is somewhat higher than it is in eukaryote biology).

    As for web references, if they cite the primary literature then you either have to show they are mis-using the literature, or that the literature itself is wrong.  Theobald cites a large number of papers discussing the difference between arbitrary and natural hierarchies -- designed objects like cars and planes produce the former, copied & gradually modified objects (like languages, scribe-copied documents, and...organisms) produce the latter.

    I'll include some of Theobald's refs so that interested parties can look them up:

    Archie, J. W. (1989) "A randomization test for phylogenetic information in systematic data." Systematic Zoology 38: 219-252.

    Faith, D. P., and Cranston, P. S. (1991) "Could a cladogram this short have arisen by chance alone?: on permutation tests for cladistic structure." Cladistics 7: 1-28.

    Farris, J. S. (1989) "The retention index and the rescaled consistency index." Cladistics 5:417-419.

    Felsenstein, J. (1985) "Confidence limits on phylogenies: an approach using the bootstrap." Evolution 39: 783-791.

    Hillis, D. M. (1991) "Discriminating between phylogenetic signal and random noise in DNA sequences." In Phylogenetic analysis of DNA sequences. pp. 278-294 M. M. Miyamoto and J. Cracraft, eds. New York: Oxford University Press.

    Hillis, D. M., and Huelsenbeck, J. P. (1992) "Signal, noise, and reliability in molecular phylogenetic analyses." Journal of Heredity 83: 189-195. PubMed

    Ringe, D. (1999) "Language classification: scientific and unscientific methods." in The Human Inheritance, ed. B. Sykes. Oxford: Oxford University Press, pp. 45-74.


    You seem to be extrapolating from the discussion given there on arbitrary design decisions to conclude that designed objects cannot produce nested hierarchies. Perhaps I am misunderstanding you.

    Of course designed objects can produce just about anything, because a hypothetical designer can always be invented who wants to produce X for goodness-knows-what reason.  This is a major problem for ID "theory", no predictions are made unless some specifications are put on the hypothetical IDer, and no one wants to even hypothesize any such specifications (you don't have to have foreknowledge of the designer, just a hypothesis...this is how science proceeds).

    But you said that ID predicts congruent phylogenies.  I am arguing that this is not established or even likely based on what we know about designed objects.  


    Is there more than one cost function?

    This section seems like you are trying to say something about how the designer would design things so that congruent phylogenies resulted due to functional constraints, or something.  But what you have to explain, in order to explain things as well as current theory, is how all of those arbitrary characters (many of them, such as DNA degeneracy, absolutely known to be functionless differences) produce statistically the same nested hierarchical trees!  If you can't do that then there's no reason to switch from the current explanation.


    Can homologies arise from different genes?

    You next go on to discuss homologies, but I'm not sure what the point is. You state that paleontologists can easily distinguish between the placental wolf and marsupial wolf skulls, as though I had stated otherwise. Of course they can, they can also easily distinguish between the bat's wing and human hand, but this does not prevent the pentadactyl pattern from being claimed as evidence for evolution. You pasted a figure of the two skulls which appear highly similar yet are supposed to have evolved independently. You say the similarities are "superficial." I have heard this said many times before, but how is it that these similarities are superficial whereas homologies such as the pentadactyl pattern, which exhibit a large degree of variance (compare the porpoise, bat and horse) are significant?

    Because the homologies all correlate with each other to a high degree of statistical confidence, producing a Linnean-type classification, whereas those features that you would expect would be the important features (as revealed by you example of classification of gas-driven machines based on function, or John Bracht's imaginings that amino acid sequence won't turn out to be largely degenerate with respect to structure and function after all) in fact don't correlate with the Linnean-type classification.

    If the genes and proteins of penguins, sharks, dolphins, seals, etc. grouped together, and bats and birds grouped together, etc., then you'd have an argument, but they don't.  This is a massive mystery from an ID perspective but easily explained by evolution.


    We should also note that homologies can develop from different genes, or otherwise follow different development patterns.

    This is an argument of Wellsian origin and depends largely on obfuscatory use of quotes and words like "different" (and Wells' unique views about the unimportance of DNA, which are rebutted in detail this ISCID thread).  Similar genes perform similar developmental functions a very long ways back, e.g. Hox genes and front-to-back patterning:


    An interesting challenge?

    Finally, you issued a challenge which sounded interesting but, forgive me if I am slow this morning, I had trouble following. You wrote:

    If the hypothesized IDer decided that there needed to be some carnivorous canine-type critters in Australia, why bother with all the genetic engineering that would be required, when a simple aboriginal boat sufficed to bring dingos to Australia only ~15,000 years ago? -- Yersinia

    Can you elaborate a bit?

    In short:

    You and Cre8tionist have proposed that convergences like the placental/marsupial wolf are better explained by intelligent design for the same function.

    I pointed out that rather than the "same" design being transplanted, it looks more like it was independently invented by modification of different starting points, and that the convergence is superficial in that the true relationships of the organisms remain clear based on homologies.

    But, if you are going to maintain the hypothesis that ID accounts for the complex carnivory specializations of wolves and thylacines, you have to explain why it appears that the design wasn't transplanted, but rather re-invented.  If a designer wanted carnivores in Australia, it would have been much easier just to put some dogs on a boat, as the stone-age Aborigines did, rather than do all of that complex creative genetic engineering twice in two different ways.

    Ditto for carnivorous marsupial "cats" in isolated south America, cacti vs. south African succulents, lemurs in Madagascar, Hawaiian honeycreepers, and of course Darwin's finches.  Why should independent design correlate so well with geographical isolation?  Did the IDer not know of boats?

    Date: 2002/12/26 16:57:06, Link
    Author: niiicholas
    I think I started a thread on this back in before The Great Server crash; there was a PNAS paper on yucca moth mouthparts, or something.

    Here is another case:


    T.o. discussion: here


    UC Riverside Study Suggests Placentas Can Evolve In 750,000 Years Or Less; Guppy-Like Fish Help Fill In The Gaps In The Evolution Of Complex Organs

    RIVERSIDE, Calif. -- Dec. 20, 2002 -- Evolutionary biologists have long been intrigued by how natural selection -- the process in nature by which the organisms best suited to their environment are the ones most likely to survive and leave descendants -- gradually creates a complex organ such as the eye, heart, or kidney.
    Now UC Riverside biologists, David Reznick and Mark Springer, along with Mariana Mateos, research associate at the University of Arizona, present in the journal Science a model system for studying the evolution of complex organs. They focus on the placenta (the organ that provides nutrients for the fetus and eliminates its waste products) in the fish genus, arguing that placentas serve as a good stand-in for complex organs whose histories have eluded evolutionary biologists.

    The dilemma posed by complex adaptation, which are organs of extreme complexity that have evolved through the action of natural selection, is that these organs demand contributions from a large number of adaptations at individual genetic loci to function properly. Darwin addressed the difficulty of complex adaptations with his treatment of the evolution of the eye. "He had to use organisms from different classes," explained Reznick, "because there isn't a living group of related organisms that have all the steps for making an eye." The organisms in Darwin's model are, however, distantly related to one another.

    Darwin proposed that complex eyes could have been formed with a succession of photosensitive organs, each a bit more complex than its predecessor and each favored by natural selection because of the advantages that the possessor received. Visualizing such a process would be easiest if steps in this sequence were preserved in closely related living organisms; but no such sequence exists for eyes because the intermediate stages have been lost through extinction.

    Reznick and his colleagues studied guppy-like fish in the genus Poeciliopsis. They report that placentas have evolved independently three times in closely related Poeciliopsis species. Other species in the genus lack placentas, and some have partial maternal provisioning via tissues that may be precursors of placentas. "Thus the fish present the full trajectory of steps involved in the evolution of this organ," said Reznick. "It allows researchers to examine what's been added, or what has changed, and eventually identify the genes associated with the evolution of each trait."

    The study by Reznick and colleagues first argues that the placenta is a complex organ, in the sense that it represents a composite of many adaptations and is controlled by many genes. "The origin of complex, novel organs plays a key role in evolution since they often define new categories of animals, such as the placenta for placental mammals," said Reznick. "They are also a source of controversy both within evolutionary biology and between evolutionary biology and the religious public. This is because their origin unfolds on a time scale considerably longer than human existence, so the process must be inferred indirectly."

    In the Science paper, the researchers show that: 1) Fish in the genus Poeciliopsis have placentas in various stages of evolution, and 2) There are clusters of closely related species that either have highly evolved placentas, placentas in intermediate stages of evolution, or no placentas at all. These provide ideal material for studying how such complexity evolves.

    The researchers then use the combination of molecular and geological data to yield estimates for how long it took the placenta to evolve in some lineages. Based on collected data, they find that the shortest time interval between a poeciliid species with a placenta and its last common ancestor without one was 750,000 years, suggesting that placentas can evolve in 750,000 years or less.

    "This result demonstrates that complex organs can evolve rapidly, on the same scale as predicted by a theoretical estimate of 400,000 years for the evolution of the eye," said Springer.

    Reznick has been collecting comparative life history data for around 15 years. For the study, he traveled around Latin America collecting the fish, going to museums to work with their collections, and then doing the appropriate dissections at UC Riverside. Several UC Riverside undergraduate students contributed to the dissections. Reznick also worked on live fish in his laboratory on campus.

    The molecular work for the study was done by Mateos over the past two years. Springer did the phylogenetic work for the study. His statistical methods helped the researchers make inferences about how traits have evolved from the combination of DNA sequence data (collected by Mateos) and the descriptions of modes of reproduction (generated by Reznick).

    The UC Riverside Department of Biology serves three main functions: undergraduate instruction, graduate education, and research in basic biology. The department conducts research and teaching in many areas of life science including cell biology, conservation biology, developmental biology, ecology, evolution, molecular biology, physiology, and population biology. The department is part of the College of Natural and Agricultural Sciences, a multi-departmental unit dedicated to instruction and basic research in the physical and life sciences, and also to 'mission-oriented' applied research in the agricultural sciences. The Biology major is a popular undergraduate major on the UC Riverside campus, with approximately 1000 students currently enrolled. Biology also provides much of the undergraduate instruction for majors in other life science departments and other science majors.

    Date: 2002/12/26 19:34:24, Link
    Author: niiicholas
    Another post:

    Well, I am glad that Cornelius concedes that ID-design is different from regular design inferences, in that while we always have (even if approximate) models for the designer in the cases of forensics, archaeology, and even SETI, no such model shall be forthcoming for ID.  Therefore we can expect nothing in particular if ID is true, and thus have no way to strengthen or weaken our confidence in the hypothesis.

    I say this somewhat in jest, because Hunter in fact only uses the "there ain't no hypothetical model for the designer" argument as a defense, in fact he makes a few characterizations at times.  Things have to "make sense" with regard to some unspecified criteria:


    With regard to the complex carnivory specializations you mention, ID is more interested in understanding the function and reason (or perhaps lack thereof) behind the different designs, not trying to justify the actions of the designer. So your challenge, as it stands, is fairly weak. To beef it up you need to show that those different specializations are unnecessary or absurd. As I said to RBH, the way to falsify design is:

    1) Show that the designer's actions make little sense,
    2) Show that naturalistic mechanisms are sufficient to explain the origin of species,
    3) Show that the preponderance of scientific evidence/analysis strongly points to evolution.

    Any of these is sufficient to falsify ID, or at least effectively falsify it by rendering ID redundant.

    The "origin of species" is a somewhat different topic and can be address elsewhere; I expect that if the usual examples of observed speciation or inferred very-recent-speciation were cited, he would back up the goalposts to the level of genus, family, order, phylum, etc.  But that's another thread.

    I think, though, that #1 and #3 are pretty easily satisfied by the Thylacine example:


    Sarcastic and rhetorical barbs about how the designer didn't create according to your personal sensibilities will only backfire, but a serious and plausible challenge on #1 will work for you. For example, in this example you bring up, show that one of the specializations is unquestionably superior to the other, even if transplanted into those other species in that other environment and niche.

    Well, how's this: the introduction of the dingo appears to have quite rapidly caused the extinction of the thylacine, which was extinct from mainland Australia before Europeans arrived.  Thylacine species persisted for tens of millions of years in the Australian fossil record, into the period of human habitation, and yet some stone-age boat people (unintentionally) killed them off by transplanting an apparently superior design, the dingo.

    The only place that thylacines hung on until the 1900's was in the isolated island of Tasmania, where dingos and bounty hunters reduced their population to fatally low numbers by the 1930's.

    (one of several web sources on this)

    As if this wasn't enough, this appears to be a general pattern with only a few exceptions: placentals have proven to be superior competitors for the same ecological niches, which is why there are precious few marsupials in South America (formerly an Australia-like place before the Panamanian isthmus connected it to North America), and why so many marsupials are endangered in Australia, while things like feral rats, cats, rabbits, and dogs (dingo) are thriving wildly.

    By any standard of "good design", it appears that the hypothetical IDer's actions "make little sense": to carefully craft all of these marsupial species for parallel ecological niches on separate landmasses, let them be fruitful and multiply for millions of years, followed by prompt extermination once tectonic accidents or stone-age boats allow apparently superior designs to invade.

    Date: 2002/12/27 00:54:53, Link
    Author: niiicholas
    It appears that the thread has devolved into several subtopics that are not strictly related to phylogenetic tree (non)congruence.  Hunter's non-congruence reasons for why we should doubt the common descent of (say) Animalia appear to have been rebutted, as he is now raising numerous different issues that would take their own threads to address:

    - Arguments about genes/development/homology
    - Can speciation occur by natural processes?
    - Can mutation+selection produce creative evolution?

    I think that these questions are perhaps the real reasons that Hunter doubts common descent of animal species, not because the phylogenetic evidence is against it.

    I think that the thylacine example is worth cogitating on further regarding ID vs. evolution, as it is not an isolated event but rather an instance of a very common phenomenon in biology: in geographically isolated regions, relatively unrelated organisms adapt to fill quite specific niches, but do it by "reinvention" that always differs in the details.  Information transplants are not seen.  

    I would humbly note that this is what Darwin realized about the Galapagos species of turtles (and later, finches) once the taxonomists got to work on them back in Britain.  He and many other world travellers have made remarks like "it is as if different creators acted in different places" or words to that effect.

    When convergent organisms are transplanted by humans or natural events, a very common occurence is extinction of the native species.  It's almost like whatever the creative force is draws its power from the size and time of isolation of the land mass in question...

    Date: 2002/12/30 08:49:00, Link
    Author: niiicholas
    In the "cytoskeletal protein homologs found in prokaryotes" category:


    II thread

    Science News Article

    Week of March 31, 2001; Vol. 159, No. 13

    Bacterial cells reveal skeletal structures
    Jessa Netting

    Bacteria are different from you and me. Always the minimalists, they lack features that plant and animal cells usually can't do without: a nucleus, special organelles, and an internal skeleton made of protein, to name a few. But research reported in the March 23 Cell knocks out one plank of this standard profile—bacteria, too, have a protein skeleton, or cytoskeleton.

    A fluorescent tag for a specific bacterial protein reveals a helical skeleton.

    "This is akin to finding the platypus, a mammal that lays eggs," says Laura J.F. Jones, who revealed the skeleton in Bacillus subtilis with her colleagues Rut Carballido-López and Jeffery Errington, all of Oxford University in England.

    The researchers say their finding helps illuminate the origins of our own cell structure and eliminates a fundamental difference between two of the most basic groups of organisms, prokaryotes (bacteria and blue-green algae) and eukaryotes (plants, animals, and protozoans).

    "Spectacular" is the how cell-mechanics researcher Piet De Boer of Case Western Reserve University in Cleveland rates the Oxford team's unmasking of a bacterial cytoskeleton. "Bacteria have really been thought of as bags of enzymes without much of an internal structure at all," says De Boer.

    Bacteria were believed to have only a tough cell wall for support. Even powerful electron microscopes have failed to turn up any distinct internal structure. In contrast, eukaryotic cells, which evolved after bacteria, have a network of filaments for support and movement. A protein known as actin forms much of this cytoskeleton, which can look like a bushy spray of fibers.

    In the past decade, bacteriologists have searched for complex structures in bacteria by using techniques for tagging proteins with fluorescent markers. These studies, which can illuminate otherwise hidden structures, have yielded evidence of a higher level of organization than previously believed, says De Boer.

    Using fluorescent tags made with antibodies that can bind to specific proteins, the Oxford investigators looked for a bacterial cytoskeleton in the rod-shaped B. subtilis. "It seemed likely to me that something as important as the cytoskeleton must have evolved quite early, so I almost expected to find actin in bacteria even though the textbooks say it is absent," says Errington.

    He and his colleagues focused on two bacterial proteins, MreB and Mbl, because of evidence that the genes coding for them have roles in determining cellular shape. Disabling the gene for MreB resulted in rounded cells, while disabling the gene for Mbl yielded elongated, twisted bacteria. Using a different fluorescent antibody to light up the intact protein in each altered cell, the researchers revealed complex internal structures made of either MreB or Mbl.

    "We were ecstatic when we saw the first MreB and Mbl images, because they immediately told us that the proteins probably made filaments like actin," says Errington. Coiling within the cell as they did, the filaments clearly could determine cell shape in normal bacteria, he says.

    Errington likens the filamentous structure to a scaffold: It doesn't have great strength itself, but instead provides the internal framework for a sturdier exterior shell, in this case the bacterium's tough cell wall.

    The finding suggests that the cytoskeleton evolved before bacteria and our own cellular ancestors split into two groups, says Errington. Having a cytoskeleton isn't a defining feature of eukaryotic cells after all, he asserts.


    Jones, L.J.F., R. Carballido-Lopez, and J. Errington. 2001. Control of cell shape in bacteria: Helical, actin-like filaments in Bacillus subtilis. Cell 104(March 23):913.

    Date: 2002/12/31 17:16:02, Link
    Author: niiicholas
    If I had a month or two, I would review the literature on the question of "optimality" of the genetic code.  It seems to me that there are many different ways that the code could be optimal, and other variations which might not make any difference.

    E.g., if every amino acid kept the same number of codons, etc., but the standard table was simply "flipped" right-to-left, would this make any difference?

    I have no idea myself, but such things are important to think about.  Wes had some pretty good stuff on this posted somewhere at one point...

    Date: 2002/12/31 17:21:59, Link
    Author: niiicholas
    Regarding Google, Dunk has a very good post here.


    (Go to )

    find the desired thread    view thread  
    find the desired post       view this message alone

    then the unique message ID will be displayed at the top of the message.  It will be something like

    You must store the google groups prefix in a convinient place.

    It is:

    Next, append the ID to the prefix: (be sure you don't leave a space
    after the '='.



    E.g., Dunk's post is:


    PS: If you surf with Internet Explorer, don't forget about the Google Search Toolbar (*very* cool):

    Date: 2002/12/31 17:37:05, Link
    Author: niiicholas
    Please give us your informed opinion when you get a chance to read it.  A freely online 2001 PNAS article (from related articles) provides something of a preview:


    Sheehan J, Templer M, Gregory M, Hanumanthaiah R, Troyer D, Phan T, Thankavel B, Jagadeeswaran P.

    Demonstration of the extrinsic coagulation pathway in teleostei: identification of zebrafish coagulation factor VII.

    Proc Natl Acad Sci U S A 2001 Jul 17;98(15):8768-73

    Department of Cellular and Structural Biology, South Texas Veteran's Health Care System, Audie Murphy Division, University of Texas Health Science Center, San Antonio, TX 78229, USA.

    It is not known whether the mammalian mechanism of coagulation initiation is conserved in fish. Identification of factor VII is critical in providing evidence for such a mechanism. A cDNA was cloned from a zebrafish (teleost) library that predicted a protein with sequence similarity to human factor VII. Factor VII was shown to be present in zebrafish blood and liver by Western blot analysis and immunohistochemistry. Immunodepletion of factor VII from zebrafish plasma selectively inhibited thromboplastin-triggered thrombin generation. Heterologous expression of zebrafish factor VII demonstrated a secreted protein (50 kDa) that reconstituted thromboplastin-triggered thrombin generation in immunodepleted zebrafish plasma. These results suggest conservation of the extrinsic coagulation pathway between zebrafish and humans and add credence to the zebrafish as a model for mammalian hemostasis. The structure of zebrafish factor VIIa predicted by homology modeling was consistent with the overall three-dimensional structure of human factor VIIa. However, amino acid disparities were found in the epidermal growth factor-2/serine protease regions that are present in the human tissue factor-factor VIIa contact surface, suggesting a structural basis for the species specificity of this interaction. In addition, zebrafish factor VII demonstrates that the Gla-EGF-EGF-SP domain structure, which is common to coagulation factors VII, IX, X, and protein C, was present before the radiation of the teleosts from the tetrapods. Identification of zebrafish factor VII significantly narrows the evolutionary window for development of the vertebrate coagulation cascade and provides insight into the structural basis for species specificity in the tissue factor-factor VIIa interaction.


    This investigation demonstrates the presence of coagulation factor VII in the zebrafish, providing molecular evidence for an extrinsic coagulation pathway in a nonmammalian species. Similarities between zebrafish and human primary protein sequence, domain organization (Gla-EGF-EGF-SP), and postulated three-dimensional structure suggest that this cDNA is orthologous to human factor VII. These sequence similarities include conservation of a single activation cleavage site, the cysteines participating in disulfide bonds, and residues that contribute to the formation of specific binding sites for sodium and calcium ions. The presence of the predicted protein was demonstrated in zebrafish plasma and liver with specific rabbit antisera vs. a unique zebrafish factor VII peptide. Immunodepletion of zebrafish plasma with the antipeptide antisera selectively inhibited thromboplastin-triggered thrombin generation. Finally, the zebrafish cDNA directed the expression of a secreted mature protein that was similar in size to human factor VII, which reconstituted thromboplastin-triggered thrombin generation in immunodepleted plasma. These structural and functional correlates reflect the conservation of factor VII gene function between zebrafish and man.

    The coagulation serine proteases arose from the family of trypsin-like genes, characterized by protease domains that use the AGY codon for the catalytic serine {195}, and contain a specific sodium ion-binding motif, Tyr/Phe {225} (23, 27). The organization of the N terminus propeptide is unique to these proteases, composed of a ¦Ã-carboxylation (Gla) domain followed by two EGF or kringle domains. Although Gla, EGF, and SP modules exist in invertebrates such as Drosophila melanogaster, there is no evidence for this unique domain organization (28). Likewise, serine proteases responsible for hemolymph coagulation in Tachypleus tridentatus (Japanese horseshoe crab) and other invertebrates species differ significantly in N terminus domain content and organization from mammalian coagulation proteases (29¨C31). Evidence for prothrombin (which contains kringle domains) exists in the primitive jawless hagfish (Myxinidae) (11). However, zebrafish factor VII now provides the earliest known evolutionary appearance of the Gla-EGF-EGF-SP domain structure common to factors VII, IX, and X and protein C. Demonstration of both zebrafish prothrombin (18) and factor VII indicates that the relevant domain assembly for the coagulation proteases had occurred (presumably by exon shuffling) (32) at or before the time of the last common ancestor of humans and zebrafish, ¡Ö450 million years ago (33).

    Significant species specificity exists in the tissue factor¨Cfactor VIIa interaction between mammalian species and appears relatively complete between zebrafish and man (15). The human soluble tissue factor¨Cfactor VIIa structure demonstrates three major intermolecular contacts involving the Gla, EGF-1, and EGF-2/SP domains, respectively (24). Inspection of homologous surfaces on the zebrafish factor VIIa model suggests that intermolecular interactions are conserved largely for the Gla and EGF-1 contact regions. In contrast, surface residues in the EGF-2/SP contact region are poorly conserved, suggesting that the intermolecular interactions with human tissue factor are largely disrupted. This disruption includes the protease insertion loop Leu-371¨CGlu-385 {170¨C178}, which appears to undergo a conformational change between the bound and unbound structures of human factor VIIa (25). In the zebrafish protein, this loop demonstrates a 5-aa deletion and replacement of a neighboring conserved Met with Arg-348 {164}. These differences in the EGF-2/SP intermolecular contact region between zebrafish and man suggest a structural basis for the observed species specificity in the tissue factor¨Cfactor VIIa interaction. Hybrid recombinant human/zebrafish factor VII proteins in which the EGF-2/SP intermolecular contact regions are exchanged could directly test their contribution to the species specificity of this interaction.

    Identification of zebrafish factor VII has important implications for the relevance of this powerful genetic model to the study of hemostasis and thrombosis. The ability to trigger (and selectively inhibit) tissue thromboplastin-dependent coagulation in a species-specific manner provides indirect evidence for tissue factor in the zebrafish. Functional data also suggest the presence of a contact-activated coagulation pathway that is independent of factor VII and factor X-like activity in the zebrafish (15). Factor X-like activity (based on RVV-X activator) is not affected by immunodepletion of factor VII, demonstrating that these activities are distinct. The degree of similarity between zebrafish and mammalian coagulation suggests that the zebrafish is a relevant animal model for the study of genes that affect hemostasis. Phenotypic screens of mutagenized zebrafish may identify novel genes that regulate the initiation of coagulation.

    In conclusion, the structural features of factor VII in the zebrafish suggest that domain assembly for the coagulation proteases occurred before radiation of the ancestral Actinopterygii (ray-finned fishes) and Sarcopterygii (lungfish and tetrapods). The gene structure (intron/exon boundaries) of coagulation factors VII, IX, and X and protein C indicates that these genes are paralagous, suggesting a common origin via gene duplication (34). Thus, it appears likely that the vertebrate coagulation cascade arose rapidly during proposed genome duplications between ancestral chordates and the development of jawed vertebrates (35¨C37). Given the functional and structural similarities to mammalian coagulation demonstrated thus far, the zebrafish should be a powerful model to identify novel genes involved in vertebrate coagulation.

    Doolittle and Patthy are referenced, unfortunately little of Doolittle's and none of Patthy's blood-clotting stuff is in widely available online journals...they all seem to be down at UCSD however.

    Date: 2003/01/03 20:59:18, Link
    Author: niiicholas
    Quote (Wesley R. Elsberry @ Jan. 01 2003,01:59)

    Ah, that's it.  Lots of good material there.

    Briefly, here is an important argument rarely made:

    1) Number of combinatorially possible codes:
    Lots and lots and lots

    2) Number of "optimal" codes:
    A lot less, but probably still lots

    If #2 is true, then the argument for the monophyly of extant life based simply on the canonical code (leaving aside all of the other evidence for the monophyly of life) remains strong, because there would be no reason for independent origination events to land on one or the other of the equally optimal codes.

    E.g., if n = # of equally optimal codes = 10, then the random probability of (say) the three domains of life landing on the same code is p = 1*1/10*1/10, or 1/100.  This is already quite a coincidence on the independent origins hypothesis.  The probability of (say) 20-odd animal phyla landing choosing the same code out of a range of 10 equally optimal codes would be 1/10^20, already quite astronomical.

    And of course if there were more like 1000 or 1 million equally optimal codes, then the random probability of independent origins hitting on the same code goes up exponentially factor.

    Note that these results hold even if the canonical code is literally "one in a million", since there are many more combinatorially possible codes than a mere million.

    The only way for the independent design hypothesis to produce nonrelated organisms with the same code is to postulate some motive for the IDer to design things this way on purpose -- but postulating motives is something that IDists refuse to do, at least officially.


    Date: 2003/01/07 21:20:14, Link
    Author: niiicholas
    Hey Nelson, welcome to AE.

    Unfortunately I don't have a week to really wrap my head around the cytosine deamination issue.  However I guess I was the "provoker" of the Mike Gene article you cite in that I posted the article "Confounded cytosine" which he is reacting to.

    So if debate of this topic begins (by people other than me), let's start by accumulating the relevant links etc. on this thread and then go from there.

    Here is an ARN post with some discussion, including some quotations from the article, with the hopes of laying out what Poole et al. were arguing.  Unfortunately this argument is embedded in a more complex discussion of various topics related to RNAworld and the origin of the genetic code which makes simple quoting difficult and I think confused subsequent discussion as it is not at all clear that the IDists involved accept or reject either RNAworld or a gradual origin of the genetic code and DNA.

    ARN thread

    Begin re-post of summary of Poole et al.:

    I do believe I provoked this particular MG essay when I posted this reference on ISCID:


    Nat Rev Mol Cell Biol 2001 Feb;2(2):147-51
    Confounded cytosine! Tinkering and the evolution of DNA.

    Poole A, Penny D, Sjoberg BM.

    Institute of Molecular BioSciences, PO Box 11222, Massey University, Palmerston North, New Zealand.

    Early in the history of DNA, thymine replaced uracil, thus solving a short-term problem for storing genetic information--mutation of cytosine to uracil through deamination. Any engineer would have replaced cytosine, but evolution is a tinkerer not an engineer. By keeping cytosine and replacing uracil the problem was never eliminated, returning once again with the advent of DNA methylation.
    Here is the direct link although you may need subscription access.

    There argument is complex but here is the gist:


    The origin of DNA is a fundamental question in evolution. Early on, DNA replaced RNA, reflecting the superior information-storage capacity of DNA1, 2. Modern biochemical pathways provide an insight into this transition, as do RNA and uracil-DNA (U-DNA) viruses2, 3, suggesting that the replacement took place in two steps (Figs 1, 2a): replacement of ribose with deoxyribose, then replacement of uracil (U) with thymine (T)4. The first step was probably very complex, and has recently been reviewed elsewhere2, 5. Here we look at the second (UT) replacement, which is emerging as another example of why evolution is best viewed as a tinkerer, not as an engineer with an eye for 'good' design (Box 1).


    Central to the story is cytosine ©, which readily deaminates to form U. This turns CG pairs into UG mispairs, and is an ongoing process in DNA6, 7 (Fig. 2b). Without repair, replication of a UG mispair would give one UA pair (which is read as a TA pair) and one CG pair. All organisms carry the machinery for repair of C deaminations — uracil-N-glycosylase (UNG), which recognizes and removes any U that it detects, leaving an abasic site. This is patched up by base-excision repair8, 9 (Fig. 3), which creates a gap in the DNA opposite G. DNA polymerase then fills the gap with dC, thus repairing the mutation. Occasionally, U (from dUTP) is incorporated opposite A, so both UG and UA pairs turn up in DNA. The UNG recognizes and removes U arising from either C deamination or misincorporation, allowing DNA to be faithfully repaired10-12.


    Before T was a constituent of DNA, it would have been harder to detect C deaminations, because U was a bona fide constituent of early DNA at UA pairs. It is widely accepted that U--&gt;T replacement solved this problem because it allowed any U arising by C deamination to be detected unambiguously.


    François Jacob14 has likened evolution to "tinkering". In contrast to an engineer, who works by design, obtaining all the necessary materials needed for construction of a prototype and finally testing it before putting it to work, a tinkerer makes use of whatever is at hand. This means that the result, although functional, is often far from perfect. A consequence of this modus operandi is that if something works in the short term it will be used, even if a better alternative is conceivable. New innovations cannot arise only to become useful when a subsequent function evolves, because there is no selection to maintain such innovations before they become useful.

    Recent progress on the biochemistry of U removal reveals an unexpected diversity of reactions catalysed by members of the uracil-DNA glycosylase family (even though they all share a common origin), and allows the U--&gt;T conundrum to be resolved. New data15 on a closely related phenomenon — the repair of deaminated 5-methylcytosine (5-meC, which deaminates to T, resulting in a TG mismatch; Fig. 2b) — highlights the usefulness of the tinkering analogy for evolution. The problems solved by replacing U with T resurfaced once again when C methylation became a feature of the genome, with a member of the U-DNA glycosylase family being recruited to repair 5-meCT deaminations.


    The trouble with T

    As eukaryotic genomes became more complex, additional mechanisms of gene regulation developed. One such mechanism is DNA methylation, where a methyl group is added to position 5 on the cytosine ring, forming 5-meC (Ref. 15). The ability to regulate genes by C methylation would have been beneficial, but it came with a catch: 5-meC deaminates to T at a rate 2–4-fold higher than C deaminates to U (Fig. 2)21, meaning that a new form of mismatch became a problem. In eukaryotes, thymine-DNA glycosylase (TDG), which is evolutionarily related to UNG and MUG, repairs TG mismatches arising from deamination of 5-meC (Refs 17,25).


    Replacing U with T provided a means by which to fine-tune repair of C--&gt;U deaminations, but the problem of C deamination was never eliminated — it re-emerged in the form of 5-meC deamination. Tinkering also makes sense of the evolution of the 5-meC apparatus, which subsequently drove the recruitment of the U-excision apparatus into T excision because of the 'unforeseen' side effect of 5-meCT deamination. All this could have been avoided simply by eliminating C early in the evolution of the genetic material — but how boring life would be if evolution worked by engineering.

    Date: 2003/01/11 18:16:37, Link
    Author: niiicholas
    If you get an IDist to give you a non-question-begging definition of information, let us know...

    Date: 2003/01/13 22:17:00, Link
    Author: niiicholas
    Originally posted here.


    January 13, 2003

    ID and Human Cloning

    By Paul Nesselroade

    Does the Intelligent Design (ID) movement have anything to say about current experimentation with human cloning?

    Clearly, starting points are critical in shaping how we view the appropriateness of any action. If our starting point is the belief that human life was accidental and brought about solely by the impersonal forces of natural selection and random mutation, then, any purpose or meaning for life has to be assigned by us, chiseled out of the void of meaninglessness with our own hands. Starting here, the idea of cloning new life explicitly for the enhancement of our own lives (through organ replacement, stem cell harvesting, or for reproductive purposes) can be legitimized. The human ‘cost’ associated with both fine-tuning the cloning process (animal cloning rarely results in birth and virtually all of those born have serious abnormalities and/or die early) and creating life expressly for sacrificial purposes, may be considered unfortunate, but can hardly be considered wrong.

    (bolds added)

    Strange that this ARN missive doesn't recognize the Raelian's oh-so-crucial "starting point":



    Supporting evidence

    Welcome to the Evidence page, a subsection of the Raelian Revolution website.

    If we truly were created by people from space, then there would be traces of this creation in our history, mythology and religion, be it Judaic, Buddhist, Christian, Islamic or other. Science should confirm this and there should be UFOlogical evidence of them monitoring our progres and even visitations.

    In fact, if one takes the trouble to look, this is exactly the case and the horisontal navigation bar above provides links to such evidence including a bibliography section listing references and authors whose totally independent conclusions support the validity of the Raelian Message.


    Supporting evidence p. 3

    For 20 years, the Raelian vision of "scientific creationism" : a step ahead of science ?

    It is striking to note that while the Raelian theory is being confirmed by a continual series of scientific discoveries, the theory of Evolution is, on the other hand, being increasingly challenged as its old questions remain unanswered and even more embarrassing new questions are appearing.

    An anti-evolutionist system in our genes:

    Perhaps the most awkward question today for the theory of evolution is the one raised by the recently discovered p53 and since then a mutlitude of others - the DNA repair mechanism. This has been found to be common to all mammals and repairs damaged DNA. If the damage is too great to repair, it organises the cell's self-destruction.

    Therefore if any defect in the transcription of the genetic code arises, (the foundation on which evolution is based) then this repair or programmed cell death mechanism will remove such a mutation. If not, then the organism as a whole will die of cancer.

    This control system is clearly present to avoid all mutation. Thus, if this system is common to all mammals, according to the theory of Evolution, it should also be present in the common ancestors of mammals.

    If it were present in our ancestors, how were they able to diversify in order to render so many different species ? This is clearly a major contradiction which can only put a serious doubt on the theory of evolution.



    Here you will find other resource material  which support the messages given  to Rael by the Elohim
    - in whole or in part.


    The Triumph of Design

    The Triumph of Design clearly and dramatically shows the gaping holes in Darwinian theory and the mounting evidence for the intelligent design of the universe. This video features Phillip Johnson, the distinguished law professor from the University of California, Berkeley whose best-selling book, Darwin On Trial, re-ignited the evolution controversy in the early 1990's. (more info)

    Evolution - Fact or Belief ?
    ( also released in French as "Enquetes & Reportages")

    More and more scientists are abandoning the Evolution Theory on the grounds that it is contrary to the basic laws of modern science. They maintain that it is a philosophy, not a science.
    This video interviews scientists from around the world to find out why they do not accept evolution as a reasonable explanation for the origin of man and the universe.

    I do agree with the ARN wedge update about one thing: your starting point is important.  For instance, if you start out by ignoring evidence contrary to your position, there is no end to the silly conclusions you will come to.

    Date: 2003/01/13 23:05:54, Link
    Author: niiicholas

    Ever see a thread/post and said "Hey!  That thread/post is so good it should be recorded for posterity"?  I have.

    Here is an example.  Art wrote a great post, with pics, over on this ARN thread:;f=13;t=000568

    ...on how the widely divergent Silversword alliance clearly demonstrates how Jonathan Wells is wrong about RM-NS and morphological "macroevolution".

    Art's post repeated below
    Originally posted by Geoff:
    Seriously, so yours and Charlie's examples show, in my limited understanding, that at least different, apparently viable types at least, can be produced by changes in developmental genes within the species.  So, to that extent, I guess Wells is indeed wrong.

    Perhaps the next line of defense would ask for examples of really macroevolutionary morphologic changes via this route (or even mere speciation of a less impressive type).  I personally am really more interested in changes beyond the production of intraspecific types.

    But you guys did indeed answer the assertion that Wells made and that I then posed -- and I accept your answers and those of others (like Mike B) with thanks.


    Hi Geoff,

    About your question as to possible known correlations between mutations in developmentally-important genes and macroevolutionary events, I submit the following for your consideration.  

    First, another accursed pubmed abstract (that need not be read in detail - instead, just note that some of the genes mentioned are the same as those you have agreed represent developmentally-important ones in which non-lethal mutations are known):

    Proc Natl Acad Sci U S A 2001 Aug 28;98(18):10208-13

    Accelerated regulatory gene evolution in an adaptive radiation.

    Barrier M, Robichaux RH, Purugganan MD.

    Department of Genetics, Box 7614, North Carolina State University, Raleigh, NC 27695, USA.

    The disparity between rates of morphological and molecular evolution remains a key paradox in evolutionary genetics. A proposed resolution to this paradox has been the conjecture that morphological evolution proceeds via diversification in regulatory loci, and that phenotypic evolution may correlate better with regulatory gene divergence. This conjecture can be tested by examining rates of regulatory gene evolution in species that display rapid morphological diversification within adaptive radiations. We have isolated homologues to the Arabidopsis APETALA3 (ASAP3/TM6) and APETALA1 (ASAP1) floral regulatory genes and the CHLOROPHYLL A/B BINDING PROTEIN9 (ASCAB9) photosynthetic structural gene from species in the Hawaiian silversword alliance, a premier example of plant adaptive radiation. We have compared rates of regulatory and structural gene evolution in the Hawaiian species to those in related species of North American tarweeds. Molecular evolutionary analyses indicate significant increases in nonsynonymous relative to synonymous nucleotide substitution rates in the ASAP3/TM6 and ASAP1 regulatory genes in the rapidly evolving Hawaiian species. By contrast, no general increase is evident in neutral mutation rates for these loci in the Hawaiian species. An increase in nonsynonymous relative to synonymous nucleotide substitution rate is also evident in the ASCAB9 structural gene in the Hawaiian species, but not to the extent displayed in the regulatory loci. The significantly accelerated rates of regulatory gene evolution in the Hawaiian species may reflect the influence of allopolyploidy or of selection and adaptive divergence. The analyses suggest that accelerated rates of regulatory gene evolution may accompany rapid morphological diversification in adaptive radiations.
    Now, consider three plants from the group (pardon my taxonomical crudeness here) mentioned in this abstract:    ,

    It doesn’t take much of an eye to see stupendous morphological differences, easily dramatic enough to qualify as possibly macroevolutionary in nature.  Of course, this could only be if it could be shown that these plants share a common ancestry.

    And indeed it can be so shown.  By a standard that even the staunchest YECer accepts, it can be strongly concluded that each of these (as well as other members of the Silversword alliance) share a common ancestry.  This is because, the vast morphological differences aside, they are interfertile.  As interestingly, for a number of other reasons (biological, geographic, historical, and molecular), it can be safely concluded that these vastly-different plants diverged from a common ancestor that looked something like


    Reflect, now, on the abstract.  In this study, evidence for positive selection of alleles (that must have arisen via mutation - this follows from the natural history of the different genera) of developmentally-important genes - genes involved in flower structure and evolution - was described.  While it’s not a videotape, it stands as evidence of the sort that Wells claims does not exist - namely, that changes in developmentally-important genes are important in macroevolutionary progressions.

    (Keep in mind that among the dramatic morphological differences that are seen in these examples are ones that involve floral structures.  Also, while others might argue with me, I would claim here that the range of morphologies shown in this post exceeds the range seen in placental mammals - just to give readers an idea of the scope of the differences.)

    (These images, and many others, can be found at the Silverswords link given above.)

    (Hint: Hit "reply with quote" in UBBs to get access to the formatting)

    Date: 2003/01/15 02:53:25, Link
    Author: niiicholas
    Bump as this thread is being cited on ISCID:

    In the "origin of new information in the evolution of humans" category:


    Genetics 2002 Dec;162(4):1825-35
    Accelerated Protein Evolution and Origins of Human-Specific Features. Foxp2 as an example.

    Zhang J, Webb DM, Podlaha O.

    Department of Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, Michigan 48109.

    Genes responsible for human-specific phenotypes may have been under altered selective pressures in human evolution and thus exhibit changes in substitution rate and pattern at the protein sequence level. Using comparative analysis of human, chimpanzee, and mouse protein sequences, we identified two genes (PRM2 and FOXP2) with significantly enhanced evolutionary rates in the hominid lineage. PRM2 is a histone-like protein essential to spermatogenesis and was previously reported to be a likely target of sexual selection in humans and chimpanzees. FOXP2 is a transcription factor involved in speech and language development. Human FOXP2 experienced a >60-fold increase in substitution rate and incorporated two fixed amino acid changes in a broadly defined transcription suppression domain. A survey of a diverse group of placental mammals reveals the uniqueness of the human FOXP2 sequence and a population genetic analysis indicates possible adaptive selection behind the accelerated evolution. Taken together, our results suggest an important role that FOXP2 may have played in the origin of human speech and demonstrate a strategy for identifying candidate genes underlying the emergences of human-specific features.

    Another one for good measure:


    Science 2001 Feb 16;291(5507):1293-7
    Birth of two chimeric genes in the Hominidae lineage.

    Courseaux A, Nahon JL.

    Institut de Pharmacologie Moleculaire et Cellulaire, UMR CNRS 6097, 660 route des Lucioles Sophia Antipolis 06560 Valbonne, France.

    How genes with newly characterized functions originate remains a fundamental question. PMCHL1 and PMCHL2, two chimeric genes derived from the melanin-concentrating hormone (MCH) gene, offer an opportunity to examine such an issue in the human lineage. Detailed structural, expression, and phylogenetic analysis showed that the PMCHL1 gene was created near 25 million years ago (Ma) by a complex mechanism of exon shuffling through retrotransposition of an antisense MCH messenger RNA coupled to de novo creation of splice sites. PMCHL2 arose 5 to 10 Ma by an event of duplication involving a large chromosomal region encompassing the PMCHL1 locus. The RNA expression patterns of those chimeric genes suggest that they have been submitted to strong regulatory constraints during primate evolution.

    [added in edit: oh wait, this was discussed in detail by theyeti back on p. 1

    Some points that I think IDists in particular tend to neglect:

    1) These are not rare cases, rather discoveries like those referenced here happen every day. The origin of novel genes with divergent functions via natural processes is a ubiquitous and continuing occurrence.

    2) I think it is useful to point out how the reconstructed origins of these various genes are *not* due to some single-step process -- rather, we have alternating rounds of duplication, mutation (and *way more* than just point mutation, e.g. exon shuffling) and selection.  IDists will often say something like "gene duplication does not create new information because you just have a copy of the gene".  But no biologist invokes gene duplication alone.  Why don't IDists ever address the case of a gene duplication where one of the copies is mutated and selected, resulting in (1) the original gene and (2) a modified copy with different function.  How can the progression of one gene-->two genes with distinct useful functions *not* be an increase in genetic "information" in any biologically relevant sense?

    3) If the process described in step 2 is accepted, repeat in a few billion organisms for a few billion years.  Does this not go at least a fair distance in explaining the information content of genomes?

    4) If the leader of the ID movement, Phil Johnson, is horribly, blatantly wrong about simple biological facts, why has he not been criticized by other IDists?  Are they perhaps similarly mislead?


    Date: 2003/01/18 23:54:17, Link
    Author: niiicholas
    I noticed Charlesbois's article also, comments are here:

    Re-evolution of complex characters

    IMO this quote is the key one for putting some balance into discussions where Woese, Doolittle, etc. are cited:


    We and others have been exploring 'whole-genome trees' as a means of overcoming the noise and bias of single-protein analyses, to extract the bulk phylogenetic signals that are inherent in genomes. The input data for genome trees can be the proportions of genes or proteins that genomes hold in common, or (as we prefer) the mean pairwise similarities between shared proteins. Despite some early indications to the contrary, whole-genome trees have now largely converged on the rRNA-sequence tree.

    For us — as, presumably, for the verticalists — this convergence means that lateral gene transfer has not undermined descent with modification as the default explanation for microbial biodiversity, nor (as recently suggested by Ford Doolittle) has it thrown microbial classification into disarray. Lateral transfer is not both quantitatively important and directional. One of the few widely accepted instances of lateral gene transfer — the origin of chloroplasts from relatives of cyanobacteria — is clearly visible in our whole-genome trees, and even more so in 'sub-genome trees' based on functional subsets of genomes.


    Date: 2003/01/19 00:48:17, Link
    Author: niiicholas
    I was thinking about posting this on this ISCID thread, and then I thought, "why bother?" Besides I am too busy to start a big debate.

    Here is the thread, started by Mike Gene:

    Topic: Brainstorming Lessons
    link to thread

    I quote the end of RBH's post:


    If Mike Gene's reference to an "attempt to squelch discussions of design until we first extract a data base of definite information (i.e., actual mechanisms, identity of design, etc.)" means that speculation or questions about the mechanisms of design and the nature, identity, and/or properties of the designing agents ought to be out of bounds, then I think it is he who draws the wrong conclusion from the account of OOL he gives in the OP. I'll give him another example to think about.

    Wegener's 1915 hypothesis of continental drift was not accepted for nearly five decades because there was no known mechanism by means of which continents could be propelled across the earth. There were suggestive data that it had occurred - e.g., geographical form matches across seas, distributions of fossils, and so on - but no mechanism, and hence no broad acceptance. It wasn't until the 1960s, when actual drift rates could be measured and a plausible mechanism for drift was offered that it became broadly accepted. (I have stood in the valley at Thingvellir, in Iceland, where the mid-Atlantic Ridge crosses the island, and have seen the lasers that measure the drift rate as the North American Plate drifts west and the Eurasian Plate drifts east. It is an eerie feeling to be there, knowing that.)

    That example suggests ID itself ought not squelch questions and speculations about mechanisms and designing agents. No matter how many entries there are in the CCF, absent testable hypotheses about how they came to be IC, it will be merely a marginally interesting list of biological oddities and a set of targets for enterprising graduate students in molecular biology.


    I agree that it is ID that is squelching hypotheses, namely the details in origins scenarios that make them testable (strengthenable or weakenable, not always strict true/false).

    There is nothing wrong with going out on a limb and proposing hypotheses with specifity that goes beyond the data; this is how science proceeds into the unknown. This is why OOL researchers propose specific hypotheses, test them, and then revise -- e.g. RNAworld has become pretty well supported as a stage preceeding the origin of modern life, but difficulties in prebiotic syntheses of RNA are provoking studies of RNA precursors, e.g NA or PNA "worlds".

    The way science does *not* proceed is by maximizing vagueness, e.g. "a designer did something somewhere sometime for unhypothesized reasons by unhypothesized means". With ID, not even the laws of physics are considered legitimate constraints on the hypothesized IDer(s). I would argue that every successful (e.g. archaeology/forensics) or viable (e.g. SETI) "ID-detecting" discipline has hypothesized far more details regarding the IDer(s) than any hypothesis put forward by Mike Gene or anyone else in the ID movement.

    The problem with ultravague hypotheses is that they are explanatorily unconstrained; the problem with an unconstrained hypothesis is that there is no objective way to strengthen it or weaken it by consideration of further data.

    E.g., with Mike Gene's front-loading via mutational bias idea (leaving aside questions of what the actual biases are, which Art and others will have to work out), it seems to me that front-loading via evolution is approximately the most difficult and clumsy possible way to design something that I can think of. It would be like trying to type with your elbows even though you had fingers. Trying to get to, say, multicellularity through a nonspecific mutational bias would be rather like trying to convert from the Articles of Confederation to the Constitution via a bias in the replacement frequencies of various letters.

    Such a conversion could be accomplished either by intelligent or algorithmic selection of specific letters (in the case of biology we should convert this analogy to natural selection's *documented* ability to sweep specific beneficial nucleotide substitutions to fixation in the population, to avoid the usual Dawkins-METHINKS debates) -- but if these capabilities are in play, what's the point of the mutational bias? The mutations will happen slightly slower without the bias (well, assuming that the necessary mutations are those included in the bias, which seems completely unsubstantiated to me), but they will happen sooner or later and then can get selected. (In the case of an IDer, they would presumably not even bother with waiting for the mutations and just design straight-up whatever they wanted to design).

    Do these considerations have any weight in weakening Mike Gene's hypothesis? Only if you hypothesize some things about the designer, which Mike Gene does not, because his hypothesis is basically "someone frontloaded something for no specified reason" and thus considerations of efficiency, effectiveness, etc. (even though these are often invoked by Mike Gene and others in support of ID in other situations) will just be brushed aside as "we don't know anything about the IDer".

    IMO, this "unconstrainedness" of ID-movement "hypotheses" is their central weakness. This is a problem that supernatural hypotheses have, but is common to "superpowerful but unspecified aliens" "completely unspecified designer(s)", etc., as well. ("Unspecified natural processes" falls in the same boat, BTW) None of them predict or explain anything without further details. Full exhaustive detail is not necessary, but a least enough detail to make us expect some pattern in the data that we wouldn't otherwise expect, and which could be weakened by other patterns, is what it takes to get started.

    Vagueness will insulate an idea from refutation but will also doom it to the land of non-explanation.

    End of Saturday Night Sermon,

    [edit: cross-posted to II evo board:

    Vagueness and Explanatory Constraints


    Date: 2003/01/19 04:19:00, Link
    Author: niiicholas
    Michael Denton has said a lot of things over the years.  However on the whole he appears to have moved in a wholly evolutionary direction after he kicked off "the modern ID movement" with his 1986 book Evolution: Theory in Crisis.

    E.g., here is a quote that I'd read but never had handy:

    originally posted here

    From Darwinism Defeated?, 1999:


    In conclusion, I agree with [Phillip] Johnson that the Darwinian model is an inadequate explanation for how evolution occurred. And I think he is right to attack the exaggerated claims of certain Darwinian theorists who extend Darwinian explanations to include all aspects of human nature and behaviour. Where he does this I applaud his efforts. I also agree with him that the living organisms exhibit design. However I am not aware of any convincing arguments put forward by Johnson to show that this design necessitates special creation. I am also unaware of any serious systematic attempt by Johnson to show how the facts of biology, such as those of geographical distribution discussed above, can be accounted for more plausibly in creationist than evolutionary terms. Until he does this, academic biology will not take his antievolutionism seriously.
    In his advocacy of special creationism I believe Johnson is merely the latest in a succession of vigorous creationist advocates who have been very influential within conservative Christian circles, particularly in the United States, during the twentieth century. None of these advocates, however, has had any lasting influence among academic biologists. This is not because science is biased in favour of philosophical naturalism but because the special creationist model is not supported by the facts and is incapable of providing a more plausible explanation for the pattern of life's diversity in time and space than its evolutionary competitor. The reason why no current member of the US National Academy of Science is a special creationist is because of the facts, the same facts that in the nineteenth century convinced Darwin and Wallace and all the leading Christian biologists, including Joseph Hooker, Asa Gray, and Charles Lyell, of the reality of descent with modification

    (some typos may remain, I fixed one)

    There is no point in quote mining, so whatever anti-evolution statements one comes across from Denton are fine also.

    Date: 2003/01/23 04:54:45, Link
    Author: niiicholas
    Some good stuff I found and posted in response to Nelson Alonzo here:;f=13;t=000576;p=3


    What we see in nature is that B. subtilis, A. aeolicus, M.tuberculosis, M.
    genitalium (the smallest genome) , and H. pylor have all 8 parts needed for the F-ATP synthase to function. If this system was truly designed, we would predict that we would find no such evolutionary history for the F-ATP synthase, and we find none. Because of IC, selection would have weeded out any broken ATP synthase, which is why we see it so conserved in all these organisms. Thus an obvious design hypothesis is that the LUCA of all bacteria contained an 8-part ATP synthase which was inteligently designed.
    Or a pre-LCA ancestor got by with just a PPase, which is equally successful at generating proton energy gradients but is a heck of a lot simpler than the F1F0 ATPase (and shares some homology to boot).


    Membrane-bound proton translocating pyrophosphatases (H+-PPase) use the energy of pyrophosphate (PPi) hydrolysis to drive proton transport across biological membranes. The formed proton gradient is subsequently used to energize many cellular processes e.g. solute transport and ATP synthesis. The active H+-PPase is a dimer of 60–82 kDa polypeptide monomers, which are predicted to contain 15 transmembrane a-helices. Transmembrane helices are connected by short extracellular turns and longer cytoplasmic loops, three of which are mainly thought to form the active site for PPi hydrolysis. Overall the predicted H+-PPase structure is pretty simple which makes it a good model system for structural and functional elucidation of the mechanism by which pyrophosphate hydrolysis is coupled to proton pumping.

    3.A.10 The H+-translocating Pyrophosphatase (H+-PPase) Family

    Proteins of the H+-PPase family are found in the vacuolar (tonoplast) membrane of higher plants, algae, and protozoa, and in both bacteria and archaea. They are therefore ancient enzymes. The plant enzymes probably pump one H+ upon hydrolysis of pyrophosphate, thereby generating a proton motive force, postive and acidic in the tonoplast lumen. They establish a pmf of similar magnitude to that generated by the H+-translocating ATPases in the same vacuolar membrane . The bacterial and archaeal proteins may catalyze fully reversible reactions. The enzyme from R.rubrum contributes to the pmf when light intensity is insufficient to generate a pmf sufficient in magnitude to support rapid ATP synthesis.

    Eukaryotic members of the H+-PPase family are large proteins of about 770 amino acyl residues with fifteen putative transmembrane a-helical spanners (TMSs). The N-termini are predicted to be in the vacuolar lumen while the C-termini are thought to be in the cytoplasm. These proteins exhibit a region that shows convincing sequence similarity to the regions surrounding the DCCD-sensitive glutamate in the C-terminal regions of the c-subunits of F-type ATPases (TC #3.A.2).
    Baltscheffsky is da guy to look at for beginning work on the origin of ATPases; brief online summary:


    2. PPi and PPi synthase in the early evolution of biological energy conversion

    After our discovery (with von Stedingk, Heldt and Klingenberg) of the first alternative biological electron transport phosphorylation system, leading in bacterial photophosphorylation to PPi rather than to ATP, we have sought evidence for or against the possibility that, in early biological evolution, PPi preceded ATP as the central energy carrier. At present we investigate active site motifs in the proton-pumping PPase family of enzymes (PPase = inorganic pyrophosphatase), to which also bacterial PPi synthase belongs. Of special significance may be certain recurring tetrapeptidyl motifs, which contain 75 - 100 % very early amino acids (Gly, Ala, Asp and Val). These motifs seem to play a central role in PPase function and may be particularly important for obtaining a first detailed picture of the molecular origin and early evolution of biological energy conversion with phosphate compounds. The motifs also show some similarity to corresponding, phosphate binding, regions in both ATP synthases and P-type ATPases.
    Note that pyrophosphate can be produced by common inorganic processes.


    So lets review. A de-novo design hypothesis entails:

    1. No evolutionary history

    2. IC tied in with functional constraint (selection weeding out mutants because of ICness .
    Hmm, neither seems quite completely so true for the ATPase, because of the PPase.  A simpler, partially sequence-similar system can perform the task.  So even for a system older than the flagellum scientists are beginning to get hints indicating that ICness tain't all it's cracked up to be.


    In the near future I want to bring Dembski into the mix. However, unless any relevant criticism of a specific system is brought up, I'm simply going to list them for now. And we can bring up another thread to discuss each system's history. For now, I'm just concerned with listing them.
    Well for starters, for the flagellum your reliance on Mike Gene has left you a bit out of date:


    Biochemistry 2001 Oct 30;40(43):13041-50
    Conformational change in the stator of the bacterial flagellar motor.

    Kojima S, Blair DF.

    Department of Biology, University of Utah, Salt Lake City, Utah 84112, USA.

    MotA and MotB are integral membrane proteins of Escherichia coli that form the stator of the proton-fueled flagellar rotary motor. The motor contains several MotA/MotB complexes, which function independently to conduct protons across the cytoplasmic membrane and couple proton flow to rotation. MotB contains a conserved aspartic acid residue, Asp32, that is critical for rotation. We have proposed that the protons energizing the motor interact with Asp32 of MotB to induce conformational changes in the stator that drive movement of the rotor. To test for conformational changes, we examined the protease susceptibility of MotA in membrane-bound complexes with either wild-type MotB or MotB mutated at residue 32. Small, uncharged replacements of Asp32 in MotB (D32N, D32A, D32G, D32S, or D32C) caused a significant change in the conformation of MotA, as evidenced by a change in the pattern of proteolytic fragments. The conformational change does not require any flagellar proteins besides MotA and MotB, as it was still seen in a strain that expresses no other flagellar genes. It affects a cytoplasmic domain of MotA that contains residues known to interact with the rotor, consistent with a role in the generation of torque. Influences of key residues of MotA on conformation were also examined. Pro173 of MotA, known to be important for rotation, is a significant determinant of conformation: Dominant Pro173 mutations, but not recessive ones, altered the proteolysis pattern of MotA and also prevented the conformational change induced by Asp32 replacements. Arg90 and Glu98, residues of MotA that engage in electrostatic interactions with the rotor, appear not to be strong determinants of conformation of the MotA/MotB complex in membranes. We note sequence similarity between MotA and ExbB, a cytoplasmic-membrane protein that energizes outer-membrane transport in Gram-negative bacteria. ExbB and associated proteins might also employ a mechanism involving proton-driven conformational change.


    The occurrence of significant conformational change in the stator has implications not only for the present-day mechanism but also for the evolution of the flagellar motor. A membrane complex that undergoes proton-driven conformational changes could perform useful work in contexts other than (and simpler than) the flagellar motor, and ancestral forms of the MotA/MotB complex might have arisen independently of any part of the rotor. We queried the sequence database using the sequence of the best-conserved part of MotA (the segment containing membrane segments 3 and 4) from Aquifex aeolicus, a species whose lineage is deeply branched from other bacteria. In addition to the expected MotA homologues, the search returned a protein sequence from the archaeal species Methanobacterium thermoautotrophicum (protein MTH1022) that shows significant sequence similarity not only to MotA but also to the protein ExbB (Figure 9). ExbB is a cytoplasmic-membrane protein that functions in conjunction with ExbD, TonB, and outer-membrane receptors to drive active transport of certain essential nutrients across the outer membrane of Gram-negative bacteria. The energy for this transport comes from the proton gradient across the inner membrane. Thus, MotA and ExbB are both components of systems that tap the proton gradient to do work some distance away (at either the rotor-stator interface or the outer membrane; Figure 9).

    Other features also point to a connection between the Mot and Exb systems. MotA functions in a complex with MotB, which as noted contains the critical residue Asp32 near the cytoplasmic end of its single membrane segment. ExbB functions in a complex with ExbD, which likewise has a single membrane segment with a critical Asp residue near its cytoplasmic end (Asp25 in ExbD of E. coli; ref 59). Although ExbB has only three membrane segments in contrast to the four in MotA, the membrane segments that show sequence similarity have the same topology. The protein TonB is also present in the complex with ExbB and ExbD (59, 60) and would provide an additional membrane segment to round out the topological correspondence (Figure 9). ExbB contains a well-conserved Pro residue (Pro141 in E. coli ExbB) that is the counterpart of Pro173 of MotA. Although MotB and ExbD do not share close sequence similarity apart from the critical Asp residue, in certain positions in the membrane segment the residues most common in MotB proteins are also common in ExbD proteins. Finally, like the MotA/MotB complex the ExbB/ExbD complex contains multiple copies of each protein (61). Together, these facts make a reasonable case for an evolutionary connection between the Mot proteins of the flagellar motor and the Exb proteins of outer-membrane transport (and by extension the TolQ/TolR proteins, which are related to ExbB/ExbD but whose functions are less understood).

    The number of parts in a flagellum that don't have homologs with different, non-flagellar functions is getting to be rather low; mostly they are filament and shaft proteins, which all may be homologous with each other, and of course nonmotile filaments are known to have a wide degree of uses in bacteria...

    So even for systems that are remote from us by 3 billion years there has been some recent progress.  

    What I'd really be interested in, Nelson, is your opinion on the vertebrate immune system.  IC or not?  Evolved or not?  Behe says IC, and intelligently designed.

    Date: 2003/01/24 04:34:13, Link
    Author: niiicholas
    For the fossil record's first feat, I submit:

    Microraptor gui

    Nature 421, 335 - 340 (2003); Four-winged dinosaurs from China

    Freely online:

    lots of discussion at II evo board

    Since the paper is up for free I will put the pics in here:

    Figure 1 Microraptor gui. a, Skeleton of Microraptor gui (IVPP V13352). Scale bar, 5 cm. b, A computerized tomography (CT) image of the major part of the IVPP V13352. Scale bar, 13 cm. Scanning was performed using a CT machine (LightSpeed Qx/i) at an energy level of 140 kV and 250 mA. The images were collected at a size of 800  600 pixels. On the basis of comparison of adjacent fracture-face geometries, density of adjacent pieces, and continuity across fractures of bones (see ref. 45), we find a few pieces are unverified or assembled in the wrong position (marked by asterisks). For example, one small piece containing the anterior end of the skull and a medium-sized piece near the right forelimb preserving some arm feathers are dubious. The latter is actually from the counter slab. However, the CT information suggests that most pieces lie together in their natural relationships, including pieces containing the forelimb, hindlimb and associated feather impressions. This is concordant with microscopic observations. c, A reconstruction of M. gui showing the morphology and distribution of the pennaceous feathers. Scale bar, 6 cm.

    And check out 2g for the definitely non-trivial (although the exact function may be up for grabs) hind leg feathers:

    Figure 2 Feathers of IVPP V13352 and TNP00996. Feathers attached to the skull (a), the tail (d), the forelimb (f), the manual digit I (i), and the hindlimb (g) of IVPP V13352, and to the skull (b) and the tail (e) of TNP00996; close-up of the skull feathers of TNP 00996 ©, and of secondaries (h) and large pennaceous feathers on distal metatarsus (j) of IVPP V13352. Note the pennaceous feathers attached to the digit (i) that might be a precursor to the alula. This is concordant with the fact that M. gui has a short manual digit I, because the alula is often associated with a reduced alular digit except in Protopteryx24. Scale bar, 5 cm.

    At the end they say:


    We carefully examined the specimens under the microscope and with high-resolution X-ray computerized tomography (CT) to test the authenticity of one of the studied specimens45 (IVPP V13352) and can guarantee the accuracy of the information that we provide in this study. case this wasn't clear, ref 45 is to the Archaeoraptor forgery, meaning that one of the pieces of the Archaeoraptor was a chunk of M. gui.

    Truth was stranger than fiction in this case...

    Date: 2003/01/25 18:00:34, Link
    Author: niiicholas
    Charlie D gives a great brief intro on why adaptive mutation ain't:

    ARN thread:
    Topic: Directed mutation;f=13;t=000588

    Originally posted by charlie d:
    I have no idea when that paper was written, but it lists no references later than 1995.  Thus, its enthusiasm for the "targeted mutation" phenomenon, its belief that it represents a fundamental challenge to the prevailing genetic paradigm, and its conclusion that "there is no explanation for it", is not surprising, considering that the hypothesis itself began to crumble in earnest in 1996 with the publication of this article by Prival and Cebula:
    Prival MJ, Cebula TA Adaptive mutation and slow-growing revertants of an Escherichia coli lacZ amber mutant. Genetics 1996 Dec;144(4):1337-41,
    and eroded further after this article by Patricia Foster (who was one of the original discoverers of the adaptive mutations phenomenon):
    Foster PL. Nonadaptive mutations occur on the F' episome during adaptive mutation conditions in Escherichia coli. J Bacteriol. 1997 Mar;179(5):1550-4.

    These and other findings prompted Foster herself to write the now classic review (available for free here): Foster PL. Adaptive mutation: has the unicorn landed? Genetics. 1998 Apr;148(4):1453-9,
    a virtual obituary for the "lamarckian" interpretation of the phenomenon.

    A more detailed review is this one (but subscription is required to access the actual paper): Foster PL. Mechanisms of stationary phase mutation: a decade of adaptive mutation. Annu Rev Genet. 1999;33:57-88.

    At the current state of affairs, it is very clear that mutations during "adaptive mutagenesis" are not specifically directed towards the gene(s) under selection, i.e. they are entirely darwinian (random wrt to fitness), and are often the result of generalized hypermutation mechanisms (the last important piece of the puzzle being the publication of this paper last year):  Hendrickson H, Slechta ES, Bergthorsson U, Andersson DI, Roth JR. Amplification-mutagenesis: evidence that "directed" adaptive mutation and general hypermutability result from growth with a selected gene amplification. Proc Natl Acad Sci U S A. 2002 Feb 19;99(4):2164-9.

    For those interested in the most recent and actual history of the "targeted mutation" saga, I recommend this recent excellent review of the issue, available for free here: Rosenberg SM Evolving responsively: adaptive mutation. Nat Rev Genet 2001 Jul;2(7):504-15


    Date: 2003/01/25 19:17:43, Link
    Author: niiicholas
    Re-posting my reply:

    It is quite interesting how hostile and demanding "open-minded skeptic" Mike Gene is towards MDT given his continual begging for leniency regarding the almost unbelievably vague and subtle form of ID that he advocates.  It is clearly a result of his uniteleological bias, and once this is exposed we can see the reason of his persecution of us.

    But MDT follows quite naturally from several premises followed regularly by Mike Gene:

    1) Loosen up on science's preference for parsimony

    2) Take "it looks as if it were designed for..." intuitions seriously

    3) Always keep in the front of one's mind the perceived biases of your opponents

    The central insight of MDT is that an awful lot of things "look like they were designed for" subverting other designs.  If this intuition is to be taken seriously, then MDT is the obvious outcome -- and a revolutionary one given the SDT-focus of the ID movement to date.  There are, to be sure, some cases in things like development where "conflicting" designs may appear to result in a larger goal, but in all these cases both designs are explained by co-replicating genomes that have the same interest in survival, so this is easily identifiable.

    In that ARN thread, MG also points to some of the widespread commonalities amongst life.  Does this point to SDT or MDT?  Neither; it points to common descent.  As Dembski and others have pointed out, SDT is fully compatible with common descent; so is MDT.

    Of course MDT advocates believe, in common with all other ID theories, that the first life was designed; however, the great thing about MDT is that it gives us much more insight into *how* it was designed compared to MG ID or SDT in general, which all advocate the "poof" model.

    If I might for a moment advocate my own subspecies of MDT, namely ITWA theory (Invisible Tinkering Warring Army theory), this point will soon become clear.  The basic biochemistry of life has been shown by nonteleological scientists to have several peculiar features:

    1) A strange dependence on RNA for core processes, which just happens to have both self-replication and enzymatic capabilities, unlike DNA and proteins

    2) A considerable degree of optimization, but optimization that appears to have simpler precursors -- e.g. the genetic code is thought to have started with just a few amino acids, which happen to be the most common ones in various core protein processes

    3) A limited number of "basic" protein folds, DNA motifs, etc.

    This list could be greatly expanded.

    The point of all this is that it appears that the last common ancestor (not necessarily a single cell, perhaps a "gene pool" of laterally-transferring bacteria) was not itself a "design from scratch", but instead the product of a tinkering of earlier, simpler designs.  ITWA theory assimilates all of the work of nonteleologist scientists on RNAworld etc. and incorporates it into its own theory.  Some version RNAworld existed at some stage, but in order to gain an advantage over other ITWAs, one ITWA added DNA to store genetic information.  This allowed for much longer genomes and greater complexity.  Further tinkers expanded the genetic code, etc.

    One of these variants was so superior that all competitors, except perhaps things like parasitic viruses and RNA viroids, were exterminated.  And this is the LCA of life.  (this may be a somewhat oversimplified picture, extermination was not necessarily a sudden process and we could have had multiple "tinker sweeps to fixation" as various innovations took over; but I am just exploring here).

    So one of the ITWAs "won" the battle.  So why, a skeptic would ask, did the process not stop here?  Victory had been had!

    Well, as anyone who studies the history of combat knows, once one army triumphs, a common result is for the army to split up and fight over the spoils.  Repetition of this process results in the modern world of innumerable battling (and sometimes self-serving cooperating) ITWAs.

    This is a far more detailed and testable explanation than "somebody designed some things for no detailed reason a few billion years ago", which appears to be what the more subtle forms of ID amount to.

    Date: 2003/01/27 19:39:19, Link
    Author: niiicholas
    Reposting from:

    Topic: List of IC systems

    First off,

    An awful lot of entries in the NCBI protein database listing MotA, ExbB, and TolQ as being a "family", in opposition to what Mike Gene has been suggesting

    Originally posted by Mike Gene:
    Nic: Hey, I'm just following the peer-reviewed lit., man. Take it up in the pages of Biochemistry if you like...

    The authors never claim MTH1022 is a homolog of motA. And even if they did, the claim would be unsupported.  
    People can read the quote I posted and decide for themselves exactly what the authors meant.  Mentioning significant sequence similarity in the middle of a discussion of homologs seems like a strong indication to me that they meant homolog or at least "likely homolog".  And see below for what some of those proteins are labeled as in the NCBI database.


    Actually, running a PSI-BLAST of ExbB gets me four hits on archaeabacteria, but whatever.

    With e values of 0.005 and higher.  That's not very impressive.  Furthermore, even if there is a non-convergent and real relationship here, note that it is not widely distributed and would thus seem to have evolved long after archaea appeared.  

    A much stronger point is that the ExbB homologs are very widely distributed in eubacteria, in very basal lineages.

    Think so?  What groups did you have in mind?[/qb]

    Hmm, well a standard protein BLAST  on E coli ExbB gives me this taxonomy report:

    An E. coli "biopolymer transport exbB protein"

    Here is the link

    Here are some of the results *outside* the proteobacteria:

    Code Sample
     Chlamydophila pneumoniae CWL029 [chlamydias] taxid 115713
    gi|15618694|ref|NP_224980.1| Macromolecule transporter [Ch...      61  1e-08

     Cytophaga hutchinsonii [CFB group bacteria] taxid 985
    gi|23136461|gb|ZP_00118181.1| hypothetical protein [Cytoph...      60  1e-08
    gi|23136843|gb|ZP_00118557.1| hypothetical protein [Cytoph...      36  0.35

     Chlamydia trachomatis [chlamydias] taxid 813
    gi|15605326|ref|NP_220112.1| polysaccharide transporter [C...      59  4e-08

     Chlamydia muridarum (agent of mouse pneumonitis) [chlamydias] taxid 83560
    gi|15835499|ref|NP_297258.1| MotA/TolQ/ExbB proton channel...      58  8e-08

     Aquifex aeolicus [aquificales] taxid 63363
    gi|15606982|ref|NP_214364.1| TolQ homolog [Aquifex aeolicu...      55  5e-07
    gi|15606823|ref|NP_214203.1| biopolymer transport exbB [Aq...      42  0.005


     Deinococcus radiodurans [eubacteria] taxid 1299
    gi|15805483|ref|NP_294179.1| biopolymer transport protein,...      47  1e-04

     Methanothermobacter thermautotrophicus str. Delta H [euryarchaeotes] taxid 187420
    gi|15679040|ref|NP_276157.1| biopolymer transport protein ...      43  0.002

     Synechocystis sp. PCC 6803 [cyanobacteria] taxid 1148
    gi|16329196|ref|NP_439924.1| biopolymer transport ExbB pro...      41  0.013
    gi|16329550|ref|NP_440278.1| biopolymer transport ExbB pro...      40  0.018

    Note below that *even* some proteobacteria ExbB proteins have "unimpressive" similarity scores and yet are still called ExbB proteins (as are some **archaeabacteria** ExbB-family proteins):

    Code Sample
    Photobacterium damselae subsp. piscicida [g-proteobacteria] taxid 38294
    gi|19577341|emb|CAD27898.1| ExbB protein [Photobacterium d...      33  1.9

     Plesiomonas shigelloides [enterobacteria] taxid 703
    gi|13774064|gb|AAG23397.1| ExbB [Plesiomonas shigelloides]         33  2.0

     Sulfolobus solfataricus [crenarchaeotes] taxid 2287
    gi|15899059|ref|NP_343664.1| Amino acid transporter, putat...      33  2.6


     Methanosarcina acetivorans C2A [euryarchaeotes] taxid 188937
    gi|20089242|ref|NP_615317.1| MotA/TolQ/ExbB proton channel...      33  3.4
    gi|20093212|ref|NP_619287.1| MotA/TolQ/ExbB proton channel...      33  3.8
    gi|20093420|ref|NP_619495.1| MotA/TolQ/ExbB proton channel...      32  6.7
    MotA and ExbB appear to have equally wide distributions

    The distribution taxonomy report for ExbB is, in fact, rather like the taxonomy report for standard protein blast of E. coli's MotA protein: lots and lots of enterobacteria and proteobacteria, and a few hits out in spirochetes and other various deeply divergent bacteria.

    Here is said taxonomy report

    Are we to conclude that MotA is just as likely to be of late origin and derived as ExbB?

    ...methinks the database may be a wee bit biased towards certain intensively-studied gram-negative bacteria groups and that therefore seeing many hits in those groups and few outside means very little in terms of relative significance.  As I showed, you have to put MotA and ExbB in the same distribution bucket regardless.

    Regarding low e-values:

    Based on your blanket skepticism of marginal e-values, you may want to argue that some MotA proteins are of independent origins and convergent on standard MotA's.  Many of these scores are non too impressive, yet some are MotAs (or PomA, a related motor) despite this:

    Code Sample
     Treponema denticola [spirochetes] taxid 158
    gi|4426945|gb|AAD20619.1| flagellar motor protein MotA [Tr...      53  3e-06

     Pseudomonas putida [g-proteobacteria] taxid 303
    gi|2853602|gb|AAC08066.1| MotA [Pseudomonas putida]                53  5e-06

     Leptospira interrogans serovar lai str. 56601 [spirochetes] taxid 189518
    gi|24213362|ref|NP_710843.1| Chemotaxis motA protein [Lept...      52  6e-06
    gi|24216276|ref|NP_713757.1| motility protein A [Leptospir...      39  0.056

     Bacillus anthracis str. A2012 [eubacteria] taxid 191218
    gi|21402555|ref|NP_658540.1| MotA_ExbB, MotA/TolQ/ExbB pro...      52  8e-06
    gi|21399546|ref|NP_655531.1| MotA_ExbB, MotA/TolQ/ExbB pro...      51  1e-05

     Shewanella oneidensis MR-1 [g-proteobacteria] taxid 211586
    gi|24375769|ref|NP_719812.1| chemotaxis motA protein [Shew...      51  1e-05
    gi|24373102|ref|NP_717145.1| chemotaxis motA protein [Shew...      38  0.13

     Thermotoga maritima [thermotogales] taxid 2336
    gi|15643440|ref|NP_228484.1| motility protein A [Thermotog...      50  3e-05

     Campylobacter jejuni [e-proteobacteria] taxid 197
    gi|15791705|ref|NP_281528.1| putative flagellar motor prot...      48  9e-05

     Rhodopseudomonas palustris [a-proteobacteria] taxid 1076
    gi|22963976|gb|ZP_00011582.1| hypothetical protein [Rhodop...      42  0.006

     Magnetococcus sp. MC-1 [proteobacteria] taxid 156889
    gi|22999422|gb|ZP_00043404.1| hypothetical protein [Magnet...      41  0.011
    gi|23000123|gb|ZP_00044067.1| hypothetical protein [Magnet...      33  3.5

     Vibrio alginolyticus [g-proteobacteria] taxid 663
    gi|3024412|sp|O06873|POMA_VIBAL Chemotaxis pomA protein >g...      40  0.038

     Bacillus halodurans [eubacteria] taxid 86665
    gi|15615802|ref|NP_244106.1| flagellar motor apparatus [Ba...      39  0.058

     Vibrio vulnificus CMCP6 [g-proteobacteria] taxid 216895
    gi|27363787|ref|NP_759315.1| Flagellar motor component Mot...      37  0.18

     Clostridium thermocellum ATCC 27405 [eubacteria] taxid 203119
    gi|23021959|gb|ZP_00061601.1| hypothetical protein [Clostr...      35  0.87

     Vibrio cholerae [g-proteobacteria] taxid 666
    gi|15640908|ref|NP_230539.1| chemotaxis protein PomA [Vibr...      32  5.6
    Regarding the e-values of archaeal ExbB homologs, PSI-BLAST on E. coli ExbB gives an archaeabacterial homolog with e-value of 2e-17, which ought to be good enough for Mike Gene:

    PSI-BLAST search

     Methanothermobacter thermautotrophicus str. Delta H [euryarchaeotes] taxid 187420
    gi|15679040|ref|NP_276157.1| biopolymer transport protein ...      90  2e-17
    gi|15678698|ref|NP_275813.1| unknown [Methanothermobacter ...      43  0.003
    gi|15678311|ref|NP_275426.1| protein kinase [Methanothermo...      33  3.4
    My point

    These kinds of things ought to at least be mentioned and discussed before reckless statements are made about absolutely no evidence for precursors to flagellar proteins, that's my only point.  For some reason you guys prefer to sweep it under the rug by unsupported arguments about ExbB's narrow distribution.  Just acknowledge that this little bit of the biological world is a bit disharmonious with the flagellum-was-specially-created thesis.  All I've been saying, and now documenting, is that ExbB homologs are at least as widely distributed as MotA, and possibly more widely distributed.

    Date: 2003/01/28 04:00:49, Link
    Author: niiicholas
    [deleted] reposting formatting didn't work.

    The thing to do would be to plot the daily normalized recapture rates (and capture rates of wild moths) for all the different experiments one could find (or at least Kettlewell) vs. days past full moon or some such.  Based on the Dorset 1955 data and on the daily (rather than aggregated into phase bins) Birmingham 1953 data it would appear that recapture rates increase as the full moon is decreasing.  Birmingham 1955 shows the opposite pattern however.

    Better yet would be to plot nightly lunar radiance or some such vs. capture & recapture rates, and delineating different traps (pheromone vs. light) -- although, both kinds of traps could show a response as the moths could be influenced by moon phase regardless of trap type.

    We should archive Tom Curtis' posts or maybe get him to synthesize them into a Wells FAQ subFAQ however, they are quite the debunking of Wells and Wells defender Steve Jones who does some really atrocious statistics...


    PS: I find it hard to believe that there is no published literature on moon phase (and related factors, e.g. cloud cover) vs. capture/recapture rates for moths.  Those moth guys spend a lot of time hanging around at night...

    Date: 2003/01/28 21:38:27, Link
    Author: niiicholas
    FWIW this page on a survey protocol for an endangered moth species (Silphium Borer Moth) says:


    Surveying for Adults

    Sampling period: Sept. 1 to Sept. 20.

    Weather conditions:

    Air temp: > 50 F
    Wind speed: < 15mph
    Sky: overcast to partly cloudy (clear is OK if moonlight is minimal)
    Moon phase: new moon is best (need minimal moonlight)
    Humidity: > 60%

    Time of day: 9:00 pm until 2 am.

    Number of visits per site: 2 visits per season, with not less than 5 days between visits.

    Sample effort per site: One for every 10 acres of Silphium occupied habitat.

    Sampling method: Night-lighting using a UV-light and a white sheet. The sheet must be monitored for a 5-hour period each time (a non-lethal funnel trap may also be used). Specimens should be released after handling and field identification, except for one voucher per site.

    (bolds added)

    link to google archive page

    And Shapiro says in his essay:

    "Moth collectors agree broadly that light traps attract very little when the moon is full."


    BTW, this page has some older moth lit (well, short news bits from New Scientist), e.g. Cherfas 1986 and 1987:

    Hang on, I just came up with some lit.

    Date: 2003/01/28 22:05:09, Link
    Author: niiicholas
    Unfortunately most fields don't have the nice PubMed-style search engine.  But with the annoying-but-relevant BIOSIS I was able to turn up quite a bit.

    Quoted below are the results of a search on "moon moth", removing only the totally irrelevant:


    Citation 1.

    Accession Number

    Das S B [a]; Katyar N P [a].

    [a] J. N. K. V. V. Zonal Agricultural Research Station, Khargone, M. P., 451 001 India.

    Title (English)
    Effect of moon light and lunar periodicity on the pheromone trap catches of tobacco caterpillar (Spodoptera litura Fab.) moths.

    Crop Research (Hisar). [print] 21(2). March, 2001. 229-236.

    The effect of moon light and its periodicity on the sex pheromone trap catches of male moths of tobacco caterpillar, Spodoptera litura (Fab.) (Lepidoptera : Noctuidae) was studied for 12 years i. e. 1986-1997 at JNKVV Zonal Agricultural Research Station, Khargone (259 m above MSL, latitude 21degree22'-21degree59' N and longitude 75degree50'-76degree12'E), M. P., India. The influence of moon light lumination response of male moths towards pheromone traps was measured by the number of the trap catches, which were correlated with illumination intensity of different days of a lunar cycle (both ascending and descending phases). Analysis of the data revealed that the trap catches were low on intensive moonlit nights i. e. on and around full moon nights. Significant negative correlation was observed between illumination of moon i. e. degree of moon phase and trap catches. The response of catches was in the increasing trend during the descending phase (full moon to no moon) and vice-versa for the ascending phase (no moon to full moon). Further, the total catches recorded were higher in the latter phase than that of former one. Highest catches were observed in the ascending and descending phase of lunar cycle during the months of October and March, respectively i. e. changing weather time which might be enhancing the mating/flight activity. Hence, this study supports the theory that the response of the moths is suppressed on and around full moon, for which a number of factors are responsible.

    Citation 2.

    Accession Number

    Kolligs Detlef [a].

    [a] Faunistisch-Okologische Arbeitsgemeinschaft, Olshausenstr. 40, 24098, Kiel Germany.

    Title (English)
    Ecological effects of artificial light sources on nocturnally active insects, in particular on butterflies (Lepidoptera).

    Faunistisch-Oekologische Mitteilungen Supplement. [print] (28). 2000. 1-136.

    It is a well known phenomena that night-active insects are attracted by artificial light sources. With a growing urban environment and a high number of street lamps and other light emitting sources, the response of night active insects to artificial light becomes of in-creasing importance for nature protection. This study focuses on the behavioural response of different insect orders, families and species to the most frequently used exterior lighting and street lamps (mercury- and sodium-vapour lamps). These artificial sources of light distinctly increased in the last decades. In the city of Kiel (North-Germany) the number of streetlights was fifty times higher in 1998 than in 1949. The investigations were carried out at two sites in Schleswig-Holstein (North-Germany): in Albersdorf / Dithmarschen (western Schleswig-Holstein) and in Kiel on the university campus (eastern Schleswig-Holstein). In Albersdorf, the insects were attracted by a light emitting greenhouse (10,000 m2) and by two punctually radiating light sources (light traps with mercury and sodium-vapour lamps) and became comparative investigated in 1994 to 1995. Two different methods were used to record insects at the greenhouse. Butterflies (Lepidoptera) were sampled by hand. The remaining insects were trapped in two 1.5 m2 large sample areas using a suction trap. Insects from each of the four sides of the green-house were sampled and trapped separately. The two light traps caught the insects automatically. On the campus of Kiel University insects were studied from 1994 to 1996. For this purpose four street lamps equipped with mercury-vapour lamps had traps attached to the socket. On one of the four street lamps the mercury-vapour lamp was exchanged by a sodium-vapour lamp with the same light intensity. In 1996 two additional street lamps were equipped with a different type of trap (describe the trap!;). 72,267 insects from 114 insect families and 96,725 insects from 138 families were redorded at Albersdorf and at Kiel, respectively. Butterflies (Lepidoptera), beetles (Coleoptera), caddies flies (Trichoptera) and sciarid flies (Sciaridae) were determined to the species level. An analysis of the catches gave the following resuits: Mosquitos (Nematocera) made up the majority of all captured insects (40 - 90 %). The other most conunon groups were butterflies (Lepidoptera), flies (Brachycera) and beetles (Coleoptera). In both study areas Hymenopterans (Hymenoptera), aphids (Aphidina), cicadas (Cicadina), true bugs (Heteroptera), neuropterans (Neuroptera), caddis flies (Trichoptera), psocids (Psocoptera) and mayflies (Ephemeroptera) made up less than 1 % of the total catch. Catches from adjacent street lamps (25 m apart) were distinctly different in their insect compositions. These differences seem to be caused by the surrounding habitats and the wind exposure of the lamps. Significant differences between the compositions of samples from different street lamps were oniy found between May and the end of August. In spring and autumn the sample 13sizes were small and species compositions were not significantly different. In contrast to hand sampling not all insects that flew into street lamps were caught by the automatic light traps (e. g. only 30-40 % of the Lepidoptera were caught by the traps) No significant correlation was found between the size of a light source and the number of Lepidoptera attracted by it. Rather the intensity and the light spectrum seem to control butterfly abundance at a light source. The light spectrum of the sodium-vapour lamp attracted fewer species and individuals than the mercury-vapour lamp. Otherwise from some species, e.g. he swift mohs (Hepialidae) or the geometric moth Idaea dimidiata, more individuals were registrated at the sodium-vapour lamps. Only single individuals of endangered butterfly species were found at the different light sources, while 31 beetle species of the Red List of Schleswig-l-Iolstein were captured in the study area in Kiel. The rove beetles (Staphylinidae) Megarthus nitidulus and Oxytelus piceus were recorded for the first time in decades in Schleswig-Holstein. Both the weevil (Curculionidae) Euophryunz confine and the rove beetle Atheta griepi were found for the first respectively the second time in Schleswig-Holstein. Three Red List species of pond colonising cacldis flies (Trichoptera) were also recorded. Insect behaviour on artificial light sources depends on the species and the sex. An experiment showed that insects were attracted by artificial light over a maximum distance of 130 m. Caterpillars were found on trees and bushes in the direct surroundings of the artificial light sources. I was concluded that, although their habitat was influenced by an artificial light regime, several species could develop successfully. Not all moths in the surrounding of a light source exhibited a positively photo-tactic reaction. Some species, e.g. the Red Underwing (Catocala nupta) or the Copper Underwing (Aniphypira pyramidea) were caught predominantly at natural sources of food or by bite instead at the artificial light. Temperature and iliurniination by the moon distinctly influenced the insect abundance at artificial light sources. On nights with high temperature insects were more abundant, whereas an increase in illumination by the moon resulted in lower abundance. Mosquitoes (Nematocera) were more abundant on nights with increasing air pressure. Small and/or less mobile insects were sensitive to strong winds and preferred to fly on wind shielded light sources. High abundance of insects at the artificial light sources was only recorded on a few days of the year when the weather was particularly favourable. Less mobile or rare species whose distribution is restricted to natural habitats seem to be most endangered by their attraction to artificial light sources. In our cultural landscape natural habitats are often isolated and even a small increase in mortality could-result in negative effects for the population development of k-strategists. In contrast, r-strategists which aggregate in large numbers at artificial light sources, are often able to compensate for additional losses with their high reproductive rate. Common and abundant species often play a key role in the nutrient cycles and food webs of ecosystems (e.g. a decrease in caterpillar density of some abundant Lepidoptera species may ha-ye a negative effect on the breeding success of insectivorous bird species). It is recommended that only sodium-vapour lamps should be used for street illumination, because of their low attractiveness to insects. However, before street lamps get installed it should be always checked whether and for how long an illumination is needed. Natural and close to natural habitats should be protected against artificial light emission because additional losses of individuals may endanger populations of rare species.

    Citation 3.

    Accession Number

    Parajulee M N [a]; Slosser J E [a]; Boring E P, III.

    [a] Tex. Agric. Exp. Stn., 11708 Highway 70 South, P.O. Box 1658, Vernon, TX 76385-1658 USA.

    Title (English)
    Seasonal activity of Helicoverpa zae and Heliothis virescens (Lepidoptera: Noctuidae) detected by pheromone traps in the rolling plains of Texas.

    Environmental Entomology. 27(5). Oct., 1998. 1203-1219.

    Bollworm, Helicoverpa zea (Boddie), and tobacco budworm, Heliothis virescens (F.), male moth activity were monitored for 15 yr (1982-1996) in sex pheromone traps in the Rolling Plains of Texas. The study consisted of 2 types of survey as follows: (1) weekly monitoring of bollworm and tobacco budworm moths in Hardeman and Knox counties to investigate their long-term seasonal activity patterns, and (2) daily monitoring of bollworm moths in Haskell, Knox, and Wilbarger counties to quantify the effect of lunar cycles on moth generation cycles. Moths were active from early April to late October, with increasing activity as the growing season of cotton, Gossypium hirsutum L., progressed through September. Although the bollworm-budworm complex in the region consisted of apprxeq93% bollworms and only apprxeq7% tobacco budworms, the seasonal trends in activity patterns were similar for both species. Correlation analyses showed a significant positive relationship between weekly trap catch and temperatures, but a significant negative relationship was observed between trap catch and wind velocity for both species. Although the average monthly activity levels were positively correlated between adjacent months, there was no significant correlation between the activity of the moth population that contributed to the overwintering generation and the following spring population. Mean seasonal abundance curves, with upper confidence limits, were constructed for each species based on 15-yr averages. The mean abundance curves of this type are useful for identifying years with unusual moth severity. Daily trap catch data showed that the moon phase influenced the capture of bollworm moths in pheromone traps, as indicated by a significant positive correlation between trap catch and percentage moon illumination. Daily trap catch data also showed that the maximum trap catch occurred 71% of the time during the full moon, followed by 1st quarter (11%), last quarter (9%), and the new moon (9%). However, the relationship between the trap catch and the lunar cycles was not apparent when the traps were serviced weekly, indicating the importance of sampling frequency in detecting the relationship between trap catch and moon phase.

    Citation 4.

    Accession Number

    Trivedi T P [a]; Rajagopal D; Tandon P L.

    [a] Central Potato Res. Station, Kufri, Shimla-171 012, Himachal Pradesh India.

    Title (English)
    Environmental correlates of potato tuber moth Phthorimaea operculella (Zeller) (Lepidoptera: Gelechiidae).

    International Journal of Pest Management. 40(4). 1994. 305-308.

    Field experiments were conducted to study the relationship of environmental factors for the survival of the potato tuber moth, Phthorimaea operculella (Zeller), in the states of Kamataka (sub-tropical climate) and Ootacamund Tamil Nadu (temperate) during 1987-1989. The sex pheromone-baited water trap was designed for mass trapping the adult potato tuber moths. It was found that the peak populations of 545 moths/trap/2 weeks and 410/moths/trap/2 weeks were recorded at Ootacamund (Tamil Nadu) and Chikaballapur (Kamataka) during March and June respectively, which coincided with the planting season in these regions. The peak population was 247 moths/trap/2 weeks during November at APMC market yard, Yeshwanthpur, Bangalore. The moth population had positive correlations with temperature and wind velocity for two locations, viz. Chikaballapur and Ootacamund. The correlation coefficient values were 0.61 and 0.53 for temperature, and 0.65 and 0.66 for wind velocity at Ootacamund and Chikaballapur, respectively. Rainfall had a negative correlation at Ootacamund. A significant correlation was observed with sunshine hours at Ootacamund whereas a negative correlation was observed at Chikaballapur. The population showed significant positive multiple correlation with weather parameters and the values of the multiple correlation coefficient were 0.84 for Chikaballapur and 0.86 for Ootacamund. The coefficient of determination (R-2) predicted 70-74% changes in trap catches. Peak population catches were observed between 18.00 and 20.00 and moon-light was shown to have no effect.

    Citation 5.

    Accession Number



    Title (English)

    Acta Phytopathologica et Entomologica Hungarica. 23(1-2). 1988. 167-186.

    One of the most important abiotic factors modifying the results of light-trap catches, is the illumination of environment, that consists of illuminations generated by the sun, the moon and the night sky, together with the function of the clouds. On the basis of the data of fractioned light-trap, the authors.sbd.using a particularly elaborated computer method.sbd.investigated the influence of the general illumination of the environment, the common and polarized light of the moon upon the results of the catches of turnip moth. It was concluded that one can observe fundamental differences between the same groups of illumination generated by the moon or by twilight with regard of many similarities. When the moon is staying above the horizon, this phenomenon extends the duration of the flying activity. If the intensity of the reflected light from the moon increases, we can observe increasing catches in case of positive polarization, and decreasing one in negative case, respectively. As a new result the authors found that, the individuals of species investigated use the so called Babinet point, on the sky (this point has no polarization) for their spatial orientation. The behaviours can be given methematically by equations to obtain the expected values of the catches.

    Citation 6.

    Accession Number

    BAKER R R [a].


    Title (English)

    Animal Behaviour. 35(1). 1987. 94-101.

    Use of the moon as a compass during migration appears difficult due to the complexity of the moon's change in azimuth during the lunar month. These apparent difficulties would be eased if the moon's position were calibrated at intervals against a constant reference source, such as the geomagnetic field. Yet, until now, no animal has been shown to integrate moon and magnetic compasses for orientation. In this study, light-traps were used on 15 nights during a lunar month to obtain samples of heart-and-dart moths, Agrotis exclamationis, characterized by a preference to fly 'toward' (i.e. .+-. the moon's azimuth. The compass orientation of each sample was then tested in normal and reversed geomagnetic fields, out of sight of the moon. Compass orientation relative to the ambient magnetic field coincided with the compass bearing of the moon at the time of capture. Directional preference changed during the lunar month in a way that tracked the change in the moon's azimuth. It is concluded that moths use the geomagnetic field to calibrate a moon compass.

    Citation 7.

    Accession Number

    MIZUTANI M [a].


    Title (English)

    Applied Entomology & Zoology. 19(2). 1984. 133-141.

    A quantitative evaluation of the influences of weather and moonlight conditions on the light trap catches of moths was needed to compare samples of different stands and time. Multiple regression analyis was employed to establish which factors were important in determining the collected number of species and individuals and other characteristics of a moth sample. Data of 17 Aug. samplings taken from 20:00-21:00 and the weather and moonlight conditions prevailing at that same time were used. Regression analyses showed that most of the variation in the number of collected species could be described by an equation involving wind velocity, fog density, change in temperature from the previous night and lightness of the sky during the night. Standard partial regression coefficient showed that fog density was the most important positive effect component and wind velocity the main negative effect component. The equation for estimating the number of collected individuals described a smaller portion of the variability than the number of species. Air temperature did not significantly affect either the number of species or individuals.

    Citation 8.

    Accession Number

    ALINIAZEE M T [a].


    Title (English)

    Ecological Entomology. 8(3). 1983. 241-248.

    Flight of M. latiferreanus (Walsingham) was influenced by a number of environmental factors including temperature, wind and rainfall. Few M. latiferreanus moths were trapped in light or suction traps or found in sweep nets samples when air temperatures were above C or below C. Moth captures were optimum when prevailing temperature was between 21 and C. Typically moth flights began at about sunset and continued throughout the night with a peak at 2200 h, about an hour after sunset. Very few moths were trapped under showery and gusty conditions, when wind velocity was over 16 km h-1. More moths were captured in light traps during dark nights than on full moon nights. The pattern of captures indicated that females flew earlier than males.

    Citation 9.

    Accession Number

    BAKER R R [a]; MATHER J G.


    Title (English)

    Animal Behaviour. 30(2). 1982. 543-548.

    Many animals are now known to have a magnetic sense which they use when moving from 1 place to another. Among insects, this sense has only been studied in any detail in the honey bee. A role for a magnetic compass sense in cross-country migration has not so far been demonstrated for any insect. On clear nights the large yellow underwing moth, N. pronuba, orientates by both the moon and the stars. Radar studies showed moths to be well-oriented on overcast nights as well as clear nights. When large yellow underwings are placed in an orientation cage on overcast nights and the Earth's normal magnetic field is reversed, the orientation of the moth reverses also. This species makes use of the Earth's magnetic field in maintaining compass orientation on overcast nights. The preferred compass orientation to the Earth's magnetic field is the same as the compass direction that results from orientation to the moon and stars.

    Citation 10.

    Accession Number



    Title (English)

    Bulletin of Entomological Research. 71(2). 1981. 207-226.

    Hourly and nightly catches of H. armigera (Hb.) and H. punctiger Wllgr. at a site adjacent to 2000 ha of commercial cotton in the Namoi Valley of New South Wales [Australia], were analyzed in relation to various environmental factors and showed that wind speed, temperature, night-length and (H. armigera only) moonlight exerted a significant influence on trap-catch. For H. punctiger and H. armigera, respectively, these factors accounted for 80 and 60% of the deviance in hourly catches but only 70 and 40% of the variation in nightly catches. Wind speeds of > 1.7 m/s suppressed the catch of both species but had a greater effect on H. punctiger than H. armigera. Whereas with both species, the optimum temperature for trapping was .apprx. C, temperature had a greater influence on the catch of H. punctiger than of H. armigera. Bright moonlight reduced the catch of H. armiger by 49%, but no significant effect was detected for H. punctiger. With H. armigera, inconsistencies in the catches appeared associated with changes in population due to adult emergence, whereas for H. punctiger the cause seemed to be changes due to movement. The combined effects of wind speed, temperature, night-length and moonlight were used to adjust the nightly catches of each species according to the environmental conditions prevailing on a standard night. This was defined as a typical summer's night with temperatures decreasing from C at dusk to C at dawn and ideal catching conditions, i.e., no moon and wind speed never exceeding 1.7 m/s. The adjusted catches were taken as indices of moth abundance. H. armiger had 3 discrete periods of abundance, characterized by the presence of large numbers of young moths and spaced at intervals suggesting successive generations. A similar pattern was lacking in H. punctiger, which was abundant only during the 1st 1/2 of the season. The aerial application of insecticides to the cotton adjacent to the light-trap resulted in reductions in the populations of both species.

    Citation 11.

    Accession Number



    Title (English)

    Zeitschrift Fuer Angewandte Entomologie. 91(4). 1981. 403-411.

    A correlation was found between the summarized values of the horizontal component change of the geomagnetic field-strength measured at night, and the amount of light-trap catches of fall webworm moth (H. cunea Drury). The change of geomagnetic field strength significantly influences the catches, but it varies with the different moon phases. A new hypothesis was elaborated for the spatial orientation of insects. Results of the study are useful in plant protection forecasting.

    Citation 12.

    Accession Number



    Title (English)

    Zeitschrift Fuer Angewandte Entomologie. 88(4). 1979. 337-353.

    Material was collected for 14 yr at 20 sites in the Hungarian forestry and agricultural light-trap network system. The effect of polarization and intensity of the reflected moonlight on the abundance of 5 lepidopteran and 2 coleopteran species in the trap catches was examined. The material consisted of 55,003 specimens. The relative abundance of the insects in catches per day was calculated for each swarming time and all were arranged by species and flights according to moon phases, and the catches of the corresponding days of lunations were averaged. The mean relative abundances (MRA) vs. moon phase, characteristic for the species, were calculated. Then these daily MRAs of the 7 spp. [European cockchafer, Melolontha melolontha L., grape colaspis, Serica brunnea L., cutworms, Scotia segetum Schiff, Orthosia gotica L, O. cruda Den. et Schiff. winter moth, Operophtera brumata L., fall webworm moth, Hyphantria Drury] were average; these general MRAs served as a basis of further analysis. Moonlight effects both the extension of the collecting area and flight activity of the insects by the cyclic changes of light intensity and polarization rate. The number of insects caught is influenced by the lunar cycle.

    Citation 13.

    Accession Number



    Title (English)

    Animal Behaviour. 27(3). 1979. 786-800.

    A portable semi-automatic flight monitor is described that permits continuous recording of the orientation of flying but tethered moths under field and other conditions. In light winds the compass orientation of tethered large yellow underwing moths, N. pronuba, is independent of wind direction. On moonlit nights the moon's azimuth is used as an orientation cue. On starlit nights, in the absence of the moon, stellar orientation using stars about from the pole star is strongly implicated. There is no compensation for the shift of these celestial cues during the night. In a darkroom or when their eyes are painted over, N. pronuba are disorientated. A model of the mechanism of nocturnal moth migration is presented.

    Citation 14.

    Accession Number


    Title (English)

    Australian Journal of Zoology. 24(1). 1976. 65-73.

    Field observations on the flight activity of E. postvittana [an apple and pear pest] showed a diel and a lunar periodicity of flight. There was a single daily flight peak at 21 h (Australian Eastern Standard Time); further analysis clearly showed 2 peaks, 1 large, 2-3 h after sunset, and 1 small, 3-4 h after sunrise. Males were active longer than females at both flight periods. Peak activity occurred shortly after new moon, around full moon, and shortly before new moon. As flight activity is controlled by light intensity, it is argued that the flight 2-3 h after sunrise and the peak in nocturnal flight activity at full moon are behavioral adaptations towards wind-assisted dispersal.

    Quick summary based on a non-thorough read-through of the abstracts:

    Authors peak captures during:

    New moon: 4 articles

    (1 pheromone; 1 light trap; 1 artificial lights (noctural insects in general but Leptioptera in particular; one couldn't tell)

    Full moon: 1 article

    (2 species in the same genera though)

    Significant effect, direction not specified in abstract:: 4 articles

    (all light traps IIRC)

    Lack of effect reported: 1 article


    Other, discusses moon & moths but not capture rates: 3 articles

    Peak "activity" at *both* new and full moon: 1 article

    So it would appear that in general Shapiro's contention is supported.  Note that peppered moths are not included in any of the studies, and that it is apparent that different moth species do different things.

    It would be nice to know the direction of effect for the 4 studies where this is not clear...

    If anyone knows Tom Curtis they might let him know about this thread, he might be interested.


    Date: 2003/02/01 17:14:48, Link
    Author: niiicholas
    Link to the other peppered moth thread:;t=11

    ...contains my review of Hooper...

    Date: 2003/02/01 18:22:00, Link
    Author: niiicholas
    Link to thread discussing the moon phases and moth capture rates:;st=0

    Date: 2003/02/01 18:29:43, Link
    Author: niiicholas
    In the "another whole kind of motility" category:


    Molecular Microbiology
    Volume 47 Issue 3 Page 657  - February 2003
    Motility modes of Spiroplasma melliferum BC3: a helical, wall-less bacterium driven by a linear motor
    Rami Gilad1, Asher Porat2 and Shlomo Trachtenberg1*


    Spiroplasma are members of the Mollicutes (Mycoplasma, Acholeplasma and Spiroplasma) - the simplest, minimal, free-living and self-replicating forms of life. The mollicutes are unique among bacteria in completely lacking cell walls and flagella and in having an internal, contractile cytoskeleton, which also functions as a linear motor. Spiroplasma are helical, chemotactic and viscotactic active swimmers. The Spiroplasmal cytoskeleton is a flat ribbon composed of seven pairs of fibrils. The ribbon is attached to the inner side of the cell membrane along its innermost (shortest) helical line. The cell's geometry and dynamic helical parameters, and consequently motility, can be controlled by changing differentially and in a co-ordinated manner, the length of the fibrils. We identified several consistent modes of cell movements and motility originating, most likely, as a result of co-operative or local molecular switching of fibrils: (i) regular extension and contraction within the limits of helical symmetry (this mode also includes straightening, beyond what is allowed by helical symmetry, and reversible change of helical sense); (ii) spontaneous and random change of helical sense originating at random sites along the cell (these changes propagate along the cell in either direction and hand switching is completed within 0.08 second); (iii) forming a deformation on one of the helical turns and propagating it along the cell (these helical deformations may travel along the cell at a speed of up to 40 µm s1); (iv) random bending, flexing and twitching (equivalent to tumbling). In standard medium (viscosity = 1.147 centipoise) the cells run at 1.5 µm s1, have a Reynolds number of 3.5  106 and consume 30 ATP molecules s1. Running velocity, duration, persistence and efficiency increase with viscosity upon adding ficoll, dextran and methylcellulose to standard media. Relative force measurements using optical tweezers confirm these findings.

    If all Mycoplasma are derived parasites of eukaryotes (?) then presumably this motility system is of relatively late origin.

    Date: 2003/02/02 05:53:36, Link
    Author: niiicholas
    Put your favorite examples here!

    Discussed on Evolving Inventions:


    Before I attempt to answer your question, John, I would like to try and narrow down the exact, final, definitive definition of "inventive solution" in TRIZ-terms.  The best I can seem to find are terms like "non-routine" and "resolving a technical contradiction", which help a bit but are difficult to apply.

    Is there perhaps an authoritative quote you could post that would constitute the best-available definition?

    Perhaps (especially since you focused on morphological evolution in your reply) answering the following would help:

    Regarding morphology/development, would the following set of stages, if evolved through, constitute an "inventive" or "routine" solution:

    1) Start with segmented metazoan.

    2) Duplicate a segment (e.g. the corresponding Hox gene is serially duplicated).  Critter now has an extra segment somewhere in the middle (say, 5 instead of 4) and corresponding pair of legs, etc., that go with the segment.

    3) Repeat step 2 a number of times (e.g., selection for larger body size retains these duplications)

    4) Once there are a fair number of segments, mutation and selection modify one or several of the more forward pairs, e.g. to improve prey capture or food-chewing or substrate/mate clasping (large number of possibilities here, lots of arthropods have these kinds of specializations).

    Below is a slightly less abstract case (in arthropods, but dealing with the origin of a novel structure not from legs but from another structure).  Would we have a novel or routine kind of solution here?

    Proc Natl Acad Sci U S A 2002 Apr 16;99(8):5498-502

    [which is free online I think]

    Origin of a complex key innovation in an obligate insect-plant mutualism.

    Pellmyr O, Krenn HW.

    Evolutionary key innovations give organisms access to new ecological resources and cause rapid, sometimes spectacular adaptive radiation. The well known obligate pollination mutualism between yuccas and yucca moths is a major model system for studies of coevolution, and it relies on the key innovation in the moths of complex tentacles used for pollen collecting and active pollination. These structures lack apparent homology in other insects, making them a rare example of a novel limb. We performed anatomical and behavioral studies to determine their origin and found evidence of a remarkably simple mechanism. Morphological analyses of the tentacles and adjacent mouthparts in pollinators and closely related taxa showed that the tentacle appears abruptly in female pollinating yucca moths. Several morphological synapomorphies between the galeae, which constitute the characteristic lepidopteran proboscis, and the tentacle suggest that the tentacle evolved quickly through expression of the genetic template for the galea at an apical growth bud on the first segment of the maxillary palp. Behavioral data indicate that tentacle and proboscis movements are controlled by a shared hydraulic extension mechanism, thus no new mechanism was needed for tentacle function. Known developmental paths from other insects can explain the origin of this sex-specific key innovation in a few steps.

    Other relevant articles:


    J Exp Zool 2003 Feb 15;295B(1):1-11 Related Articles, Links  

    Hox genes as synchronized temporal regulators: Implications for morphological innovation.

    Crawford M.

    Department of Biological Sciences, University of Windsor, Windsor, Ontario, N9B 3P4, Canada.

    In vertebrates, clusters of Hox genes express in a nested and hierarchical fashion to endow the embryo's segments with discrete identities. Later in development, members of the same gene family are employed again to pattern the limb, intestinal, and reproductive systems. A careful analysis of the morphologies of Hox mutant mice suggests that the genes provide qualitatively different cues during the specification of segments than they do during the development of more recently derived structures. In addition to the regulatory differences noted by others, the activity of Hox genes during specification of the vertebrate metameres in some recent deletion experiments is inconsistent with a role for them as strictly spatial determinants. On the contrary, the phenotypes observed are suggestive of a role for them as elements of a generic time-keeping mechanism. By contrast, the specification of more recent evolutionary structures appears to be more spatial and gene-specific. These differences in role and effect may suggest some simple mechanisms by which the Hox clusters operate, and rules by which gene networks can be diverted to create new structures over the course of evolution. Specific predictions and experiments are proposed. J. Exp. Zool. (Mol. Dev. Evol.) 295B:1-11, 2003. Copyright 2003 Wiley-Liss, Inc.

    Curr Biol 2002 Oct 1;12(19):1711-6
    Diverse adaptations of an ancestral gill: a common evolutionary origin for wings, breathing organs, and spinnerets.

    Damen WG, Saridaki T, Averof M.

    Institute for Genetics, University of Cologne, Weyertal 121, D-50931, Koln, Germany.

    Changing conditions of life impose new requirements on the morphology and physiology of an organism. One of these changes is the evolutionary transition from aquatic to terrestrial life, leading to adaptations in locomotion, breathing, reproduction, and mechanisms for food capture. We have shown previously that insects' wings most likely originated from one of the gills of ancestral aquatic arthropods during their transition to life on land. Here we investigate the fate of these ancestral gills during the evolution of another major arthropod group, the chelicerates. We examine the expression of two developmental genes, pdm/nubbin and apterous, that participate in the specification of insects' wings and are expressed in particular crustacean epipods/gills. In the horseshoe crab, a primitively aquatic chelicerate, pdm/nubbin is specifically expressed in opisthosomal appendages that give rise to respiratory organs called book gills. In spiders (terrestrial chelicerates), pdm/nubbin and apterous are expressed in successive segmental primordia that give rise to book lungs, lateral tubular tracheae, and spinnerets, novel structures that are used by spiders to breathe on land and to spin their webs. Combined with morphological and palaeontological evidence, these observations suggest that fundamentally different new organs (wings, air-breathing organs, and spinnerets) evolved from the same ancestral structure (gills) in parallel instances of terrestrialization.

    A detailed review of the origin of feathers:


    Q Rev Biol 2002 Sep;77(3):261-95

    The evolutionary origin and diversification of feathers.

    Prum RO, Brush AH.

    Department of Ecology and Evolutionary Biology, and Natural History Museum, University of Kansas, Lawrence, Kansas 66045, USA.

    Progress on the evolutionary origin and diversification of feathers has been hampered by conceptual problems and by the lack of plesiomorphic feather fossils. Recently, both of these limitations have been overcome by the proposal of the developmental theory of the origin of feathers, and the discovery of primitive feather fossils on nonavian theropod dinosaurs. The conceptual problems of previous theories of the origin of feathers are reviewed, and the alternative developmental theory is presented and discussed. The developmental theory proposes that feathers evolved through a series of evolutionary novelties in developmental mechanisms of the follicle and feather germ. The discovery of primitive and derived fossil feathers on a diversity of coelurosaurian theropod dinosaurs documents that feathers evolved and diversified in nonavian theropods before the origin of birds and before the origin of flight. The morphologies of these primitive feathers are congruent with the predictions of the developmental theory. Alternatives to the theropod origin of feathers are critique and rejected. Hypotheses for the initial function of feathers are reviewed. The aerodynamic theory of feather origins is falsified, but many other functions remain developmentally and phylogenetically plausible. Whatever their function, feathers evolved by selection for a follicle that would grow an emergent tubular appendage. Feathers are inherently tubular structures. The homology of feathers and scales is weakly supported. Feathers are composed of a suite of evolutionary novelties that evolved by the duplication, hierarchical organization, interaction, dissociation, and differentiation of morphological modules. The unique capacity for modular subdivision of the tubular feather follicle and germ has fostered the evolution of numerous innovations that characterize feathers. The evolution of feather keratin and the molecular basis of feather development are also discussed.

    Body plans:


    Evol Dev 2002 Nov-Dec;4(6):459-99

    Hox genes and the evolution of the arthropod body plan.

    Hughes CL, Kaufman TC.

    Howard Hughes Medical Institute, Department of Biology, Indiana University, Bloomington, IN 47405, USA.

    In recent years researchers have analyzed the expression patterns of the Hox genes in a multitude of arthropod species, with the hope of understanding the mechanisms at work in the evolution of the arthropod body plan. Now, with Hox expression data representing all four major groups of arthropods (chelicerates, myriapods, crustaceans, and insects), it seems appropriate to summarize the results and take stock of what has been learned. In this review we summarize the expression and functional data regarding the 10 arthropod Hox genes: labial proboscipedia, Hox3/zen, Deformed, Sex combs reduced, fushi tarazu, Antennapedia, Ultrabithorax, abdominal-A, and Abdominal-B. In addition, we discuss mechanisms of developmental evolutionary change thought to be important for the emergence of novel morphological features within the arthropods.


    Philos Trans R Soc Lond B Biol Sci 1995 Sep 29;349(1329):313-9

    Hox genes and the evolution of diverse body plans.

    Akam M.

    Wellcome/CRC Institute and Department of Genetics, Cambridge, U.K.

    Homeobox genes encode transcription factors that carry out diverse roles during development. They are widely distributed among eukaryotes, but appear to have undergone an extensive radiation in the earliest metazoa, to generate a range of homeobox subclasses now shared between diverse metazoan phyla. The Hox genes comprise one of these subfamilies, defined as much by conserved chromosomal organization and expression as by sequence characteristics. These Hox genes act as markers of position along the antero-posterior axis of the body in nematodes, arthropods, chordates, and by implication, most other triploblastic phyla. In the arthropods this role is visualized most clearly in the control of segment identity. Exactly how Hox genes control the structure of segments is not yet understood, but their differential deployment between segments provides a model for the basis of segment diversity. Within the arthropods, distantly related taxonomic groups with very different body plans (insects, crustaceans) may share the same set of Hox genes. The expression of these Hox genes provides a new character to define the homology of different body regions. Comparisons of Hox gene deployment between insects and a branchiopod crustacean suggest a novel model for the derivation of the insect body plan.


    Annu Rev Cell Dev Biol 2002;18:53-80
    Gene co-option in physiological and morphological evolution.

    True JR, Carroll SB.

    Department of Ecology and Evolution, State University of New York at Stony Brook, Stony Brook, New York 11794-5245, e-mail:

    Co-option occurs when natural selection finds new uses for existing traits, including genes, organs, and other body structures. Genes can be co-opted to generate developmental and physiological novelties by changing their patterns of regulation, by changing the functions of the proteins they encode, or both. This often involves gene duplication followed by specialization of the resulting paralogous genes into particular functions. A major role for gene co-option in the evolution of development has long been assumed, and many recent comparative developmental and genomic studies have lent support to this idea. Although there is relatively less known about the molecular basis of co-option events involving developmental pathways, much can be drawn from well-studied examples of the co-option of structural proteins. Here, we summarize several case studies of both structural gene and developmental genetic circuit co-option and discuss how co-option may underlie major episodes of adaptive change in multicellular organisms. We also examine the phenomenon of intraspecific variability in gene expression patterns, which we propose to be one form of material for the co-option process. We integrate this information with recent models of gene family evolution to provide a framework for understanding the origin of co-optive evolution and the mechanisms by which natural selection promotes evolutionary novelty by inventing new uses for the genetic toolkit.

    In fact, right now we are living through the merging of developmental biology with the modern synthesis, e.g.:


    Genetica 2001;112-113:45-58

    Toward a new synthesis: population genetics and evolutionary developmental biology.

    Johnson NA, Porter AH.

    Department of Entomology and Program in Organismic and Evolutionary Biology, University of Massachusetts, Amherst 01003, USA.

    Despite the recent synthesis of developmental genetics and evolutionary biology, current theories of adaptation are still strictly phenomenological and do not yet consider the implications of how phenotypes are constructed from genotypes. Given the ubiquity of regulatory genetic pathways in developmental processes, we contend that study of the population genetics of these pathways should become a major research program. We discuss the role divergence in regulatory developmental genetic pathways may play in speciation, focusing on our theoretical and computational investigations. We also discuss the population genetics of molecular co-option, arguing that mutations of large effect are not needed for co-option. We offer a prospectus for future research, arguing for a new synthesis of the population genetics of development.

    Date: 2003/02/02 06:43:20, Link
    Author: niiicholas
    Originally posted over at ARN, perhaps this could serve as starting material for an overall "progressive case for the origins of complexity" FAQ, i.e. that starts with the small processes and then builds them up.

    Feel free to add relevant links, posts, etc., especially to threads that better document specific points, e.g. adaptive radiation, transitional fossils, IC, etc.

    Original thread:


    Berthajane, Vivid, et al.,

    I've often thought that there should be a FAQ somewhere specifically on the evolution of complexity, since that is what is the sticking point for a lot of people.

    I don't really have the time to write a FAQ or even do more than hit-and-run post, but perhaps I can communicate how I think it might go.  Perhaps you can comment if you think all of this is old hat and would be pointless and unconvincing to you in a FAQ or if you think it would be worth reading.

    OK, here goes.

    The case for RM & NS producing complexity is cumulative.  You start from small-scale processes and then work up.

    1) "Microevolution" -- local adaptation: drug resistance, peppered moths, pesticide resistance, guppy size change, etc.  Presumably everyone accepts this.level of evolution.

    It is worth considering, for a moment, some of the implications of even this minor level of evolution:

    a) Microevolutionary forces can, in short order, take a single mutation in a single individual and spread it to fixation, so that it exists in every member of a population of millions.  All of the millions of bad mutations don't matter a bit, they rarely made it further than a generation or two.  That one-in-a-million lucky mutation is the one that natural selection picks (even if it is lost by chance the first few times, sooner or later it or an equivalent mutation will spread far enough that its success becomes guarenteed).

    Also, note that even at this minor level we have a fair bit of design-mimicking occurring.  Peppered moths, for example, don't change color in any random direction, they change color to match the color of tree bark (please refer to the Wells FAQ before critiquing the peppered moth example).  Modern militaries only got around to producing decent camoflague in the mid-1900's.

    Now think about all the other amazing instances of camoflague in the animal (and plant!;) world.

    A few examples:

    A frog in Madagascar:

    Those were fairly modest examples.

    Look for the plants in this picture, they're in plain view:

    The well-named Lithops:

    And here, which one is the ant and which one is the ant-mimicking spider?

    (hint: count legs)

    Here is a fairly decent webpage on mimicry (Kimballs pages are about the best online pseudo-bio text I've seen, decent pictures etc)

    Camoflague and prey-mimicry combined in this one:

    (Click here for an II thread discussing anglerfish evolution BTW)

    Anyhow, I went on a tangent with camoflague and mimicry.  My point: I submit that all of these cases are rather easily explained by "microevolution" of the peppered moth type (and there are many other studies of natural selection for camoflague BTW) -- indeed, many of these impressive designs are specific to species in genera or families with completely different coloration...e.g. anglerfish that live so deep that no light reaches them don't bother with camoflague.

    If this kind of thing is conceeded, then we've already allowed that microevolution has a rather substantial ability for "creativity" and acheiving very specific "designs".

    (b) Returning to the population-genetics-level processes described at the top of (a)...Now think about them happening continually (many different mutations will be under the influence of selection in any given species at any given point in time) for millions of years.  Here we add in speciation, both due to geographical separation (allopatric) and niche partitioning (sympatric).  Many species going in many different directions.  Many recent adaptive radiations of species, where very-closely related species are morphologically very different and "designed" for very different niches, could be cited.  Here are a few:

    Kimball's speciation page

    Darwin's Finches (Darwin did not even realize they were all finches for years after he collected them; they fill the niches fufilled by various birds on continents -- seed eaters, insect eaters, woodpecker, warbler, etc.):

    (this, BTW, is the most important point about Darwin's Finches, although Peter & Rosemary Grant's studies of recent natural selection are also interesting)

    The Hawaiian honeycreepers are even better examples.  These are all closely related (well, were, some were driven extinct when Europeans and their pets invaded):

    And be sure to check out Art's post on the Hawaiian Silversword Alliance (sounds like an army in an online wargame, I know...):

    Some of these Silverswords are trees, some are little herbs, and yet they are all closely related and many are even interfertile

    © If it is conceeded that RM & NS can account for the rather astounding diversity of the above groups, then we've agreed that natural evolutionary processes can account for family-level diversity.  Now, if the same processes produced orders (e.g. the various mammal groups) and classes (e.g., reptiles, amphibians, etc.), we should see some fossil evidence of this, and we do.  In the case of vertebrates, rather a lot, and a bunch of new ones in the last 10 years.  Just to review what we've got intermediates or close-offshoots for:

    walking sirienians (manatees etc., forget what they're descended from)
    ...and of course, humans.

    Why any of these should exist, except on the hypothesis that all modern organisms originated by modification of previous organisms by a process limited to fairly gradual changes (like RM&NS) is a useful question to consider.

    2) Turning from morphology to molecules: while the lower levels of evolution and adaptation might be explained basically by selection of point mutations, at some point new genetic information has to be created.  There is a mechanism for this, namely the combination of gene duplication (and variations on this, e.g. deletions, rearrangments, etc.) with the mutation-and-selection processes discussed back in 1a.

    Even unmodified gene duplications are often selected; e.g., some DDT resistant mosquitos have 100+ copies of a DDT-resistance gene (see Weiner, Beak of the Finch).  Plus we have genome duplications, duplication of whole segments of chromosomes, etc.  These kinds of processes give evolution a lot of material to play with, and there are numerous documented and published cases of observed or recent origins of novel genes by various combinations of the above processes.

    Lots of them are described in this origin of information thread

    And of course the same kinds of adaptive radiation patterns found in morphology can be found in molecules, and here we even have hard-and-fast evidence that directional natural selection was operating millions of years back in the unobservable past, in the form of substitution biases, e.g.:


    Gene 2000 Dec 30;261(1):43-52
    Adaptive evolution of animal toxin multigene families.

    Kordis D, Gubensek F.

    Department of Biochemistry and Molecular Biology, Jozef Stefan Institute, Jamova 39, 1000, Ljubljana, Slovenia.

    Animal toxins comprise a diverse array of proteins that have a variety of biochemical and pharmacological functions. A large number of animal toxins are encoded by multigene families. From studies of several toxin multigene families at the gene level the picture is emerging that most have been functionally diversified by gene duplication and adaptive evolution. The number of pharmacological activities in most toxin multigene families results from their adaptive evolution. The molecular evolution of animal toxins has been analysed in some multigene families, at both the intraspecies and interspecies levels. In most toxin multigene families, the rate of non-synonymous to synonymous substitutions (dN/dS) is higher than one. Thus natural selection has acted to diversify coding sequences and consequently the toxin functions. The selection pressure for the rapid adaptive evolution of animal toxins is the need for quick immobilization of the prey in classical predator and prey interactions. Currently available evidence for adaptive evolution in animal toxin multigene families will be considered in this review.
    And here is the tip of the iceberg (Drosophila is always the tip of the iceberg) for the molecules giving us an even better handle on just how important a force directional natural selection is on genomes:


    Adaptive protein evolution in Drosophila.

    Nature 2002 Feb 28;415(6875):1022-4
    Smith NG, Eyre-Walker A.

    Centre for the Study of Evolution and School of Biological Sciences, University of Sussex, Brighton BN1 9QG, UK.

    For over 30 years a central question in molecular evolution has been whether natural selection plays a substantial role in evolution at the DNA sequence level. Evidence has accumulated over the last decade that adaptive evolution does occur at the protein level, but it has remained unclear how prevalent adaptive evolution is. Here we present a simple method by which the number of adaptive substitutions can be estimated and apply it to data from Drosophila simulans and D. yakuba. We estimate that 45% of all amino-acid substitutions have been fixed by natural selection, and that on average one adaptive substitution occurs every 45 years in these species.
    If this is not impressive enough, think about what the population of a species of fruit fly must be (billions? trillions?).

    As for the origin of new morphology, the combination of the origins-of-genes processes described above, with recent knowledge of the genes patterning development, has made this much clearer.  E.g.:


    Philos Trans R Soc Lond B Biol Sci 1995 Sep 29;349(1329):313-9

    Hox genes and the evolution of diverse body plans.

    Akam M.

    Wellcome/CRC Institute and Department of Genetics, Cambridge, U.K.

    Homeobox genes encode transcription factors that carry out diverse roles during development. They are widely distributed among eukaryotes, but appear to have undergone an extensive radiation in the earliest metazoa, to generate a range of homeobox subclasses now shared between diverse metazoan phyla. The Hox genes comprise one of these subfamilies, defined as much by conserved chromosomal organization and expression as by sequence characteristics. These Hox genes act as markers of position along the antero-posterior axis of the body in nematodes, arthropods, chordates, and by implication, most other triploblastic phyla. In the arthropods this role is visualized most clearly in the control of segment identity. Exactly how Hox genes control the structure of segments is not yet understood, but their differential deployment between segments provides a model for the basis of segment diversity. Within the arthropods, distantly related taxonomic groups with very different body plans (insects, crustaceans) may share the same set of Hox genes. The expression of these Hox genes provides a new character to define the homology of different body regions. Comparisons of Hox gene deployment between insects and a branchiopod crustacean suggest a novel model for the derivation of the insect body plan.

    Annu Rev Cell Dev Biol 2002;18:53-80
    Gene co-option in physiological and morphological evolution.

    True JR, Carroll SB.

    Department of Ecology and Evolution, State University of New York at Stony Brook, Stony Brook, New York 11794-5245, e-mail:

    Co-option occurs when natural selection finds new uses for existing traits, including genes, organs, and other body structures. Genes can be co-opted to generate developmental and physiological novelties by changing their patterns of regulation, by changing the functions of the proteins they encode, or both. This often involves gene duplication followed by specialization of the resulting paralogous genes into particular functions. A major role for gene co-option in the evolution of development has long been assumed, and many recent comparative developmental and genomic studies have lent support to this idea. Although there is relatively less known about the molecular basis of co-option events involving developmental pathways, much can be drawn from well-studied examples of the co-option of structural proteins. Here, we summarize several case studies of both structural gene and developmental genetic circuit co-option and discuss how co-option may underlie major episodes of adaptive change in multicellular organisms. We also examine the phenomenon of intraspecific variability in gene expression patterns, which we propose to be one form of material for the co-option process. We integrate this information with recent models of gene family evolution to provide a framework for understanding the origin of co-optive evolution and the mechanisms by which natural selection promotes evolutionary novelty by inventing new uses for the genetic toolkit.
    In fact, right now we are living through the merging of developmental biology with the modern synthesis, e.g.:


    Genetica 2001;112-113:45-58

    Toward a new synthesis: population genetics and evolutionary developmental biology.

    Johnson NA, Porter AH.

    Department of Entomology and Program in Organismic and Evolutionary Biology, University of Massachusetts, Amherst 01003, USA.

    Despite the recent synthesis of developmental genetics and evolutionary biology, current theories of adaptation are still strictly phenomenological and do not yet consider the implications of how phenotypes are constructed from genotypes. Given the ubiquity of regulatory genetic pathways in developmental processes, we contend that study of the population genetics of these pathways should become a major research program. We discuss the role divergence in regulatory developmental genetic pathways may play in speciation, focusing on our theoretical and computational investigations. We also discuss the population genetics of molecular co-option, arguing that mutations of large effect are not needed for co-option. We offer a prospectus for future research, arguing for a new synthesis of the population genetics of development.
    I have put the above articles and some others over in this thread.

    3) OK, so at this point we perhaps have reached the amount of evolution that Mike Behe accepts or at least doesn't argue about, that is: a heck of a lot.  I tend to be of the opinion that if natural evolutionary processes can produce new genes, novel morphological traits, and even body plans, we ought to expect that it's powerful enough to do just about anything that that we see in biology today.  But, some will raise IC at this point, arguing that, sure, evolution could have produced mammals, humans, wings, whales, innumerable new genes and adaptations, but that a designer still intervened to produce a certain class of system (*really* complex or rather simple-but-irreducible, depending on who you talk to...) that Behe calls IC.

    This has been discussed to death in numerous places, but suffice it to say that for the most complicated of Behe's IC systems, namely the vertebrate immune system, Behe's claims about lack of evidence for an evolutionary origin, and lack of scientific publications on the topic of the origin of the immune system, he has been decisively refuted.


    Read this: Evolving Immunity by Matt Inlay

    Then read: This ISCID thread where IDists were hapless in their attempt to defend Behe

    If natural processes can produce even ridiculously complex IC like this, then there is no particular reason to invoke ID to explain IC.

    4) Finally, once all of the above is accepted or considered probable, we are in a position to consider the origin of eukaryotes and prokaryotes.  In my opinion, if RM&NS processes can create something like the metazoan phyla and the immune system, there's no reason to suspect that anything else was responsible for earlier events.

    We are however getting into events that occurred on a microscopic scale 1+ billion years ago, so details are necessarily much more speculative.  All I can recommend is some of the better reading I've found on these topics:

    Maynard Smith and Szathmary, Major Transitions in Evolution, 1995.  Here is a brief review by someone.

    The short version of the above is their 1998 Origins of Life but it is pretty much pointless compared to the bigger book.

    The other good source is pretty much anything written by Cavalier-Smith (type his name in here), e.g. this series of articles:


    J Mol Evol 2001 Oct-Nov;53(4-5):555-95
    Obcells as proto-organisms: membrane heredity, lithophosphorylation, and the origins of the genetic code, the first cells, and photosynthesis.

    Cavalier-Smith T.

    Department of Zoology, University of Oxford, South Parks Road, Oxford, OX1 3PS, United Kingdom.

    I attempt to sketch a unified picture of the origin of living organisms in their genetic, bioenergetic, and structural aspects. Only selection at a higher level than for individual selfish genes could power the cooperative macromolecular coevolution required for evolving the genetic code. The protein synthesis machinery is too complex to have evolved before membranes. Therefore a symbiosis of membranes, replicators, and catalysts probably mediated the origin of the code and the transition from a nucleic acid world of independent molecular replicators to a nucleic acid/protein/lipid world of reproducing organisms. Membranes initially functioned as supramolecular structures to which different replicators attached and were selected as a higher-level reproductive unit: the proto-organism. I discuss the roles of stereochemistry, gene divergence, codon capture, and selection in the code's origin. I argue that proteins were primarily structural not enzymatic and that the first biological membranes consisted of amphipathic peptidyl-tRNAs and prebiotic mixed lipids. The peptidyl-tRNAs functioned as genetically-specified lipid analogues with hydrophobic tails (ancestral signal peptides) and hydrophilic polynucleotide heads. Protoribosomes arose from two cooperating RNAs: peptidyl transferase (large subunit) and mRNA-binder (small subunit). Early proteins had a second key role: coupling energy flow to the phosphorylation of gene and peptide precursors, probably by lithophosphorylation by membrane-anchored kinases scavenging geothermal polyphosphate stocks. These key evolutionary steps probably occurred on the outer surface of an 'inside out-cell' or obcell, which evolved an unambiguous hydrophobic code with four prebiotic amino acids and proline, and initiation by isoleucine anticodon CAU; early proteins and nucleozymes were all membrane-attached. To improve replication, translation, and lithophosphorylation, hydrophilic substrate-binding and catalytic domains were later added to signal peptides, yielding a ten-acid doublet code. A primitive proto-ecology of molecular scavenging, parasitism, and predation evolved among obcells. I propose a new theory for the origin of the first cell: fusion of two cup-shaped obcells, or hemicells, to make a protocell with double envelope, internal genome and ribosomes, protocytosol, and periplasm. Only then did water-soluble enzymes, amino acid biosynthesis, and intermediary metabolism evolve in a concentrated autocatalytic internal cytosolic soup, causing 12 new amino acid assignments, termination, and rapid freezing of the 22-acid code. Anticodons were recruited sequentially: GNN, CNN, INN, and *UNN. CO2 fixation, photoreduction, and lipid synthesis probably evolved in the protocell before photophosphorylation. Signal recognition particles, chaperones, compartmented proteases, and peptidoglycan arose prior to the last common ancestor of life, a complex autotrophic, anaerobic green bacterium.

    Int J Syst Evol Microbiol 2002 Jan;52(Pt 1):7-76
    The neomuran origin of archaebacteria, the negibacterial root of the universal tree and bacterial megaclassification.

    Cavalier-Smith T.

    Department of Zoology, University of Oxford, UK.

    Prokaryotes constitute a single kingdom, Bacteria, here divided into two new subkingdoms: Negibacteria, with a cell envelope of two distinct genetic membranes, and Unibacteria, comprising the new phyla Archaebacteria and Posibacteria, with only one. Other new bacterial taxa are established in a revised higher-level classification that recognizes only eight phyla and 29 classes. Morphological, palaeontological and molecular data are integrated into a unified picture of large-scale bacterial cell evolution despite occasional lateral gene transfers. Archaebacteria and eukaryotes comprise the clade neomura, with many common characters, notably obligately co-translational secretion of N-linked glycoproteins, signal recognition particle with 7S RNA and translation-arrest domain, protein-spliced tRNA introns, eight-subunit chaperonin, prefoldin, core histones, small nucleolar ribonucleoproteins (snoRNPs), exosomes and similar replication, repair, transcription and translation machinery. Eubacteria (posibacteria and negibacteria) are paraphyletic, neomura having arisen from Posibacteria within the new subphylum Actinobacteria (possibly from the new class Arabobacteria, from which eukaryotic cholesterol biosynthesis probably came). Replacement of eubacterial peptidoglycan by glycoproteins and adaptation to thermophily are the keys to neomuran origins. All 19 common neomuran character suites probably arose essentially simultaneously during the radical modification of an actinobacterium. At least 11 were arguably adaptations to thermophily. Most unique archaebacterial characters (prenyl ether lipids; flagellar shaft of glycoprotein, not flagellin; DNA-binding protein lob; specially modified tRNA; absence of Hsp90) were subsequent secondary adaptations to hyperthermophily and/or hyperacidity. The insertional origin of protein-spliced tRNA introns and an insertion in proton-pumping ATPase also support the origin of neomura from eubacteria. Molecular co-evolution between histones and DNA-handling proteins, and in novel protein initiation and secretion machineries, caused quantum evolutionary shifts in their properties in stem neomura. Proteasomes probably arose in the immediate common ancestor of neomura and Actinobacteria. Major gene losses (e.g. peptidoglycan synthesis, hsp90, secA) and genomic reduction were central to the origin of archaebacteria. Ancestral archaebacteria were probably heterotrophic, anaerobic, sulphur-dependent hyperthermoacidophiles; methanogenesis and halophily are secondarily derived. Multiple lateral gene transfers from eubacteria helped secondary archaebacterial adaptations to mesophily and genome re-expansion. The origin from a drastically altered actinobacterium of neomura, and the immediately subsequent simultaneous origins of archaebacteria and eukaryotes, are the most extreme and important cases of quantum evolution since cells began. All three strikingly exemplify De Beer's principle of mosaic evolution: the fact that, during major evolutionary transformations, some organismal characters are highly innovative and change remarkably swiftly, whereas others are largely static, remaining conservatively ancestral in nature. This phenotypic mosaicism creates character distributions among taxa that are puzzling to those mistakenly expecting uniform evolutionary rates among characters and lineages. The mixture of novel (neomuran or archaebacterial) and ancestral eubacteria-like characters in archaebacteria primarily reflects such vertical mosaic evolution, not chimaeric evolution by lateral gene transfer. No symbiogenesis occurred. Quantum evolution of the basic neomuran characters, and between sister paralogues in gene duplication trees, makes many sequence trees exaggerate greatly the apparent age of archaebacteria. Fossil evidence is compelling for the extreme antiquity of eubacteria [over 3500 million years (My)] but, like their eukaryote sisters, archaebacteria probably arose only 850 My ago. Negibacteria are the most ancient, radiating rapidly into six phyla. Evidence from molecular sequences, ultrastructure, evolution of photosynthesis, envelope structure and chemistry and motility mechanisms fits the view that the cenancestral cell was a photosynthetic negibacterium, specifically an anaerobic green non-sulphur bacterium, and that the universal tree is rooted at the divergence between sulphur and non-sulphur green bacteria. The negibacterial outer membrane was lost once only in the history of life, when Posibacteria arose about 2800 My ago after their ancestors diverged from Cyanobacteria.

    Int J Syst Evol Microbiol 2002 Mar;52(Pt 2):297-354
    The phagotrophic origin of eukaryotes and phylogenetic classification of Protozoa.

    Cavalier-Smith T.

    Department of Zoology, University of Oxford, UK.

    Eukaryotes and archaebacteria form the clade neomura and are sisters, as shown decisively by genes fragmented only in archaebacteria and by many sequence trees. This sisterhood refutes all theories that eukaryotes originated by merging an archaebacterium and an alpha-proteobacterium, which also fail to account for numerous features shared specifically by eukaryotes and actinobacteria. I revise the phagotrophy theory of eukaryote origins by arguing that the essentially autogenous origins of most eukaryotic cell properties (phagotrophy, endomembrane system including peroxisomes, cytoskeleton, nucleus, mitosis and sex) partially overlapped and were synergistic with the symbiogenetic origin of mitochondria from an alpha-proteobacterium. These radical innovations occurred in a derivative of the neomuran common ancestor, which itself had evolved immediately prior to the divergence of eukaryotes and archaebacteria by drastic alterations to its eubacterial ancestor, an actinobacterial posibacterium able to make sterols, by replacing murein peptidoglycan by N-linked glycoproteins and a multitude of other shared neomuran novelties. The conversion of the rigid neomuran wall into a flexible surface coat and the associated origin of phagotrophy were instrumental in the evolution of the endomembrane system, cytoskeleton, nuclear organization and division and sexual life-cycles. Cilia evolved not by symbiogenesis but by autogenous specialization of the cytoskeleton. I argue that the ancestral eukaryote was uniciliate with a single centriole (unikont) and a simple centrosomal cone of microtubules, as in the aerobic amoebozoan zooflagellate Phalansterium. I infer the root of the eukaryote tree at the divergence between opisthokonts (animals, Choanozoa, fungi) with a single posterior cilium and all other eukaryotes, designated 'anterokonts' because of the ancestral presence of an anterior cilium. Anterokonts comprise the Amoebozoa, which may be ancestrally unikont, and a vast ancestrally biciliate clade, named 'bikonts'. The apparently conflicting rRNA and protein trees can be reconciled with each other and this ultrastructural interpretation if long-branch distortions, some mechanistically explicable, are allowed for. Bikonts comprise two groups: corticoflagellates, with a younger anterior cilium, no centrosomal cone and ancestrally a semi-rigid cell cortex with a microtubular band on either side of the posterior mature centriole; and Rhizaria [a new infrakingdom comprising Cercozoa (now including Ascetosporea classis nov.), Retaria phylum nov., Heliozoa and Apusozoa phylum nov.], having a centrosomal cone or radiating microtubules and two microtubular roots and a soft surface, frequently with reticulopodia. Corticoflagellates comprise photokaryotes (Plantae and chromalveolates, both ancestrally with cortical alveoli) and Excavata (a new protozoan infrakingdom comprising Loukozoa, Discicristata and Archezoa, ancestrally with three microtubular roots). All basal eukaryotic radiations were of mitochondrial aerobes; hydrogenosomes evolved polyphyletically from mitochondria long afterwards, the persistence of their double envelope long after their genomes disappeared being a striking instance of membrane heredity. I discuss the relationship between the 13 protozoan phyla recognized here and revise higher protozoan classification by updating as subkingdoms Lankester's 1878 division of Protozoa into Corticata (Excavata, Alveolata; with prominent cortical microtubules and ancestrally localized cytostome--the Parabasalia probably secondarily internalized the cytoskeleton) and Gymnomyxa [infrakingdoms Sarcomastigota (Choanozoa, Amoebozoa) and Rhizaria; both ancestrally with a non-cortical cytoskeleton of radiating singlet microtubules and a relatively soft cell surface with diffused feeding]. As the eukaryote root almost certainly lies within Gymnomyxa, probably among the Sarcomastigota, Corticata are derived. Following the single symbiogenetic origin of chloroplasts in a corticoflagellate host with cortical alveoli, this ancestral plant radiated rapidly into glaucophytes, green plants and red algae. Secondary symbiogeneses subsequently transferred plastids laterally into different hosts, making yet more complex cell chimaeras--probably only thrice: from a red alga to the corticoflagellate ancestor of chromalveolates (Chromista plus Alveolata), from green algae to a secondarily uniciliate cercozoan to form chlorarachneans and independently to a biciliate excavate to yield photosynthetic euglenoids. Tertiary symbiogenesis involving eukaryotic algal symbionts replaced peridinin-containing plastids in two or three dinoflagellate lineages, but yielded no major novel groups. [...abstract too long... (!!!;)]

    Heredity 2002 Feb;88(2):125-41
    Origins of the machinery of recombination and sex.

    Cavalier-Smith T.

    Department of Zoology, University of Oxford, South Parks Road, Oxford, OX1 3PS, UK.

    Mutation plays the primary role in evolution that Weismann mistakenly attributed to sex. Homologous recombination, as in sex, is important for population genetics--shuffling of minor variants, but relatively insignificant for large-scale evolution. Major evolutionary innovations depend much more on illegitimate recombination, which makes novel genes by gene duplication and by gene chimaerisation--essentially mutational forces. The machinery of recombination and sex evolved in two distinct bouts of quantum evolution separated by nearly 3 Gy of stasis; I discuss their nature and causes. The dominant selective force in the evolution of recombination and sex has been selection for replicational fidelity and viability; without the recombination machinery, accurate reproduction, stasis, resistance to radical deleterious evolutionary change and preservation of evolutionary innovations would be impossible. Recombination proteins betray in their phylogeny and domain structure a key role for gene duplication and chimaerisation in their own origin. They arose about 3.8 Gy ago to enable faithful replication and segregation of the first circular DNA genomes in precellular ancestors of Gram-negative eubacteria. Then they were recruited and modified by selfish genetic parasites (viruses; transposons) to help them spread from host to host. Bacteria differ fundamentally from eukaryotes in that gene transfer between cells, whether incidental to their absorptive feeding on DNA and virus infection or directly by plasmids, involves only genomic fragments. This was radically changed by the neomuran revolution about 850 million years ago when a posibacterium evolved into the thermophilic cenancestor of eukaryotes and archaebacteria (jointly called neomurans), radically modifying or substituting its DNA-handling enzymes (those responsible for transcription as well as for replication, repair and recombination) as a coadaptive consequence of the origin of core histones to stabilise its chromosome. Substitution of glycoprotein for peptidoglycan walls in the neomuran ancestor and the evolution of an endoskeleton and endomembrane system in eukaryotes alone required the origin of nuclei, mitosis and novel cell cycle controls and enabled them to evolve cell fusion and thereby the combination of whole genomes from different cells. Meiosis evolved because of resulting selection for periodic ploidy reduction, with incidental consequences for intrapopulation genetic exchange. Little modification was needed to recombination enzymes or to the ancient bacterial catalysts of homology search by spontaneous base pairing to mediate chromosome pairing. The key innovation was the origin of meiotic cohesins delaying centromere splitting to allow two successive divisions before reversion to vegetative growth and replication, necessarily yielding two-step meiosis. Also significant was the evolution of synaptonemal complexes to stabilise bivalents and of monopolins to orient sister centromeres to one spindle pole. The primary significance of sex was not to promote evolutionary change but to limit it by facilitating ploidy cycles to balance the conflicting selective forces acting on rapidly growing phagotrophic protozoa and starved dormant cysts subject to radiation and other damage.
    Even if one disagrees with TCS on certain issues (his late-dating of the origin of eukaryotes and archaeabacteria is certainly a minority position), this gives one some vague idea (read the 200+ pages of articles to get a somewhat improved but still incomplete idea) of the kind of background knowledge level one must be at to even begin to discuss the Really Long Ago issues of evolution in an informed fashion.

    Hope that helps,

    Reposting this to AE...

    Date: 2003/02/06 03:00:49, Link
    Author: niiicholas
    Hey Micah,

    I think it all depends on what your (group) goals really are.  If one of the goals is to promote ID/provide a forum for IDists to publish, or to critique modern evolutionary theory, then just say it up front and go ahead and do it, it's your journal.

    If on the other hand you want something with broader appeal, you will have to find some method of editing/review that excludes things like "Yet Another Article Based on a Misunderstanding of the 2nd Law of Thermodynamics" or "Re-publication of Article by IDist X" or "Miscellaneous Antievolutionary Ramblings".  Perhaps some requirement that contributions represent something *novel*, that "move the ball foward" (or backward, even), whatever the ball may be, would be a position-neutral way of doing this.

    E.g., "A Hypothetical Explicit Model for the Main Periods of Intervention in the Evolution of Life by an Intelligent Designer".  IMO the most important thing is not going around trying to prove evolution wrong, it is for ID to come up with its own explicit hypotheses and proposing/conducting tests of them.  Explicit hypotheses "advance the ball" of the discussion even if they are wrong.

    Date: 2003/02/07 01:12:06, Link
    Author: niiicholas
    Although the basics of how the eubacterial flagellum works are reasonably well-known

    (see Howard Berg's article in Physics Today, Motile Behavior of Bacteria for a good introduction) remaining mystery surrounds the exact mechanism by which the flow of H+ powers rotary motion.  


    Here is Berg's figure of the flagellum:

    H+, aka protons, hydrogen ions, or "acid", flow from the inter-membrane space (where ATPases, photosynthesis, and other processes store them at high concentration) into the cell (down, in Berg's figure) where they are at lower concentration.

    Somehow this energy is converted into motion of the cell.  A number of diverse models have been proposed for how exactly this might occur.  Mike Gene briefly reviews a couple of them in his argument for the nonevolution of the flagellum here.

    He includes a figure derived from a paper on the question of motor mechanism:

    The grey round thing represents the FliG protein (the part of the C-ring that interacts with the motor proteins, MotA and MotB) and the pinkish things with the H+ or Na+ flowing through them represent the MotAB complex.

    [WARNING: beginning marginally informed speculation section.  Treat as one would treat a mathematical "conjecture" -- or rather just a conjecture, I'm sure math is more formal about such things]

    Perhaps we can imagine two main classes of models:

    1) Those in which the H+ flow plays a *direct* role in rotating the flagellum (e.g., the "proton turbine model" in the left of the figure).  This is, BTW, an appealingly simple model for motor operation: the protons just flow on through and the charges interact with the diagonally-positioned charges on the C-ring, sort of like wind blowing on a windmill.  Presumably a conformation change in FliC could reverse the diagonal direction and presto, rotation in the opposite direction.

    2) Those in which the H+ flow causes some conformation (shape) change in the MotAB complex, which then interacts to "push" (speaking very basically; could be a Brownian ratchet for instance) on the C-ring.  How a conformation change in FliC would produce reverse rotation on this model is obscure to me, although I'm sure there's a way.

    Based on the idea that MotAB had flagellum-independent origins in the form of proteins homolgous to ExbB (and ExbD IIRC), can we make any guess as to which of these might be more likely?

    The difficulty with #1 would appear to be that both the proto-FliC and proto-ExbB would have to be at least crudely adapted to accepting proton flow.

    It seems to me that #2 might be more likely if MotAB evolved from ExbB-like ion channels and if those channels functioned by conducting H+ through them and using the resulting conformation changes to perform work elsewhere at a distance.  The proto-MotB (already adapted for performing H+-powered work on some other protein) might be the only thing that would have to mutate in order to get some crude purchase on the proto-FliC (the base of a transport system, but that's another part of the story).

    Anyway, the basic idea is that it would be cool, for instance, if one could predict which functional model to prefer based on an evolutionary based on homology with ExbB...

    All of this depends upon further understanding of how the Exb complex works however.  Something to work on...

    [/ramble concluded]

    (PS: THis is one of the Mot-homolog articles, it appears that they go for the conformation-change model also):


    Biochemistry 2001 Oct 30;40(43):13041-50
    Conformational change in the stator of the bacterial flagellar motor.

    Kojima S, Blair DF.

    Department of Biology, University of Utah, Salt Lake City, Utah 84112, USA.

    MotA and MotB are integral membrane proteins of Escherichia coli that form the stator of the proton-fueled flagellar rotary motor. The motor contains several MotA/MotB complexes, which function independently to conduct protons across the cytoplasmic membrane and couple proton flow to rotation. MotB contains a conserved aspartic acid residue, Asp32, that is critical for rotation. We have proposed that the protons energizing the motor interact with Asp32 of MotB to induce conformational changes in the stator that drive movement of the rotor. To test for conformational changes, we examined the protease susceptibility of MotA in membrane-bound complexes with either wild-type MotB or MotB mutated at residue 32. Small, uncharged replacements of Asp32 in MotB (D32N, D32A, D32G, D32S, or D32C) caused a significant change in the conformation of MotA, as evidenced by a change in the pattern of proteolytic fragments. The conformational change does not require any flagellar proteins besides MotA and MotB, as it was still seen in a strain that expresses no other flagellar genes. It affects a cytoplasmic domain of MotA that contains residues known to interact with the rotor, consistent with a role in the generation of torque. Influences of key residues of MotA on conformation were also examined. Pro173 of MotA, known to be important for rotation, is a significant determinant of conformation: Dominant Pro173 mutations, but not recessive ones, altered the proteolysis pattern of MotA and also prevented the conformational change induced by Asp32 replacements. Arg90 and Glu98, residues of MotA that engage in electrostatic interactions with the rotor, appear not to be strong determinants of conformation of the MotA/MotB complex in membranes. We note sequence similarity between MotA and ExbB, a cytoplasmic-membrane protein that energizes outer-membrane transport in Gram-negative bacteria. ExbB and associated proteins might also employ a mechanism involving proton-driven conformational change.

    Date: 2003/02/07 01:31:24, Link
    Author: niiicholas
    This would appear to be in support of the "the proton passes through the MotAB complex, and the resulting change of shape moves the FliG & C-ring"


    At first sight, these two systems have little in common with the flagellar motor other than the use of a trans-membrane electrochemical gradient as an energy source. The bacterial flagellum is a complex macromolecular assemblage forming a multipartite structure composed of a long helical propeller, a flexible hook region and a rotary motor in the bacterial cytoplasmic membrane (for reviews, see Blair, 1995; DeRosier, 1998). The torque generation depends on the operation of a number of motors composed of the two proteins MotA and MotB. These proteins are believed to form the stator of the motor, arranged around the periphery of the flagellar basal body, which constitutes the rotor of the motor, and interacting specifically with the protein FliG, one of the subunits that form this basal body (Zhou et al., 1998a). The suggested mechanism is that protons traverse the membrane through a 'pore' formed by the MotA and MotB proteins. This 'pore' involves, in particular, a conserved aspartate residue of MotB (Asp-32) (Zhou et al., 1998b). Two conserved proline residues of MotA (Pro-173 and Pro-222) (Braun et al., 1999) are also particularly important in torque generation. On the basis of these studies, a model has been proposed (Braun et al., 1999) in which the first proline senses a conformational state and gates proton uptake by the aspartate residue from the periplasm. The proton uptake causes a change that either permits (via a Brownian ratchet) or drives rotation, a step involving the second proline residue. Finally, proton release into the cytoplasm restores the motor to its initial state.

    Let's see if this graphic works:


    Eric Cascales Roland Lloubès James N Sturgis Molecular Microbiology Volume 42 Issue 3 Page 795  - November 2001  
    The TolQ-TolR proteins energize TolA and share homologies with the flagellar motor proteins MotA-MotB

    Date: 2003/02/07 01:48:37, Link
    Author: niiicholas
    Bracht on the flagellum:

    The Bacterial Flagellum: A Response to Goodenough

    Date: 2003/02/07 02:27:38, Link
    Author: niiicholas
    In the "A Different Way to Control a Bacterial Flagellum" category:


    J Mol Microbiol Biotechnol 2002 May;4(3):183-6

    Sensory transduction to the flagellar motor of Sinorhizobium meliloti.

    Scharf B, Schmitt R.

    Lehrstuhl fur Genetik, Universitat Regensburg, Germany.

    Molecular mechanisms that govern chemotaxis and motility in the nitrogen-fixing soil bacterium, Sinorhizobium meliloti, are distinguished from the well-studied taxis systems of enterobacteria by new features. (i) In addition to six transmembrane chemotaxis receptors, S. meliloti has two cytoplasmic receptor proteins, McpY (methyl-accepting chemotaxis protein) and IcpA (internal chemotaxis protein). (ii) The tactic response is mediated by two response regulators, CheY1 and CheY2, but no phosphatase, CheZ. Phosphorylated CheY2 (CheY2-P) is the main regulator of motor function, whereas CheY1 assumes the role of a 'sink' for phosphate that is shuttled from CheY2-P back to CheA. This phospho-transfer from surplus CheY2-P to CheA to CheY1 replaces CheZ phosphatase. (iii) S. meliloti flagella have a complex structure with three helical ribbons that render the filaments rigid and unable to undergo polymorphic transitions from right- to left-handedness. Flagella rotate only clockwise and their motors can increase and decrease rotary speed. Hence, directional changes of a swimming cell occur during slow-down, when several flagella rotate at different speed. Two novel motility proteins, the periplasmic MotC and the cytoplasmic MotD, are essential for motility and rotary speed variation. A model consistent with these data postulates a MotC-mediated gating of the energizing MotA-MotB proton channels leading to variations in flagellar rotary speed.

    Random points:

    1) Yet another non-bidirectional flagellum

    2) This flagellum has required parts that other flagella don't require (MotC and MotD)

    3) Other flagella have required parts (e.g. CheZ) that this flagellum doesn't require

    4) I always thought it made more sense to regulate the motor rather than the C-ring (or at least it was easier to imagine); it appears that Sinorhizobium meliloti agrees.

    5) Does "rigid flagella" indicate that these guys get away without even hook proteins (the more-flexible proteins at the base of the external rod structure)?

    6) Chemotaxis systems in general are a huge mess in terms of IC-interpretation. In some cases similar systems are coupled to wildly different motility systems (and probably even to nonmotility systems; cells have to react in multiple ways including motion), and some motile cells appear to get by without the chemotaxis system at all; see:


    Microbiology 1999 Feb;145 ( Pt 2):279-81
    A twisted tale: the origin and evolution of motility and chemotaxis in prokaryotes.

    Faguy DM, Jarrell KF.

    Date: 2003/02/08 01:11:48, Link
    Author: niiicholas
    Link to extended discussion on the relative basal-ness of MotA vs. ExbB:;f=13;t=000576;p=3

    Date: 2003/02/08 02:39:54, Link
    Author: niiicholas
    Fun article, a latter day version of Purcell's "Life at Low Reynolds Number":

    The efficiency of propulsion by a rotating flagellum


    Proc. Natl. Acad. Sci. USA
    Vol. 94, pp. 11307-11311, October 1997
    The efficiency of propulsion by a rotating flagellum
    (bacteria / motility / hydrodynamics / low Reynolds number)

    Edward M. Purcell*

    Department of Physics, Harvard University, Cambridge, MA 02138

    Communicated by Howard C. Berg, Harvard University, Cambridge, MA, July 29, 1997


    [At very low Reynolds number, the regime in which fluid dynamics is governed by Stokes equations, a helix that translates along its axis under an external force but without an external torque will necessarily rotate. By the linearity of the Stokes equations, the same helix that is caused to rotate due to an external torque will necessarily translate. This is the physics that underlies the mechanism of flagellar propulsion employed by many microorganisms. Here, I examine the linear relationships between forces and torques and translational and angular velocities of helical objects to understand the nature of flagellar propulsion.]

    Note: the mathematical tractability of calculating diffusion and velocity for bacteria & their flagella should not be neglected.  E.g. it seems that the propulsion or dispersal potential of various "crude" flagella could be calculated.

    Date: 2003/02/15 00:57:38, Link
    Author: niiicholas
    Stop the presses!  Tubulin (not just the tubulin homolog FtsZ) found in prokaryotes.


    Proc Natl Acad Sci U S A 2002 Dec 24;99(26):17049-54
    Genes for the cytoskeletal protein tubulin in the bacterial genus Prosthecobacter.


    Jenkins C, Samudrala R, Anderson I, Hedlund BP, Petroni G, Michailova N, Pinel N, Overbeek R, Rosati G, Staley JT.

    Department of Microbiology, University of Washington, Seattle, WA 98195, USA.

    Tubulins, the protein constituents of the microtubule cytoskeleton, are present in all known eukaryotes but have never been found in the Bacteria or Archaea. Here we report the presence of two tubulin-like genes [bacterial tubulin a (btuba) and bacterial tubulin b (btubb)] in bacteria of the genus Prosthecobacter (Division Verrucomicrobia). In this study, we investigated the organization and expression of these genes and conducted a comparative analysis of the bacterial and eukaryotic protein sequences, focusing on their phylogeny and 3D structures. The btuba and btubb genes are arranged as adjacent loci within the genome along with a kinesin light chain gene homolog. RT-PCR experiments indicate that these three genes are cotranscribed, and a probable promoter was identified upstream of btuba. On the basis of comparative modeling data, we predict that the Prosthecobacter tubulins are monomeric, unlike eukaryotic alpha and beta tubulins, which form dimers and are therefore unlikely to form microtubule-like structures. Phylogenetic analyses indicate that the Prosthecobacter tubulins are quite divergent and do not support recent horizontal transfer of the genes from a eukaryote. The discovery of genes for tubulin in a bacterial genus may offer new insights into the evolution of the cytoskeleton.


    It is evident that at some point in their evolution, the Eucarya acquired a structural complexity unrivaled by members of the other two domains of life. One of the major structural features that separates the Eucarya from the Bacteria and the Archaea is the presence of an internal cytoskeleton composed of actin and tubulin. Notably, these cytoskeletal elements are present in all known eukaryotes, even the a-mitochondriate protozoa (1, 2). Furthermore, their acquisition represented an important step in the evolution of eukaryotic cells by facilitating the engulfment of bacterial endosymbionts, which later became chloroplasts and mitochondria (3).

    In contrast, there have been no conclusive reports of these cytoskeletal elements in the bacterial or archaeal domains. Over the years, there have been numerous reports of "microtubule-like" structures or "rhapidosomes" in members of both the Bacteria and the Archaea (summarized in ref. 4); however, thus far these observations lack any genetic basis. At present, the leading candidate for an evolutionary precursor of tubulin in the bacterial/archaeal domains is the cell division protein, FtsZ. Although there is strong evidence from their 3D structures that tubulin and FtsZ are homologous proteins (5, 6), they share only very low sequence identity, most of which is confined to the GTP-binding region (7). The strikingly low sequence identity is difficult to reconcile with the fact that tubulins and FtsZs are among the slowest-evolving proteins known and raises the question of whether any more closely related homologs of tubulin exist in members of the Bacteria or Archaea (8, 9).

    Reports of microtubule-like structures in bacterial ectosymbionts ("epixenosomes") of ciliates in the genus Euplotidium present the most compelling structural evidence yet for the existence of tubulin-containing elements in bacteria. These organisms, which belong to the little-studied division, Verrucomicrobia, have been shown to possess tubular structures with diameters of 22 ± 3 nm, the size range of eukaryotic microtubules. These structures crossreact with anti-Paramecium tubulin antibodies and display sensitivity to microtubule-depolymerizing agents (10, 11). On the basis of these observations, we searched the partially sequenced genome of a free-living member of the Verrucomicrobia, Prosthecobacter dejongeii, for genes homologous to those for tubulin. To our knowledge, P. dejongeii is the first member of the division Verrucomicrobia to be subjected to genome-sequencing studies.


    Evolutionary Origin of Prosthecobacter Tubulin Genes.

    A significant question raised by this study relates to the evolutionary origin of the Prosthecobacter tubulin genes and may be summarized as two main hypotheses. First, the genes arose via a horizontal gene transfer from a eukaryote, and second, that the bacterial tubulins are ancestral to eukaryotic tubulins.

    Relationships between the Prosthecobacter tubulins and a specific eukaryotic lineage, which would implicate a recent gene transfer, were never observed regardless of the sequence representatives, alignment subset, or mode of analysis used. Furthermore, btuba and btubb genes are present in all four species of the Prosthecobacter genus, suggesting that the genes were acquired before the divergence of this lineage. Thus, if the Prosthecobacter tubulin genes arose via horizontal transfer from a eukaryote, it was not during the recent history of the lineage.

    The second hypothesis, that the bacterial tubulin genes are ancestral to eukaryotic tubulin genes, could be explained in terms of a shared ancestry between the two groups or a gene transfer from an ancestor of the Verrucomicrobia to a protoeukaryotic organism, before the radiation of extant eukaryotes. A gene transfer between the groups could also encompass a fusion event between an ancestor of the Verrucomicrobia and another organism, such as an archaeon (25). The phylogenetic analyses superficially support this hypothesis, in that the bacterial tubulin sequences were always seen to branch more deeply than eukaryotic  and  tubulin; however, this relies on the assumption that  and  tubulins were the first members of the tubulin family to arise. Even if this assumption is correct, caution is required in the interpretation of the analyses, given that the level of sequence divergence in the bacterial sequences may cause them to migrate to the base of the tree artifactually (24). The various evolutionary models for the origin of tubulins that are implied by these hypotheses are to be discussed in detail elsewhere.

    Although the current evidence does not allow an effective distinction between the two hypotheses presented here, further indications as to the origin of the Prosthecobacter tubulin genes may be facilitated by determining the distribution of the genes within the division Verrucomicrobia. If the genes were present in members of several subdivisions of the Verrucomicrobia, this would suggest that the genes have been in these organisms for a long time. Furthermore, closer examination of the P. dejongeii genome, such as searching for other genes unique to eukaryotes, may aid in determining whether a large transfer event or a fusion occurred between members of the Verrucomicrobia and eukaryotes.

    If it were true that the bacterial tubulins are ancestral to eukaryotic tubulins, it would have a significant impact on our understanding of eukaryote cell evolution. Although FtsZ is a homolog of tubulin, the evolutionary distance between the two proteins is substantial. Indeed, it has been suggested several times that a more immediate evolutionary precursor of tubulin may reside in some as-yet-undiscovered bacterial or archaeal lineage (26) or was acquired from an extinct lineage (25, 27) or "chronocyte" (2). Whether the Prosthecobacter tubulins satisfy this role as evolutionary intermediate between FtsZ and eukaryotic tubulin remains to be seen.

    Obviously, research is just beginning on this bacterium and proteins.  However, it is interesting in light of one of Mike Gene's essays on his webpage:


    Tubulin and ftsZ: More than One Way to View Something

    For some unknown reason, many critics of ID think that design = uniqueness. That is, if a biological feature X is similar to biological feature Y, we are supposed to rule out design and instead infer common ancestry. But are things really this simple?

    Consider tubulin and ftsZ. The former is a very important eukaryotic cytoskeletal protein involved in maintaining the cell structure, coordinating intracellular movement, separating chromosomes during mitosis, and forming the backbone of the eukaryotic flagellum. The latter gene product is a bacterial protein that plays an essential role in splitting the two cells during cell division and may also have cytoskeletal roles.

    Although the two proteins have a similar role, most scientists did not originally consider them homologous (related by a common ancestral sequence). In a paper published in Cell by David Edgell and W. Ford Doolittle back in 1997, they noted that sequence identity less than 20% is attributed to chance. They also argued a "common function alone is not sufficient evidence of homology because two proteins can convergently arrive at the same mechanistic, structural, or biochemical solution to a particular biological problem." In fact, speaking directly about tubulin and ftsZ, they wrote, "amino acid alignments between these two proteins are not very convincing."

    But today, the situation has changed as most scientists now think the two proteins are homologous. Why? The 3-D structure of both proteins has been solved and have been found to be very similar. One scientist has recently explained the picture:


    There is now overwhelming evidence in favor of the idea that FtsZ is a homolog of tubulin, the ubiquitous eukaryotic cytoskeletal protein involved in many essential cellular processes including mitosis. Despite only limited primary sequence homology centered around a GTP binding motif termed the `tubulin signature sequence', the recently solved crystal structures of FtsZ and tubulin show extensive structural homology throughout the proteins. In addition, FtsZ, like tubulin, binds and hydrolyzes GTP and assembles into protofilaments that have structures similar to those within microtubules. This assembly is GTP-dependent and disassembly occurs when the GTP is exhausted, suggesting that FtsZ polymers, like microtubules, are dynamically unstable. FtsZ and tubulin also share similar responses to hydrophobic dyes: while bis-anilino-naphthalenesulfonate (bis-ANS) inhibits polymerization of both proteins, the related dye ANS has no effect on either. Another link between FtsZ and tubulin in vivo is that they can be made to coalign as polymers in mammalian cells in the presence of vinblastine, a microtubule-destabilizing drug. - Margolin, W. Themes and variations in prokaryotic cell division. Fems Microbiology Reviews, 2000 Oct, 24(4):531-48.


    While this view is quite reasonable in science, we must remember that science is looking for the best non-teleological explanation. Thus, although no calculations have been made, it seems intuitively implausible that such similarities could be due to chance. And in science, chance is the only other viable alternative explanation to common descent.

    But if we step out of this box and entertain teleological causes, structural similarity, and the similar properties that follow, are insufficient reason to infer common descent in place of design. In other words, while I would agree that both sequence and structural similarity are good evidence for common descent, this only holds true as long as we have no reason to suspect ID may be lurking in the background.

    Now, my working hypothesis entails that life appeared on this planet as a consequence of seeding and the life forms that were seeded represented a consortium of sophisticated cell types. Since tubulin is basic to eukarya and ftsZ is basic to bacteria, and since both eukarya and bacteria may have been among that consortium (or separated by two distinct seeding events), ID may be lurking in the background. So let's see how we can think about the two proteins from an ID perspective.


    Thirdly, we might expect these differences to be very important, explaining why a designer would employ the different variations on the GPD theme. And one of the facts not mention thus far in this thread is that although both ftsZ and tubulin have very different amino acid sequences when compared to each other, the sequences of both ftsZ and tubulin are highly conserved in bacteria and eukarya, respectively. In other words, when we compare ftsZ sequence within bacteria and tubulin sequence with eukarya, we find strong sequence conservation. FtsZ, for example, shows 40-50% identity when very different forms of bacteria are compared and I believe the tubulin conservation is even higher. In fact, one paper on my desk states "tubulins are among the most conserved proteins known."

    This pattern is consistent with independent origins by design. That is, the first bacteria were endowed with a GPD variant known as ftsZ that has been conserved for billions of years due to its important design objective. Similarly, the first eukaryotes were endowed with a GPD variant known as tubulin that has been conserved for billions of years due to its important design objectives.

    On the other hand, if we try to force common descent on the two distinct, highly conserved proteins, we face a strange situation. For prior to the evolution of ftsZ and tubulin from this hypothetical ftsZ/tubulin-like precursor, there was no apparent functional constraint. If there was, it is difficult to explain how the two sequences so radically drifted from each other only to be locked into place (of all places) in the last common ancestors of eukaryotes and bacteria. But wait a minute. The 3-D structure was being conserved. That's the basis for inferring the common descent. Yet what was it doing prior to the two sequences getting locked into place? Nothing bacterial. Nothing eukaryotic.

    But here we have tubulin evidently doing something prokaryotic.

    Never heard of these Prosthecobacter guys before?


    Int J Syst Bacteriol 1996 Oct;46(4):960-6

    Phylogeny of Prosthecobacter, the fusiform caulobacters: members of a recently discovered division of the bacteria.

    Hedlund BP, Gosink JJ, Staley JT.

    Department of Microbiology, University of Washington, Seattle 98195-7242,

    Prosthecobacter fusiformis is morphologically similar to caulobacters; however, it lacks a dimorphic life cycle. To determine the relatedness of the genus Prosthecobacter to dimorphic caulobacters and other prosthecate members of the alpha subgroup of the Proteobacteria (alpha-Proteobacteria), we isolated and sequenced 16S rRNA genes from four Prosthecobacter strains. Surprisingly, the results of phylogenetic analyses placed the fusiform caulobacters in a deeply rooted division of the Bacteria that was most closely affiliated with the Planctomyces-Chlamydia group and only distantly related to the alpha-Proteobacteria. The genus Prosthecobacter shares a common lineage in this division with Verrucomicrobium spinosum, a polyprosthecate, heterotrophic bacterium. Consistent with this phylogenetic placement, menaquinones were isolated from Prosthecobacter strains and menaquinones have been isolated from Verrucomicrobium strains and planctomycetes but not from members of the alpha-Proteobacteria. Thus, the genus Prosthecobacter is a second genus in the recently described order Verrucomicrobiales. Members of the genus Prosthecobacter are susceptible to beta-lactam antibiotics and contain mesodiaminopimelic acid, indicating that they, unlike members of the Planctomycetales or Chlamydiales, have peptidoglycan cell walls. This major phenotypic difference, together with the phylogenetic independence of the verrucomicrobia, indicates that these bacteria and the sources of related 16S ribosomal DNAs obtained from soils, freshwater, and the marine pelagic environment represent an unrecognized division of the Bacteria.

    Date: 2003/02/17 15:41:23, Link
    Author: niiicholas
    This thread is devoted to the Argument from Ignorance and what happens to various sciences if it were allowed the same free reign that IDists give the Argument from Ignorance in biology.



    BTW, since the Steves have no serious scientific doubt that natural selection was the major mechanism behind the origin of the bacterial flagellum, have them drop me an e-mail providing some of this evidence. The evidence must be immense, given there is no serious doubt. Oddly enough, it seems to be secret evidence. SShhh.  

    Similarly, because the origin of the rings of Saturn is still unknown except for some general models and scraps of data, we should have "serious doubt" that current physical theory can account for it.

    Any schmoe in any field can go dig up something unexplained (or only generally explained, as in the cases of both the flagellum and the rings of Saturn) in any field, that is old enough or otherwise "distant" enough to make evidence hard to come by.  None of this justifies "serious doubt" in a well-established theory, especially for problems that are routinely brought up and solved within the field ("complex adaptive structure #1241" in biology, evolutionary theory has already explained a number of complex adaptive structures so what difference does one more make?).  

    On Mike Gene's logic these mysterious, highly symmetrical structures should put mainstream geology into "serious doubt":

    ...and these should put mainstream anthropology/archeology into doubt:

    The "Bahgdad Battery" -- apparently a 2200 year old battery.

    And yes, both of these puzzles have been invoked in support of radical theories like, oh I don't know, alien intervention in the history of life.

    I guess we should be teaching this "serious doubt" about mainstream science in school earth sciences and history classes also, just to be fair.

    Post your favorite mysteries here!!

    Date: 2003/02/17 17:16:08, Link
    Author: niiicholas
    More from Dembski on the flagellum:

    ISCID thread

    Dembski's latest article:
    Still Spinning Just Fine: A Response to Ken Miller

    My reply:

    There are severe problems with basically every paragraph of Bill Dembski's latest, I will focus on just one:

    Dembski writes in Still Spinning Just Fine that:


    The Argument from Personal Incredulity:

    Miller claims that the problem with anti-evolutionists like Michael Behe and me is a failure of imagination -- that we personally cannot "imagine how evolutionary mechanisms might have produced a certain species, organ, or structure." He then emphasizes that such claims are "personal," merely pointing up the limitations of those who make them. Let's get real. The problem is not that we in the intelligent design community, whom Miller incorrectly calls "anti-evolutionists," just can't imagine how those systems arose. The problem is that Ken Miller and the entire biological community haven't figured out how those systems arose. It's not a question of personal incredulity but of global disciplinary failure (the discipline here being biology) and gross theoretical inadequacy (the theory here being Darwin's).

    However, with confronted with rather a lot of literature on the origin and evolution of the immune system (one of Behe's originally identified IC systems from Darwin's Black Box, plus lots of evidence of precursors in organisms without the full system, not a single IDist was able to defend the previous statements of Behe and Dembski along the lines of "the entire biological community ha[s]n't figured out how those systems arose."  A few of the more sophisticated ID-friendlies even appeared to agree that the gradual evolution of the "IC" immune system was a perfectly reasonable idea supported by a fair number of observations and peer-reviewed articles.

    This was all done right here on ISCID not few months ago:

    Organisms using GAs vs. Organisms being built by GAs

    And yes, this will keep getting brought up as long as Dembski keeps repeating the same false line that biologists are clueless about how complex multipart systems can originate.

    As for what things like the Type III secretion system do and do not prove (as well as for citations of important bits of evidence that Dembski failed to deal with, things like the Exb homologs of the flagellum motor proteins, and the archaeal flagellum--Type IV secretion system homologies), there's not much point in repeating them yet again, so I've been accumulating a list of the relevant links here: resource thread on the prokaryote flagella (there's more than one kind of flagellum, durnit!!! )

    Date: 2003/02/17 18:07:21, Link
    Author: niiicholas
    I got some replies to this quote I posted in response to Nelson Alonso:


    So lets review. A de-novo design hypothesis entails:

    1. No evolutionary history

    2. IC tied in with functional constraint (selection weeding out mutants because of ICness .
    Hmm, neither seems quite completely so true for the ATPase, because of the PPase.  A simpler, partially sequence-similar system can perform the task.  So even for a system older than the flagellum scientists are beginning to get hints indicating that ICness tain't all it's cracked up to be.


    In the near future I want to bring Dembski into the mix. However, unless any relevant criticism of a specific system is brought up, I'm simply going to list them for now. And we can bring up another thread to discuss each system's history. For now, I'm just concerned with listing them.
    Well for starters, for the flagellum your reliance on Mike Gene has left you a bit out of date:


    Biochemistry 2001 Oct 30;40(43):13041-50
    Conformational change in the stator of the bacterial flagellar motor.

    Kojima S, Blair DF.

    Department of Biology, University of Utah, Salt Lake City, Utah 84112, USA.

    MotA and MotB are integral membrane proteins of Escherichia coli that form the stator of the proton-fueled flagellar rotary motor. The motor contains several MotA/MotB complexes, which function independently to conduct protons across the cytoplasmic membrane and couple proton flow to rotation. MotB contains a conserved aspartic acid residue, Asp32, that is critical for rotation. We have proposed that the protons energizing the motor interact with Asp32 of MotB to induce conformational changes in the stator that drive movement of the rotor. To test for conformational changes, we examined the protease susceptibility of MotA in membrane-bound complexes with either wild-type MotB or MotB mutated at residue 32. Small, uncharged replacements of Asp32 in MotB (D32N, D32A, D32G, D32S, or D32C) caused a significant change in the conformation of MotA, as evidenced by a change in the pattern of proteolytic fragments. The conformational change does not require any flagellar proteins besides MotA and MotB, as it was still seen in a strain that expresses no other flagellar genes. It affects a cytoplasmic domain of MotA that contains residues known to interact with the rotor, consistent with a role in the generation of torque. Influences of key residues of MotA on conformation were also examined. Pro173 of MotA, known to be important for rotation, is a significant determinant of conformation: Dominant Pro173 mutations, but not recessive ones, altered the proteolysis pattern of MotA and also prevented the conformational change induced by Asp32 replacements. Arg90 and Glu98, residues of MotA that engage in electrostatic interactions with the rotor, appear not to be strong determinants of conformation of the MotA/MotB complex in membranes. We note sequence similarity between MotA and ExbB, a cytoplasmic-membrane protein that energizes outer-membrane transport in Gram-negative bacteria. ExbB and associated proteins might also employ a mechanism involving proton-driven conformational change.


    The occurrence of significant conformational change in the stator has implications not only for the present-day mechanism but also for the evolution of the flagellar motor. A membrane complex that undergoes proton-driven conformational changes could perform useful work in contexts other than (and simpler than) the flagellar motor, and ancestral forms of the MotA/MotB complex might have arisen independently of any part of the rotor. We queried the sequence database using the sequence of the best-conserved part of MotA (the segment containing membrane segments 3 and 4) from Aquifex aeolicus, a species whose lineage is deeply branched from other bacteria. In addition to the expected MotA homologues, the search returned a protein sequence from the archaeal species Methanobacterium thermoautotrophicum (protein MTH1022) that shows significant sequence similarity not only to MotA but also to the protein ExbB (Figure 9). ExbB is a cytoplasmic-membrane protein that functions in conjunction with ExbD, TonB, and outer-membrane receptors to drive active transport of certain essential nutrients across the outer membrane of Gram-negative bacteria. The energy for this transport comes from the proton gradient across the inner membrane. Thus, MotA and ExbB are both components of systems that tap the proton gradient to do work some distance away (at either the rotor-stator interface or the outer membrane; Figure 9).

    Other features also point to a connection between the Mot and Exb systems. MotA functions in a complex with MotB, which as noted contains the critical residue Asp32 near the cytoplasmic end of its single membrane segment. ExbB functions in a complex with ExbD, which likewise has a single membrane segment with a critical Asp residue near its cytoplasmic end (Asp25 in ExbD of E. coli; ref 59). Although ExbB has only three membrane segments in contrast to the four in MotA, the membrane segments that show sequence similarity have the same topology. The protein TonB is also present in the complex with ExbB and ExbD (59, 60) and would provide an additional membrane segment to round out the topological correspondence (Figure 9). ExbB contains a well-conserved Pro residue (Pro141 in E. coli ExbB) that is the counterpart of Pro173 of MotA. Although MotB and ExbD do not share close sequence similarity apart from the critical Asp residue, in certain positions in the membrane segment the residues most common in MotB proteins are also common in ExbD proteins. Finally, like the MotA/MotB complex the ExbB/ExbD complex contains multiple copies of each protein (61). Together, these facts make a reasonable case for an evolutionary connection between the Mot proteins of the flagellar motor and the Exb proteins of outer-membrane transport (and by extension the TolQ/TolR proteins, which are related to ExbB/ExbD but whose functions are less understood).

    The number of parts in a flagellum that don't have homologs with different, non-flagellar functions is getting to be rather low; mostly they are filament and shaft proteins, which all may be homologous with each other, and of course nonmotile filaments are known to have a wide degree of uses in bacteria...

    So even for systems that are remote from us by 3 billion years there has been some recent progress.  


    ...from this ARN thread:;p=3

    ...and then Nelson replied and I replied:

    Originally posted by Nelson Alonso:
    I also want to read your reference concerning bacterial flagellar motor, but to be honest, I already see it as irrelevant, since sequence similarity doesn't tell me much about how to make a bacterial flagellum via natural selection and random mutation.
    Hmm, Mike Gene didn't think that such a thing was irrelevant:

    MotA/MotB, on the other hand, could plausibly exist as some ion channel prior to the existence of the flagella, but there is no evidence of this.
    And yet soon after he wrote this, exactly such homologous-but-non-flagellar ion channel was discovered.  Looks to me like this family of enzymes couples proton flow to all kinds of mechanical processes, only one of which is rotating the base of the flagellum.

    And he also wrote:


    [snipped image for formatting sake]

    Figure 1. The EFM Hypothesis. It begins with multi-component export machinery and invokes an initial cooption even to explain the origin of the filament. But because the "filament" of the flagellum is also a multi-component system, simultaneous, not gradual cooption is being invoked. Its non-flagellar function is not provided. The second cooption event, where an ion channel is added to create the flagellum, invokes the same thing.
    But a plausibly pre-existing function for stage 2 (now) *has* been provided.  And, strangely enough (except from the perspective of the cooption hypothesis), the first reasonably strong homology evidence for a pre-existing functional subcomponent of the flagellum *just happens* to be the last two parts added in the cooption scenario, which just happen to already function together just like they do in the flagellum.  

    (I don't see any good reason for MG's breaking what is otherwise convention and splitting off FlG's C-terminal end as a "separate" part, seems to me this is a special maneuvure not utilized elsewhere)


    The bacterial motor allows movement at such a speed that, if the bacteria were resized to the weight of cars, they would supposedly break the sound barrier.
    If you follow this analogy, the car when "sitting still" would be "jiggling" many times its body length every second due to brownian motion.  Your driveway and house would be ruined.  Intuition is a poor guide to life at the very small scale.


    The Exb complex are homologs but quite distant from the Mot complex, and even the function is completely different.
    All depends on what you mean by "function".  Kojima and Blair didn't think so.  As for distance, the proposed cooption event did occur at something like the common ancestor of eubacterial, so there has been a bit o'time for divergence.

    ....And when Nelson still wasn't impressed, I wrote:

    Um, Nelson, you didn't even read the quote I provided:


    We queried the sequence database using the sequence of the best-conserved part of MotA (the segment containing membrane segments 3 and 4) from Aquifex aeolicus, a species whose lineage is deeply branched from other bacteria. In addition to the expected MotA homologues, the search returned a protein sequence from the archaeal species Methanobacterium thermoautotrophicum (protein MTH1022) that shows significant sequence similarity not only to MotA but also to the protein ExbB (Figure 9). ExbB is a cytoplasmic-membrane protein that functions in conjunction with ExbD, TonB, and outer-membrane receptors to drive active transport of certain essential nutrients across the outer membrane of Gram-negative bacteria. The energy for this transport comes from the proton gradient across the inner membrane.
    See that?  A homolog in archaebacteria.  As far as our current understanding of microbial phylogeny allows us to say anything about what is basal to what, it appears that the MotA homolog is more basally distributed than the eubacterial flagellum.  So if you're going to use distribution as a guide to what came first, you lose on this one.

    Of course, given the uncertainty surrounding phylogenetic events 3.5 billion years ago, not to mention lateral transfer events etc., the most reasonable thing to do would be to say that we have no particularly good information about what came before what.  But then there goes any confidence in the assertion that bacteria have always had flagella or have no precursor homologous proteins, which has been a big chunk
    of your argument.

    Regarding the probability of this ion channel hooking up to the base of a primitive Type III pili, the exact mechanism of coupling proton flow to motion is still up in the air.  However, you wouldn't have to get a fully functioning flagellum out of it, even undirected wiggling would enhance dispersal.  This provides the starting point for natural selection to refine the procedure.

    As you and Mike Gene point out, such a getting-the-process-started mutation is an unlikely "completely chance event" -- but just like any mutation, this is not a one-try event!!!  Give a few gaztrillion bacteria a few million years!  And we are clearly no longer dealing with the fortuitous de novo synthesis of a whole bunch of proteins, as Dembski suggests, or even the fortuitous cooption of dozens of individual proteins all at once, as Mike Gene sometimes mischaracterizes cooption.  We are just hypothesizing a mutation crudely coupling two pre-existing systems.

    As for similarity in function, Kojima and Blair note that this basic ion-channel system has been successfully coupled to diverse systems:

    Thus, MotA and ExbB are both components of systems that tap the proton gradient to do work some distance away (at either the rotor-stator interface or the outer membrane; Figure 9).
    The point with the brownian motion analogy is that "faster than the speed of sound" is not quite so impressive on the molecular scale.  Considering that some bacteria get by with relatively slow motility systems, and many get by with none at all, argues that we should keep the niftiness of the flagellum in perspective.  Another random fact: the energetic efficiency of the flagellum is at best a few percent according to Berg's Random Walks in Biology.

    And then in reply to a few objections from Mike Gene:

    First off,

    An awful lot of entries in the NCBI protein database listing MotA, ExbB, and TolQ as being a "family", in opposition to what Mike Gene has been suggesting

    Originally posted by Mike Gene:
    Nic: Hey, I'm just following the peer-reviewed lit., man. Take it up in the pages of Biochemistry if you like...

    The authors never claim MTH1022 is a homolog of motA. And even if they did, the claim would be unsupported.  
    People can read the quote I posted and decide for themselves exactly what the authors meant.  Mentioning significant sequence similarity in the middle of a discussion of homologs seems like a strong indication to me that they meant homolog or at least "likely homolog".  And see below for what some of those proteins are labeled as in the NCBI database.


    Actually, running a PSI-BLAST of ExbB gets me four hits on archaeabacteria, but whatever.

    With e values of 0.005 and higher.  That's not very impressive.  Furthermore, even if there is a non-convergent and real relationship here, note that it is not widely distributed and would thus seem to have evolved long after archaea appeared.  

    A much stronger point is that the ExbB homologs are very widely distributed in eubacteria, in very basal lineages.

    Think so?  What groups did you have in mind?[/qb]
    Hmm, well a standard protein BLAST  on E coli ExbB gives me this taxonomy report:

    An E. coli "biopolymer transport exbB protein"

    Here is the link

    Here are some of the results *outside* the proteobacteria:

    Code Sample
     Chlamydophila pneumoniae CWL029 [chlamydias] taxid 115713
    gi|15618694|ref|NP_224980.1| Macromolecule transporter [Ch...      61  1e-08

     Cytophaga hutchinsonii [CFB group bacteria] taxid 985
    gi|23136461|gb|ZP_00118181.1| hypothetical protein [Cytoph...      60  1e-08
    gi|23136843|gb|ZP_00118557.1| hypothetical protein [Cytoph...      36  0.35

     Chlamydia trachomatis [chlamydias] taxid 813
    gi|15605326|ref|NP_220112.1| polysaccharide transporter [C...      59  4e-08

     Chlamydia muridarum (agent of mouse pneumonitis) [chlamydias] taxid 83560
    gi|15835499|ref|NP_297258.1| MotA/TolQ/ExbB proton channel...      58  8e-08

     Aquifex aeolicus [aquificales] taxid 63363
    gi|15606982|ref|NP_214364.1| TolQ homolog [Aquifex aeolicu...      55  5e-07
    gi|15606823|ref|NP_214203.1| biopolymer transport exbB [Aq...      42  0.005


     Deinococcus radiodurans [eubacteria] taxid 1299
    gi|15805483|ref|NP_294179.1| biopolymer transport protein,...      47  1e-04

     Methanothermobacter thermautotrophicus str. Delta H [euryarchaeotes] taxid 187420
    gi|15679040|ref|NP_276157.1| biopolymer transport protein ...      43  0.002

     Synechocystis sp. PCC 6803 [cyanobacteria] taxid 1148
    gi|16329196|ref|NP_439924.1| biopolymer transport ExbB pro...      41  0.013
    gi|16329550|ref|NP_440278.1| biopolymer transport ExbB pro...      40  0.018

    Note below that *even* some proteobacteria ExbB proteins have "unimpressive" similarity scores and yet are still called ExbB proteins (as are some **archaeabacteria** ExbB-family proteins):

    Code Sample
    Photobacterium damselae subsp. piscicida [g-proteobacteria] taxid 38294
    gi|19577341|emb|CAD27898.1| ExbB protein [Photobacterium d...      33  1.9

     Plesiomonas shigelloides [enterobacteria] taxid 703
    gi|13774064|gb|AAG23397.1| ExbB [Plesiomonas shigelloides]         33  2.0

     Sulfolobus solfataricus [crenarchaeotes] taxid 2287
    gi|15899059|ref|NP_343664.1| Amino acid transporter, putat...      33  2.6


     Methanosarcina acetivorans C2A [euryarchaeotes] taxid 188937
    gi|20089242|ref|NP_615317.1| MotA/TolQ/ExbB proton channel...      33  3.4
    gi|20093212|ref|NP_619287.1| MotA/TolQ/ExbB proton channel...      33  3.8
    gi|20093420|ref|NP_619495.1| MotA/TolQ/ExbB proton channel...      32  6.7
    MotA and ExbB appear to have equally wide distributions

    The distribution taxonomy report for ExbB is, in fact, rather like the taxonomy report for standard protein blast of E. coli's MotA protein: lots and lots of enterobacteria and proteobacteria, and a few hits out in spirochetes and other various deeply divergent bacteria.

    Here is said taxonomy report

    Are we to conclude that MotA is just as likely to be of late origin and derived as ExbB?

    ...methinks the database may be a wee bit biased towards certain intensively-studied gram-negative bacteria groups and that therefore seeing many hits in those groups and few outside means very little in terms of relative significance.  As I showed, you have to put MotA and ExbB in the same distribution bucket regardless.

    Regarding low e-values:

    Based on your blanket skepticism of marginal e-values, you may want to argue that some MotA proteins are of independent origins and convergent on standard MotA's.  Many of these scores are non too impressive, yet some are MotAs (or PomA, a related motor) despite this:

    Code Sample
     Treponema denticola [spirochetes] taxid 158
    gi|4426945|gb|AAD20619.1| flagellar motor protein MotA [Tr...      53  3e-06

     Pseudomonas putida [g-proteobacteria] taxid 303
    gi|2853602|gb|AAC08066.1| MotA [Pseudomonas putida]                53  5e-06

     Leptospira interrogans serovar lai str. 56601 [spirochetes] taxid 189518
    gi|24213362|ref|NP_710843.1| Chemotaxis motA protein [Lept...      52  6e-06
    gi|24216276|ref|NP_713757.1| motility protein A [Leptospir...      39  0.056

     Bacillus anthracis str. A2012 [eubacteria] taxid 191218
    gi|21402555|ref|NP_658540.1| MotA_ExbB, MotA/TolQ/ExbB pro...      52  8e-06
    gi|21399546|ref|NP_655531.1| MotA_ExbB, MotA/TolQ/ExbB pro...      51  1e-05

     Shewanella oneidensis MR-1 [g-proteobacteria] taxid 211586
    gi|24375769|ref|NP_719812.1| chemotaxis motA protein [Shew...      51  1e-05
    gi|24373102|ref|NP_717145.1| chemotaxis motA protein [Shew...      38  0.13

     Thermotoga maritima [thermotogales] taxid 2336
    gi|15643440|ref|NP_228484.1| motility protein A [Thermotog...      50  3e-05

     Campylobacter jejuni [e-proteobacteria] taxid 197
    gi|15791705|ref|NP_281528.1| putative flagellar motor prot...      48  9e-05

     Rhodopseudomonas palustris [a-proteobacteria] taxid 1076
    gi|22963976|gb|ZP_00011582.1| hypothetical protein [Rhodop...      42  0.006

     Magnetococcus sp. MC-1 [proteobacteria] taxid 156889
    gi|22999422|gb|ZP_00043404.1| hypothetical protein [Magnet...      41  0.011
    gi|23000123|gb|ZP_00044067.1| hypothetical protein [Magnet...      33  3.5

     Vibrio alginolyticus [g-proteobacteria] taxid 663
    gi|3024412|sp|O06873|POMA_VIBAL Chemotaxis pomA protein >g...      40  0.038

     Bacillus halodurans [eubacteria] taxid 86665
    gi|15615802|ref|NP_244106.1| flagellar motor apparatus [Ba...      39  0.058

     Vibrio vulnificus CMCP6 [g-proteobacteria] taxid 216895
    gi|27363787|ref|NP_759315.1| Flagellar motor component Mot...      37  0.18

     Clostridium thermocellum ATCC 27405 [eubacteria] taxid 203119
    gi|23021959|gb|ZP_00061601.1| hypothetical protein [Clostr...      35  0.87

     Vibrio cholerae [g-proteobacteria] taxid 666
    gi|15640908|ref|NP_230539.1| chemotaxis protein PomA [Vibr...      32  5.6
    Regarding the e-values of archaeal ExbB homologs, PSI-BLAST on E. coli ExbB gives an archaeabacterial homolog with e-value of 2e-17, which ought to be good enough for Mike Gene:

    PSI-BLAST search

     Methanothermobacter thermautotrophicus str. Delta H [euryarchaeotes] taxid 187420
    gi|15679040|ref|NP_276157.1| biopolymer transport protein ...      90  2e-17
    gi|15678698|ref|NP_275813.1| unknown [Methanothermobacter ...      43  0.003
    gi|15678311|ref|NP_275426.1| protein kinase [Methanothermo...      33  3.4
    My point

    These kinds of things ought to at least be mentioned and discussed before reckless statements are made about absolutely no evidence for precursors to flagellar proteins, that's my only point.  For some reason you guys prefer to sweep it under the rug by unsupported arguments about ExbB's narrow distribution.  Just acknowledge that this little bit of the biological world is a bit disharmonious with the flagellum-was-specially-created thesis.  All I've been saying, and now documenting, is that ExbB homologs are at least as widely distributed as MotA, and possibly more widely distributed.

    Date: 2003/02/17 19:06:37, Link
    Author: niiicholas
    I'd forgotten that I'd accumulated these, they were posted originally in the ISCID immune system thread:

    Dr. Dembski writes:



    By your great mass of words and facts you've lost the train of the argument. The issue is not whether pieces exist for cooption (whether in the same organism or, with the immune system, even in different organisms) but whether those pieces can properly be coordinated to produce the final function in the IC system under examination. For cooption to work there has to be coordination. Design is known to have the capability to effect such coordination. You're claiming that natural selection does as well, but there is no evidence of that.
    There are no two ways about it, this is false.  I think that even Peonie and Mike Gene would agree  with me on this one.  There are dozens of examples of the origin of new genes and even multigene systems in either modern times or geologically recently enough that the direct evidence of natural selection remains in the genome, and *very* detailed pathways, on the level of individual nucleotide changes, have been traced in many instances.

    A few of the examples are described here.  

    Here is a list, just off the top of my head.  References can be found easily by searching PubMed so I trust you will not mind if for the purposes of space I just list some of the cases I know about without giving refs for all of them.

    The recent-origin Drosophila genes jingwei and sdic

    Nylon degradation genes (multiple independent origins)

    Recent origin of antifreeze genes in fish (and plants)

    Antibiotic and antipesticide genes

    Here is a case of the origin of an autotransporter (AT) gene, lav by domain shuffling; I quote just a bit, the whole rather long article with all of their documenting evidence is  freely online at pubmed:


    A mosaic origin for lav was inferred from a G+C content transition at the boundary of its presumed passenger domain with the linker and -barrel domains. Similarly, the junction of nonhomology between lav and las coincides with the G+C transition and inferred domain boundaries of both genes. On the basis of quite different evidence (discordance between phylogenies based on individual domains), Loveless and Saier have proposed that AT proteins evolve by domain shuffling (28). A functionally novel AT can arise by linking a new passenger activity to a generic -barrel pore. Our analysis provides independent evidence for the combinatorial origin and subsequent reshuffling of at least one AT protein.


    As biotype aegyptius strains and Int1 belong to different phylogenetic subgroups, it is unlikely that they inherited lav from a common ancestor. Rather, it is likely that the first H. influenzae clade to acquire the gene passed it to one or more other clades by transformation and homologous recombination within flanking DNA. Once a laterally transferred fragment has been acquired by a population of naturally transformable bacteria, it can readily be assimilated into the species by co-opting linked homologous sequence and uptake signals. Interstrain and interspecies transfer implies a shared selective advantage in certain host environments.
    For the evolution of multigene systems, even those with multiple-parts -required, see:

    Mortlock, R. P., editor (1992). The Evolution of Metabolic Function Boca Raton Fla., CRC Press, pp. 1-339.

    Table of contents:

    1) Experiments in the Evolution of Catabolic Pathways Using Modern Bacteria

    2) Natural and Experimentally Evolved Pathways for the Utilization of D-Arabinose in Enteric Bacteria

    3) The Development of a Catabolic Pathway for Ethylene Glycol

    4) Evolution of [alpha]-Aminoadipate Pathway for the Synthesis of Lysine in Fungi

    5) Common Ancestry of Escherichia coli Pyruvate Oxidase and the Acetohydroxy Acid Synthase of the Branched-Chain Amino Acid Biosynthetic Pathway

    6) Evolution of Bacterial Alcohol Metabolism

    7) Microbial Metabolism of Mandelate: Occurence, Function, Properties, and Evolution of Mandelate Dehydrogenases and Other Enzymes of the Mandelate Pathway

    8) Evolution of the Bacterial Phosphoenolpyruvate: Sugar Phosphotransferase System
    Section I: Physiologic and Organismic Considerations
    Section II: Molecular Considerations

    9) An Emerging Outline of the Evolutionary History of Aromatic Amino Acid Biosynthesis

    10) Life Before DNA: The Origin and Evolution of Early Archean Cells

    11) The Prebiotic Evolution of Complex Molecules: A Central Role for Catalyzed Cells
    ...and lots of articles published since 1992, e.g.:

    On atrazine resistance (lots of articles here)

    The degradation of pentachlorophenol by the recent assembly of a multiple-parts-required pathway, e.g.:

    Copley SD. Evolution of a metabolic pathway for degradation of a toxic xenobiotic: the patchwork approach. Trends Biochem Sci. 2000 Jun;25(6):261-5.

    Anandarajah K, Kiefer PM Jr, Donohoe BS, Copley SD. Recruitment of a double bond isomerase to serve as a reductive dehalogenase during biodegradation of pentachlorophenol. Biochemistry. 2000 May 9;39(18):5303-11.

    An even more sophisticated example is Johnson et al.'s (2002) article, "Origins of the 2,4-Dinitrotoluene Pathway". 2,4-dinitrotoluene (DNT) is another recently human-introduced compound, and yet bacteria have assembled a quite  complex pathway for its degradation. The summary of the reconstructed evolution of the pathway is also quite complex (and detailed):

    Inferences from the comparison of the structural genes of the 2,4-DNT pathway suggest that the pathway came together from three sources. The initial dioxygenase appears to have originated from a naphthalene degradation pathway like that of strain U2 (17). A large portion of the salicylate hydroxylase oxygenase component is retained but is not functional. The MNC monooxygenase was probably derived from a pathway for degradation of chloroaromatic compounds. The presence of the vestigial (with respect to 2,4-DNT degradation) ortho-ring fission dioxygenase is consistent with its recruitment from a pathway for chloroaromatic compounds. The true ring fission enzyme for 2,4-DNT degradation has a different origin. The sequence of DntD is quite dissimilar to all other described meta-ring fission enzymes, including those from naphthalene and chloroarene degradative pathways. The distinctive sequence of the ring cleavage enzyme reflects the substrate specificity observed for the THT oxygenase (28). The distant relationship between homogentisate dioxygenase and DntD and the association with homologs from amino acid metabolism (dntE and dntG) indicate that the lower pathway operon arose from a gene cluster for amino acid degradation.

    The disparate origins of the various dnt and associated genes described in this study are consistent with the difficulties that bacteria face to achieve efficient metabolism of synthetic compounds like 2,4-DNT. The organization of the pathway  genes suggests there is a progression towards a compact region en-coding the entire pathway. In that progression, remnants from assembly persist, such as the benzenetriol oxygenase (ORF3), putative maleylacetate reductase (ORF10), and putative trans-posase (ORF4). No role in nitroarene degradation is apparent for the remnants; their presence might indicate an intermediate point in the evolution of an optimal system or perhaps some of the proteins could be used in other pathways when another substrate is available.
    And numerous review articles that review the topic of cooption:

    Otto SP, Yong P. The evolution of gene duplicates. Adv Genet 2002;46:451-83 Related Articles,  Links  

    Betran E, Long M. Expansion of genome coding regions by acquisition of new genes. Genetica. 2002 May;115(1):65-80.

    Kondrashov FA, Rogozin IB, Wolf YI, Koonin EV. Selection in the evolution of gene duplications. Genome Biol 2002;3(2):RESEARCH0008  (free online)

    Eizinger A, Jungblut B, Sommer RJ. Evolutionary change in the functional specificity of genes. Trends Genet 1999 May;15(5):197-202

    Hughes A. Adaptive evolution after gene duplication. Trends Genet 2002 Sep;18(9):433

    Ganfornina MD, Sanchez D. Generation of evolutionary novelty by functional shift. Bioessays. 1999 May;21(5):432-9.

    Long M. Evolution of novel genes. Curr Opin Genet Dev 2001 Dec;11(6):673-80

    True JR, Carroll SB. Gene Co-Option in Physiological and Morphological Evolution. Annu Rev Cell Dev Biol. 2002

    Here's a case of cooption in a slightly different sense, but returning to one of my original points: microbes "designed" to subvert the immune system:


    Immunology 2001 Jan;102(1):2-7
    Co-option of endocytic functions of cellular caveolae by pathogens.
    Shin JS, Abraham SN.

    It is increasingly becoming clear that various immune cells are infected by the very pathogens that they are supposed to attack. Although many mechanisms for microbial entry exist, it appears that a common route of entry shared by certain bacteria, viruses and parasites involves cellular lipid-rich microdomains sometimes called caveolae. These cellular entities, which are characterized by their preferential accumulation of glycosylphosphatidylinositol (GPI)-anchored molecules, cholesterol and various glycolipids, and a distinct protein (caveolin), are present in many effector cells of the immune system including neutrophils, macrophages, mast cells and dendritic cells. These structures have an innate capacity to endocytoze various ligands and traffic them to different intracellular sites and sometimes, back to the extracellular cell surface. Because caveolae do not typically fuse with lysosomes, the ligands borne by caveolar vesicles are essentially intact, which is in marked contrast to ligands endocytozed via the classical endosome-lysosome pathway. A number of microbes or their exotoxins co-opt the unique features of caveolae to enter and traffic, without any apparent loss of viability and function, to different sites within immune and other host cells. In spite of their wide disparity in size and other structural attributes, we predict that a common feature among caveolae-utilizing pathogens and toxins is that their cognate receptor(s) are localized within plasmalemmal caveolae of the host cell.
    In other words, like the evidence for the evolution of the immune system, the evidence for cooption by natural processes has gobbs of evidence and literature behind it.  Yet Dembski asserts that there is "no evidence" for it.  


    The only evidence is of isolated pieces waiting to be coordinated. That's why I insist on **detailed** Darwinian pathways (and no, you haven't provided them). Pathways are continuous trajectories that connect the dots. The issue is not whether the dots are in place but how to connect them.
    The previous claim of the IC argument was that the dots couldn't exist because they wouldn't be functional.  Now you're conceding that they exist, but quibbling over how "detailed" the reconstructed pathways are, and yet you still refuse to explicitly say what counts as "detailed" for you or to justify that level of detail as an appropriate standard of judgement of evolutionary explanations.  The goalposts are on wheels.  The standard in science is clear however: testability and passed tests, and this is the one I advocate, and which I think all evolutionary immunologists would argue is being successfully applied in the field.  Compared to "IDdidit" (where's your details there, Dr. Dembski?) the reconstructed origin of the immune system is quite detailed, and getting more so all of the time.


    You've offered no evidence that natural selection can do that -- or is your evidence simply that it couldn't have been design and therefore natural selection is all that's left? That sounds like an argument from ignorance.
    Nope, the known natural processes of mutation and selection make predictions about what should be seen in the data, which I outlined in a previous post, and in this thread I'm arguing that the evidence and the literature on the origin of the IC immune system supports those predictions.  Some have made suggestions in the thread that, basically, maybe ID did it even though it looks like natural processes (employing small changes, cooption etc. predicted by RM&NS) were responsible; this cannot of course be ruled out, but my point is that ID does not *predict* these observations while RM&NS does.

    Date: 2003/02/17 20:12:31, Link
    Author: niiicholas
    Old posts on the topic:

    Mot homologies in context of Musgrave's Flagellum FAQ

    The bacterial flagellum evolved (scroll down to get the best post)

    Beating a dead horse, or, flagellating the flagellum

    Evolving the Bacterial Flagellum by Mike Gene (and unfortunately, MG's essay still hasn't been finished as far as I can tell)

    Date: 2003/02/17 22:06:54, Link
    Author: niiicholas
    Link to:

    ARN discussion

    Date: 2003/02/18 18:45:12, Link
    Author: niiicholas
    Heh.  Check this out.  I never spent much time on the nonstructural components of the bacterial flagellum, since pretty much everyone focuses on the structural parts, but Dembski in his recent essay apparently was getting nervous that too many structural parts had been given alternative functions, and so he made reference to all of the nonstructural genes involved.

    So I did a search on chemotaxis genes.  Look what I found:


    Mol Biol Evol 2000 Dec;17(12):1956-70
    Evolution of two-component signal transduction.

    free full article online

    Koretke KK, Lupas AN, Warren PV, Rosenberg M, Brown JR.

    SmithKline Beecham Pharmaceuticals, Collegeville, Pennsylvania 19426-0989, USA.

    Two-component signal transduction (TCST) systems are the principal means for coordinating responses to environmental changes in bacteria as well as some plants, fungi, protozoa, and archaea. These systems typically consist of a receptor histidine kinase, which reacts to an extracellular signal by phosphorylating a cytoplasmic response regulator, causing a change in cellular behavior. Although several model systems, including sporulation and chemotaxis, have been extensively studied, the evolutionary relationships between specific TCST systems are not well understood, and the ancestry of the signal transduction components is unclear. Phylogenetic trees of TCST components from 14 complete and 6 partial genomes, containing 183 histidine kinases and 220 response regulators, were constructed using distance methods. The trees showed extensive congruence in the positions of 11 recognizable phylogenetic clusters. Eukaryotic sequences were found almost exclusively in one cluster, which also showed the greatest extent of domain variability in its component proteins, and archaeal sequences mainly formed species-specific clusters. Three clusters in different parts of the kinase tree contained proteins with serine-phosphorylating activity. All kinases were found to be monophyletic with respect to other members of their superfamily, such as type II topoisomerases and Hsp90. Structural analysis further revealed significant similarity to the ATP-binding domain of eukaryotic protein kinases. TCST systems are of bacterial origin and radiated into archaea and eukaryotes by lateral gene transfer. Their components show extensive coevolution, suggesting that recombination has not been a major factor in their differentiation. Although histidine kinase activity is prevalent, serine kinases have evolved multiple times independently within this family, accompanied by a loss of the cognate response regulator(s). The structural and functional similarity between TCST kinases and eukaryotic protein kinases raises the possibility of a distant evolutionary relationship.


    Two-component signal transduction (TCST) pathways form the central signaling machinery in bacteria (for reviews, see Stock, Ninfa, and Stock 1989 ; Parkinson and Kofoid 1992 ; Hoch and Silhavy 1995 ). In response to a stimulus, typically extracellular, the kinase component autophosphorylates at an internal histidine (the H-box). The high-energy phosphate group is then transferred to an aspartyl residue on the response regulator component (hence, "two-component" signal transduction), which modifies cellular behavior via an effector domain (fig. 1 ). Although most systems use a linear phosphorelay from one kinase to one response regulator, some use more complicated paths, involving a branching of the signal (chemotaxis) or multiple phosphorylated components (sporulation, adaptation to anaerobic conditions).

    Code Sample

    [b]Fig. 1.[/b]—Schematic diagram illustrating phosphorelay in two-component signal transduction systems. The signal (usually coming from the extracellular environment) is transduced to the "linker" region, which is located adjacent to the last transmembrane helix of the membrane-bound protein. The linker interacts with the kinase domain to induce autophosphorylation at a histidine (shown in red) located in the His-box domain or—in [b]CheA[/b]—in the Hpt domain. The phosphate is then transferred to an aspartate residue (shown in red) in a response regulator domain. The phosphorylated response regulator elicits the appropriate response within the cell (typically via the DNA-binding activity of an effector domain). In some systems, an Hpt domain serves as a regulatory phosphate sink for the phosphorylated response regulator

    In bacteria, TCST systems mediate adaptive responses to a broad range of environmental stimuli. These include citrate uptake and catabolism (Cit), aerobic respiration (Arc), osmoregulation (EnvZ/OmpR), stress-induced sporulation (Kin/Spo), N-acetylmuramoyl-l-alanine amidase biosynthesis (Lyt), nitrate and nitrite metabolism (Nar), nitrogen regulation (Ntr), phosphate regulation (Pho), host recognition for pathogen invasion (Vir), and chemotaxis (Che) (Stock, Ninfa, and Stock 1989 ; Parkinson and Kofoid 1992 ; Hoch and Silhavy 1995 ). TCST systems also exist in certain nonanimal eukaryotes and in some Archaea (Alex and Simon 1994 ; Loomis, Shaulsky, and Wang 1997). In plants, they mediate photosensitivity (Schneider-Poetsch et al. 1991 ; Yeh and Lagarias 1998 ) and ethylene response (Chang et al. 1993 ); in fungi, they mediate osmoregulation (Maeda, Wurgler-Murphy, and Saito 1994 ; Krems, Charizanis, and Entian 1996 ; Posas et al. 1996 ) and hyphal development (Alex, Borkovich, and Simon 1996 ; Alex et al. 1998 ); and in the slime mold, they mediate Dictyostelium discoideum osmoregulation (Schuster et al. 1996 ) and fruiting body formation (Singleton et al. 1998 ). A thorough cataloguing of protein kinases found in the genome of the nematode Caenorhabditis elegans failed to find any true orthologs to prokaryotic histidine kinases, which suggests that TCST systems do not occur in metazoans (Plowman et al. 1999 ).


    An exception to the phosphorelay described here is found in the chemotaxis kinase CheA, where the H-box has lost the catalytic histidine and is used exclusively for dimerization, while an Hpt domain that may have originally served a regulatory function is now used for phosphorelay to CheY and CheB (Bilwes et al. 1999 ; Dutta, Qin, and Inouye 1999 ). Further variability in His-acceptor domains is seen in the Spo0B protein, whose H-box domain forms a dimeric four-helix bundle similar to canonical H-boxes but of opposite handedness (Varughese 1998 ).

    In addition to the three phosphorelay domains described above, a fourth domain conserved broadly in TCST systems has recently been recognized (Park and Inouye 1997 ; Aravind and Ponting 1999 ). Termed the "linker" region (or HAMP domain), it is typically found at the C-terminal end of the last transmembrane segment in many histidine kinases, chemoreceptors, bacterial nucleotidyl cyclases, and phosphatases, and mutations show that it plays a critical role in signal transduction. Some proteins contain multiple copies in tandem, suggesting that it represents an autonomously folding unit. Its ability to regulate kinase activity in trans (e.g., between chemoreceptors and CheA) and the variable nature of the segments connecting it to the H-box suggest that it acts through direct interaction with the kinase domain rather than through propagation of conformational change along the polypeptide chain. Thus, four protein domains appear to be typically involved in the signal transduction pathway from the extracellular sensor domain to the cytoplasmic effector (fig. 1 ).

    TCST systems represent one of the most studied and best understood areas of bacterial physiology. Recently, they have also emerged as attractive targets for anti-microbial drug development (Barrett et al. 1998 ; Lange et al. 1999 ; Throup et al. 2000). Here we report the results of a detailed phylogenetic and structural study of genomic TCST sequences, undertaken to explore the origin and evolution of TCST systems.


    Several interesting observations follow from the phylogenetic clusters presented here: No cluster contained proteins from both Archaea and eukaryotes, although a specific evolutionary relationship has long been postulated between these two groups (reviewed in Brown and Doolittle 1997 ). Bacterial phylogeny similarly did not correlate well with the observed clustering. Despite the considerable sizes of some clusters, none contained representatives from each bacterial species, and no bacterium had a representative in all of the clusters. Among bacteria, no cluster predominated across all species: Pho contained nearly a third of all TCST proteins detected in E. coli, B. subtilis, and Synechocystis and two thirds of those in M. tuberculosis, but none from spirochetes. In the latter, Che which is missing from A. aoelicus and M. jannaschii, was predominant (even though both organisms encode flagellar proteins and are motile). [a little garbled, I think this means these particular guys don't have Che proteins, e.g.:

    "Among the Archaea, Methanobacterium thermoautotrophicum and Archaeoglobus fulgidus contained the largest numbers of histidine kinases (16 and 14, respectively) and response regulators (10 and 11, respectively), although they still contained fewer than free-living bacteria. Pyrococcus horikoshii had only a single histidine kinase and two response regulators (corresponding to the chemotaxis proteins CheA, CheY, and CheB), while Methanococcus jannaschii, Aeropyrum pernix, and Thermoplasma acidophilum had none. "]

    Origin of the Histidine Kinase Fold
    Response regulators are not recognizably related to other known protein families beyond a general structural similarity to P-loop NTPases (such as Ras) (Lukat et al. 1991 ; Stock et al. 1993 ), which has hitherto not been considered sufficient to infer homology. Histidine kinases, however, are clearly related to Hsp90, MutL, and type II topoisomerases in the ATP-binding domain (Tanaka et al. 1998 ; Bilwes et al. 1999 ; Dutta, Qin, and Inouye 1999 ). The conserved structural core consists of an antiparallel, four-stranded ß-sheet flanked on one side by three -helices, which surround the ATP-binding site. In addition, an ß element, which is in an equivalent structural position, is circularly permuted in the sequence of histidine kinases relative to other proteins with this fold. The structural similarity is mirrored in a set of conserved sequence motifs, primarily associated with nucleotide binding, which strongly imply descent from a common ancestor (fig. 4A ). Phylogenetic analysis of the sequence data by distance methods indicates that all kinases in this superfamily arose from a single ancestral protokinase (fig. 4B ). Because of the low branch point of PDKs, it is unclear whether this ancestor had Ser- or His-phosphorylating activity.

    Histidine Kinases and Response Regulators Have Coevolved

    In this study, we analyzed the phylogenetic relationships between the TCST systems from 14 complete and 6 partial genomes. Their components represent highly evolved multigene families, and the pattern and process of proliferation of such interacting yet structurally unrelated proteins is an important problem in evolutionary biology. A priori, two competing models for the evolution of novel TCST systems appear plausible: the recruitment model and the coevolution model. The recruitment model suggests that novel TCST systems evolve through gene duplication of one component, which then co-opts components from heterologous systems to yield a new specificity. This model is supported by the structural similarity of response regulators, in which only a few residues are sufficient to determine specificity, and by the observed crosstalk of TCST systems within an organism. From the phylogenetic perspective, this mechanism would result in an incongruent clustering of cognate histidine kinases and response regulators. The coevolution model suggests that novel TCST systems evolve by global duplication of all their components and subsequent differentiation. This model is supported by the fact that many TCST systems are concurrent on the chromosome. Phylogenetically, this mechanism would produce congruent gene trees for histidine kinases and response regulators.

    Our results support the coevolution model. Despite the large number of proteins considered, which limited the resolution of the analysis by lowering the ratio of aligned residues to OTUs, the trees obtained for the histidine kinase and response regulator domains showed congruent clustering (fig. 2 ). Although the precise evolutionary relationships between clusters were not supported by strong bootstrap values, the overall topology of the NJ histidine kinase tree was verified by heuristic search results for the minimal-length MP tree. No such support was obtained for the response regulator tree, which had a lower resolution, but its validity was verified by the occurrence of two superclusters (Arf/Cit/CheY/Lyt and Nar/Mth) that were also found in the histidine kinase tree. The clusters themselves were statistically much more robust, with over half receiving bootstrap support of >50% in the distance-based analysis. As required by the coevolution model, pairs of histidine kinases and response regulators that are known to interact were overwhelmingly found in cognate clusters, as were 89% of histidine kinase and response regulator pairs that are linked on the chromosome (fig. 3 ). Coevolution has previously been proposed for eukaryotic TCST proteins, as well as for two hybrid kinases of E. coli (BarA and RcsC) (Pao and Saier 1997 ). Hybrid kinases, however, also provide evidence for a recruitment mechanism at work. For example, four of the five hybrid kinases of E. coli (ArcB, TorS, RcsC, and EvgA) are known to signal through response regulators found in noncognate clusters, and the fifth one, BarA, is thought to do so as well (via OmpR, found in the Pho cluster) (Hoch and Silhavy 1995 ). Recruitment is also observed in the chemotaxis and sporulation systems. Nevertheless, coevolution appears to be the strongly predominant mechanism by which novel TCST systems arise. Similar patterns of molecular coevolution have been observed in other interacting proteins, such as neuropeptides and their receptors (Darlinson and Richter 1999 ) and chaperonin subunits (Archibald, Logsdon, and Doolittle 1999 ).

    Coevolution is not limited to TCST proteins, but also extends to the domains forming them. Both domain shuffling and domain swapping are comparatively rare events, and, with few exceptions, response regulators having homologous carboxyl-terminal domains were found within one cluster. These results agree well with a previous study performed on 49 bacterial response regulators by Pao and Saier (1995) , who found that classes of response regulators, defined by homology of their carboxyl-termini, generally formed distinct phylogenetic clusters. Pao and Saier's (1995) classes 1–5 correspond—in order—to our phylogenetic clusters Ntr, Pho, Nar, CheB, and Hybrid; classes 6 and 7 were phylogenetically heterogeneous in both studies.

    Histidine Kinases and Eukaryotic Protein Kinases—Homology or Analogy?
    A distance-based phylogenetic analysis of proteins containing a histidine kinase–like ATP-binding domain, which include type II topoisomerases, Hsp90, and MutL, indicated that all kinase domains with this fold are monophyletic and confirmed that the PDKs form an outgroup to the histidine kinase clade (fig. 4B ). Searches for more distantly related proteins surprisingly suggested a similarity to the small lobe of protein kinases, which is also involved in ATP binding. The structurally similar region covers virtually the entire conserved core of both folds but is circularly permuted in the protein kinase small lobe (fig. 5A ). The amino- and carboxyl-termini of the histidine kinase fold are in close proximity, however (a prerequisite of circular permutation), and circular permutation events have been documented in the evolution of many protein folds (see the SCOP database at; Lo Conte et al. 2000 ), including the histidine kinase fold (Bilwes et al. 1999 ). Although the protein kinase small lobe is part of the so-called ATP-grasp fold (jointly with the peptide-binding large lobe), a recent structural analysis by Grishin (1999) has concluded that only the large lobe is homologous among the members of this fold, with the small lobe having been recruited among structurally similar but unrelated proteins. Our analysis supports an independent evolutionary origin of the small and large lobes of eukaryotic protein kinases.

    Despite the fact that the structural similarity between histidine kinases and protein kinases is remote, the signaling pathways in which the two types of kinase operate present intriguing similarities. Both form homodimers, which phosphorylate in trans and generally contain an extracellular sensory domain, which binds signaling molecules asymmetrically at the subunit interface. They have a common mode of signal transduction, as shown by the phytochromes Phy1 and Phy2 of the moss Ceratodon purpureus, which are 90% identical in the chromophore-binding domain, yet signal through protein kinase and histidine kinase domains, respectively (fig. 5C ). Functional chimeras have also been constructed between the sensory domain of the Tar chemoreceptor and both protein and histidine kinases (Moe, Bollag, and Koshland 1989 ; Utsumi et al. 1989). Finally, as discovered recently, both kinase types use adaptors with an SH3-fold for interaction with other proteins (Bilwes et al. 1999 ). Similar parallels can be drawn between response regulators and the Ras family of G-proteins (Lukat et al. 1991 ). Not only are both encoded by large multigene families, linking different sensory inputs to specific effector outputs, but they are both activated by a high-energy phoshoanhydride bond. Their striking structural similarity, particularly in the active site, has previously been interpreted as evidence for homology rather than analogy (Artymiuk et al. 1990 ). Although each of these similarities may have arisen by convergent evolution, the combination of structural and functional parallels that can be drawn throughout signaling pathways in bacteria and eukaryotes suggest that a prototypical signal transduction pathway may already have existed in the last common ancestor and that this pathway utilized protein phosphorylation. If so, yet a third group of kinases (possibly showing similarly profound structural changes) remains to be discovered in Archaea, where bacterial- and eukaryotic-type kinases are rare and clearly acquired by horizontal transfer.
    (bolds added)

    My brief summary: some good hints about the ultimate origin of histidine kinases, some faint hints about the ultimate origin of response regulators, but: clear evidence that key flagellar chemotaxis proteins served a multitude of other roles prior to being flagellar.

    Date: 2003/02/19 03:09:08, Link
    Author: niiicholas
    In the "just how precise would the organization of flagellum operons really have to be to get a minimal functioning flagellum?" category:


    Kalir S, McClure J, Pabbaraju K, Southward C, Ronen M, Leibler S, Surette MG, Alon U.

    Ordering genes in a flagella pathway by analysis of expression kinetics from living bacteria.

    Science. 2001 Jun 15;292(5524):2080-3.

    The recent advances in large-scale monitoring of gene expression raise the challenge of mapping systems on the basis of kinetic expression data in living cells. To address this, we measured promoter activity in the flagellar system of Escherichia coli at high accuracy and temporal resolution by means of reporter plasmids. The genes in the pathway were ordered by analysis algorithms without dependence on mutant strains. The observed temporal program of transcription was much more detailed than was previously thought and was associated with multiple steps of flagella assembly.


    The precise order of transcription of the various operons is probably not essential for assembling functional flagella. This is suggested by complementation experiments in which the motility of flagella mutants was
    rescued by expression of the wild-type gene from a foreign promoter (1). The detailed transcription order could, however, function to make flagella synthesis more efficient, be-cause parts are not transcribed earlier than
    needed. (p.2082)

    Date: 2003/02/20 01:34:35, Link
    Author: niiicholas
    There is a certain sad irony here, and I'm not talking about meningitis being a disease of the brain...


    SFI Working Paper Abstract

    Title: Two-Tiered Evolution of “Neiserria meningitis”: How Within-Host Ecology and Between-Host Epidemiology Expedite Phase Shifting
    Author(s): Lauren W. Ancel, Bruce R. Levin, Anthony R. Richardson, and Igor Stojiljkovic

    Abstract: Many so-called pathogenic bacteria make their living as commensals or even symbionts of the hosts that they colonize. Bacteria such as “Neiserria Meningitidis,” “Haemophilus influenzae,” “Staphylococcus aureus (1),” “Streptococcus pneumoneae,” “Helicobacter pylori,” and “Echerichia coli” are far more likely to colonize and maintain their populations in healthy individuals, asymptomatically, than to cause disease. Moreover, the members of these otherwise benign or beneficial species that are actually responsible for diseases like meningitis and sepsis, are not transmitted to new hosts and are therefore at an ecological and evolutionary dead-end. This implies that the virulence factors responsible for the pathogenicity of these bacteria must evolve in response to selection pressures other than those for causing disease. What are these pressures? Here we consider “Neisseria meningitidis”--a common member of the commensal flora of the nasal pharyngeal passages of humans that is also responsible for sporadic and epidemic meningitis. We focus on the evolution of phase shifting--a mutational process that turns genes on and off and, in particular, genes that code for virulence determinants such as pili, lipopolysaccharide, capsular polysaccharide, and outer membrane proteins.

    Using mathematical models, we offer two testable hypotheses: First, within a single human host, fast phase shifting leads to virulence. And second, although virulence may be disadvantageous within the framework of a single host, fast phase shifting may evolve in response to selection operating at a multihost epidemiological level. We discuss avenues for empirically testing these hypotheses and the implications of this work for the evolution of virulence in general.

    Keywords: evolution, epidemiology, mutation rate, phase shifting, virulence, Neisseria meningitis

    Date: 2003/02/20 02:10:10, Link
    Author: niiicholas
    [cross-posted to t.o. and AE]

    The release of this *can't* be accidental.  I don't think the DI has ever published a random "let's restate our same old arguments for no explicit reason" article like this.  But "Media Advisory on Evolution Controversies" is a particularly oblique term methinks.

    And any mention of the Stevolutionists is conspicuous by it's absence.

    Perhaps they've been getting a few skeptical calls from press people?
    Media Advisory on Evolution Controversies

    Discovery Institute
    Press Release
    February 19, 2003
    Contact: Mark Edwards, 206-292-0401 x 107

    As you report on controversies over evolution and intelligent design, here are some facts you might find useful:

    1. There is a growing scientific controversy over Darwinian evolution.

    a) Today there are critics of Darwinian evolution within the scientific community, including biologists at mainstream American universities. In 2001, more than 100 scientists including scholars at such institutions as Yale, Princeton, MIT, and the Smithsonian signed a public statement announcing that they were "skeptical of claims for the ability of random mutation and natural selection to account for the complexity of life. Careful examination of the evidence for Darwinian theory should be encouraged." [A complete list of these scientists can be found in A Scientific Dissent from Darwinism.]

    b) Because of the scientific critics of Darwin's theory, it is misleading to present the modern controversy over Darwinian evolution as a simplistic battle between "science" and "religious fundamentalists." Accurate reporting on this issue should do justice to the complexities of the real situation, not resurrect stereotypes from the fictional movie Inherit the Wind.

    2. It is constitutional and legal for teachers to teach about the scientific controversies surrounding Darwinian evolution.

    a) The courts have frowned upon raising religious objections to evolution in science classrooms, but these legal restrictions are irrelevant to discussions of scientific controversies over evolution.

    b) According to law professor David DeWolf, co-author of the leading law review article about how to teach the evolution controversy legally, there is absolutely no constitutional problem with acquainting students with scientific criticisms of Darwin's theory currently being made by scientists. [See David DeWolf et. al., Teaching the Origins Controversy: Science, Or Religion, Or Speech? Utah Law Review (2000)].

    "Teaching a variety of scientific theories about the origins of humankind to schoolchildren might be validly done with the clear secular intent of enhancing the effectiveness of science instruction."
    - U.S. Supreme Court, Edwards vs. Aguillard Ruling (1987)

    3. The failure of biology curricula to discuss the weaknesses as well as the strengths of Darwin's theory is attracting increased criticism from educators, scientists, and the general public.

    a) According to biology professor Scott Minnich of the University of Idaho, Darwinian evolution has become "the exceptional area that you can't criticize" in science education, something he considers "a bad precedent." In his view, we need to "teach it more, and teach it critically."

    b) According to a 2001 Zogby Poll, an overwhelming majority of Americans (71%) believe that "biology teachers should teach Darwin's theory of evolution, but also the scientific evidence against it."

    c) Recent scientific reports have shown that some of the most common scientific proofs for Darwin's theory that are cited in high school and college textbooks are now widely known to be flawed, notably Haeckel's embryos and the Peppered Moth experiments [see linked NY Times' articles].

    4. Federal education policy as articulated by Congress now calls for an balanced approach when teaching about controversial scientific topics such as evolution.

    a) In the Conference Report to the landmark No Child Left Behind Act of 2001, Congress clearly advised states to provide for the balanced treatment of controversial scientific issues like evolution. According to Congress, "where topics are taught that may generate controversy (such as biological evolution), the curriculum should help students to understand the full range of scientific views that exist, why such topics may generate controversy, and how scientific discoveries can profoundly affect society." (This language originally came from Sen. Rick Santorum , R-PA, and is sometimes called The Santorum Amendment.)

    b) U.S. Senator Robert Byrd (Dem-WV) expressed the sentiments of many lawmakers when he declared that "it is important that students be exposed not only to the theory of evolution, but also to the context in which it is viewed by many in our society. If students cannot learn to debate different viewpoints and to explore a range of theories in the classroom, what hope have we for civil discourse beyond the schoolhouse doors?" [Congressional Record, June 13, 2001]

    5. Darwin himself would have likely agreed to a 'teach the controversy' approach.

    In The Origin of Species Darwin wrote: "A fair result can be obtained only by fully stating and balancing the facts and arguments on both sides of each question."

    Can teachers discuss the scientific controversy over Darwinian theory? Yes, in fact, good education demands it.

    About Discovery Institute

    Discovery Institute is non-profit, non-partisan policy and research organization on issues from transportation to technology to tax policy. In science education, it supports a "teach the controversy" approach to Darwinian evolution. Its Center for Science and Culture has more than 40 affiliated biologists, biochemists, physicists, philosophers and historians of science, and public policy and legal experts, most of whom also have positions with colleges and universities.

    -------------------------------------------------------------------------------Discovery Institute is a non-profit, non-partisan, public policy think tank headquartered in Seattle dealing with national and international affairs. The Institute is dedicated to exploring and promoting public policies that advance representative democracy, free enterprise and individual liberty. For more information visit Discovery's website at

    Please report any errors to

    Date: 2003/02/20 22:54:56, Link
    Author: niiicholas

    J Bacteriol 2003 Mar;185(5):1624-33
    Role of the Cytoplasmic C Terminus of the FliF Motor Protein in Flagellar Assembly and Rotation.

    Grunenfelder B, Gehrig S, Jenal U.

    Division of Molecular Microbiology, Biozentrum, University of Basel, CH-4056 Basel, Switzerland.

    Twenty-six FliF monomers assemble into the MS ring, a central motor component of the bacterial flagellum that anchors the structure in the inner membrane. Approximately 100 amino acids at the C terminus of FliF are exposed to the cytoplasm and, through the interaction with the FliG switch protein, a component of the flagellar C ring, are essential for the assembly of the motor. In this study, we have dissected the entire cytoplasmic C terminus of the Caulobacter crescentus FliF protein by high-resolution mutational analysis and studied the mutant forms with regard to the assembly, checkpoint control, and function of the flagellum. Only nine amino acids at the very C terminus of FliF are essential for flagellar assembly. Deletion or substitution of about 10 amino acids preceding the very C terminus of FliF resulted in assembly-competent but nonfunctional flagella, making these the first fliF mutations described so far with a Fla(+) but Mot(-) phenotype. Removal of about 20 amino acids further upstream resulted in functional flagella, but cells carrying these mutations were not able to spread efficiently on semisolid agar plates. At least 61 amino acids located between the functionally relevant C terminus and the second membrane-spanning domain of FliF were not required for flagellar assembly and performance. A strict correlation was found between the ability of FliF mutant versions to assemble into a flagellum, flagellar class III gene expression, and a block in cell division. Motile suppressors could be isolated for nonmotile mutants but not for mutants lacking a flagellum. Several of these suppressor mutations were localized to the 5' region of the fliG gene. These results provide genetic support for a model in which only a short stretch of amino acids at the immediate C terminus of FliF is required for flagellar assembly through stable interaction with the FliG switch protein.

    Date: 2003/02/21 02:47:25, Link
    Author: niiicholas
    Martino Rizzotti published a book, Early Evolution, in 2000, which presents a reasonably detailed scenario deriving the flagellum from an F1F0 ATPase.  Compared to other options it is not particularly convincing, although he does rather better at it than one might otherwise expect.

    But, it is published, here are some online links:

    Google search

    Cavalier-Smith was fairly critical of the book in his review, but does cite the flagellum scenario in passing in one of his articles.


    Date: 2003/02/24 20:18:43, Link
    Author: niiicholas
    Online here:

    Evolution and Ant Agriculture: a response to Ilíon.

    Some of his other posts:
    Successful predictions of evolutionary theory

    Here's da whole thing:

    In the "Still Spinning Just Fine" thread, Ilíon brought to our attention the purportedly co-evolved ant-fungus-mold-bacterium system as a case that presents difficulties for the traditional Darwinian paradigm.  As an ant evolution researcher, I am of the opinion that the ant/fungus/mold/bacterium relationship is fascinating regardless of one's perspective, and think that the topic merits its own thread.  I also happen to think that much of what we know about the workings (and even the existence) of this complex relationship is a direct consequence of the use of Darwinian theory by biologists, and I echo Marc's sentiments that the system is a fine example of evolutionary biology in practice.

    This is a long post, and it has the following structure:

    • 1. Short ant/fungus background.
    • 2. The role of evolutionary theory in ant/fungus research.
    • 3. Some quibbles over technical issues.
    • 4. Overview of evidence for common descent and natural selection in the ant/fungus/mold/bacteria system.

    1. Quick background.

    In a nutshell, there are some 200+ species of ants in the new world tropics that are obligate fungivores. These are mostly small, inconspicuous ants, but the group also includes the famous and economically important leaf-cutter ants.  These ants are involved in a largely mutualistic relationship with a fungus.  The fungus is eaten by the ants, but the fungus also depends on the ants for its propogation: a true agricultural system.  In the past 4 years, a twist has been discovered: an Escovopsis mold that is a specialized parasite of the ant fungus, and a Streptomyces bacterium that produces an antibiotic that the ants use to combat the parasitic Escovopsis.

    The attine ants

    The discovery of the Streptomyces

    Ulrich Mueller's publications

    photo gallery of Atta leaf-cutters and gardens

    photo gallery of Acromyrmex leaf-cutters

    photo gallery of Mycocepurus, a more "primitive" attine.

    (note, the final three links are shameless self-promotion of my brand-new web site)

    2. The role of evolutionary theory in ant/fungus research.

    To say that most of what we know about fungus-growing ants and their fungi stems directly or indirectly from evolutionary research would not be an exaggeration. To say that everything we know about the Escovopsis parasite is due to evolutionary research is a simple, observational truth.

    I bring this up because Ilíon wrote:      
    "Why are 'evolutionary biologists scratching their heads?' Aside from the obvious interesting questions, I think it's because the facts don't fit the paradigm"
    I have a hard time believing that the facts cause problems for the paradigm, because "the facts" to which Ilíon refers wouldn't even be known if it weren't for the Darwinian paradigm in the first place.  Escovopsis was re-discovered, and the details of its biology were described, as the result of research into a widely-held idea that contradicted Darwinian theory.  The following passage is from the introduction to the pioneering study:

    "The longstanding assumption that ant fungal gardens are free of significant pathogenic pressure is surprising because it contradicts some fundamental theories of the evolution of parasitism... To resolve the conflict between the theoretical prediction that parasites should exist in the clonal attine fungicultural systems and the widespread yet untested belief that ants maintain their gardens free of parasites, we conducted an extensive examination of fungal parasitism of gardens of attine ants."

    Source: Currie, C.R., U.G.Mueller, and D. Malloch. 1999. The agricultural pathology of ant fungus gardens. Proc.Nat.Acad.Sci.USA. 96:7998-8002. (Download pdf)
    Briefly, evolutionary theory predicted that there should be serious parasites of this system as a consequence of prolonged asexual reproduction.  So these researchers- primarily Currie, a graduate student at the time- went chasing a Darwinian notion and discovered Escovopsis.

    But this discovery is just the tip of the iceberg.  Biologists have flocked to the attine/fungus system because the system raises so many interesting evolutionary issues, some of which may be easily resolved and others of which are real head-scratchers. Besides the discovery of the fungal parasite, here are a few other bits of knowledge that owe their existence to evolutionary theory. It is by no means an exhaustive list.  (Note: by ‘evolutionary theory', I don't mean as Ilíon insinuates that observations are merely reported in ‘Darwinspeak'. I mean that these discoveries were motivated by Darwinian research questions, or that their discovery would not have happened without knowledge of common descent or natural selection.)

    1. Ant fungi have been transmitted horizontally between ant nests, in addition to vertical transmission from parent to daughter colony. This result emerged from phylogenetic analysis (See Mueller, U.G. 2002. American Naturalist 160(supplement): s67-s98.).

    2. Attine ant species with more complex caste systems are polyandrous (See Murakami, T. et al 2000. Behav. Ecol. SocioBiol.48:276-284.)

    3. Escovopsis fungi likely had a single origin (See Currie et al 2003. Science 299:386-388.)

    4. The fungal cultivars do sometimes depart from the ant mutualism and become free-living (See Mueller, U.G. 2002. American Naturalist 160(supplement): s67-s98.).

    I don't bring up these examples as a demonstration that Darwinian evolutionary theory is ultimately the best explanation of the ant/fungus/mold/bacteria relation. Rather, I bring them up to show that Darwinian theories have been extremely fruitful in both bringing this system to light and in stimulating further research. The ability to generate questions is *extremely* important in scientific theories, and the ‘head scratching' produced by Darwinian theories is a natural consequence of their usefulness.  Head-scratching means questions, and questions mean research.  A theory that doesn't raise questions does not provide a useful substrate for science.

    It is worth noting that so far answers have been forthcoming to these questions, which I take as an indication that we are on the right track.

    It is also worth noting that little, if anything, in this system can be traced to creationist or Intelligent Design thought.  Simply put, advocates of those schools will need to provide quite a bit more detail about how, where, and when design was affected in this system before a design research program will be possible.  If you would like to see design adopted by scientists working in this system, you've got to provide an alternative that is more useful in the lab and in the field than Darwinism.  This will entail doing better than making non-committal statements about the "unknowability" of the design process of the sort that permeates writings.  Meanwhile, Darwinian reseach keeps suggesting and finding new players in the symbiosis.

    3. Some quibbles over technical issues.

    Some of my issues are with Ilíon, but most are with the NYTimes article that Ilíon cites.
    Ilíon wrote:
    Also, note that the story says the mold seems to be related to a mold that devastates commercial mushroom farms. The mushrooms we grow have not been prohibited from sexually reproducing for the last 50 million years, so by your argument they have been able to continue evolving to resist the mold attacking them. And yet, it doesn't sound as though they do a much better job than the ants' fungus does.
    I have a minor correction to make.  The fungi have not been prohibited from sexually reproducing for 50 million years.  They have been observed to reproduce sexually in both the lab and in the field.  (See again the Mueller 2002 Am Nat paper).  This may not have been clear from the NYT article, but then, the popular media has never been known for the accuracy of its reporting. Rather, the issue is that the fungal cultivar only rarely reproduces sexually, so its rate of production of genetic novelty is lower than that of the parasite.  It still is true, however,  that within each nest the fungus garden is a clonal monoculture.

    You're forgetting that the evidence indicates that all nests are using the same clonal cultivar of the mold.
    An error in the reportage of the NYTimes.  Some species of Apterostigma, one of the "lower" attines,  use a distantly-related species of fungus. But, I consider your point valid, as most species use cultivars from the same clade, and it seems clear from the phylogeny that the original domestication happened once.

    In your nice little story, the ant are becoming increasingly dependent on the fungus, but the mold is increasing, reducing their yields. During this time, and during the time that the ants are 'learning' to use the bacteris to fight the mold, some of the nests will even lose their crops, which will cause some of those nests to die, but others will restart their gardens with a new batch of 'wild' fungus - thus we should find multiple cultivars of the fungus.
    I think you've taken the simplistic reporting of the NY Times a bit too seriously.  Not your fault. The inference of a single domestication event comes from phylogeny, and you've got to be careful with what you can and cannot conclude from a phylogeny.  By "single event", what the original researchers mean is that all current fungal cultivars, and their ants, trace their ancestry back to a single fungal and a single ant species.  Beyond this inference, there is simply no resolution to distinguish an actual one ant-one fungus domestication event, and a population that did it gradually with many original cultivars.  Specifically, here are three situations that will look identical in phylogenetic retrospect:

    1. A literal single origin, where one colony picks up one fungus and the rest is history. I think this is the interpretation that you object to.  Not without  reason, IMHO.

    2. Multiple origins, but all the fungal cultivars involved are closely related and share a common ancestor.  If that ancestor left no descendants that are not cultivated by ants in the present day, then the fungi will still trace back to a single node on the phylogeny as an artifact of extinction, even though there may actually have been multiple domestication events.

    3. Multiple origins, but when the ants lose their fungi they re-acquire not from the wild but from another ant nest.  There is some evidence that this is what modern attine ants do when they lose their fungus.  This way the fungus spreads laterally among colonies, and given a stochastic process of fungal lineage loss throughout the population all colonies will eventually come to cultivate a single lineage.  The other original fungal lineages, having gone extinct, will not appear in the phylogenetic analysis and the phylogeny will trace back to a single node.  

    The take-home message is that "single origin" claims can be a bit misleading.  Currently there is no way to test between these different possibilities, so for the time being we are stuck with a "single origin" only in the broad sense.

    The three-way symbiosis of the ant (and apparently, we're talking about more than one species of ant but they're all using the same fungus clone), the fungus, and the bacterium has to be all in place from the beginning to be able to successfully fight the mold.
    Correction: there are multiple species of fungi, some of them specific to particular attine species.  The fungus is only clonal at the level of the colony.  They are all descended from a 50my or so old fungus, but they've had plenty of time to diversify.  Interestingly, the pattern of diversification is *very* suggestive of coevolution with the ants.  I'll get back to this point in a bit.

    If the queens didn't 'know' from the beginning to take a start of the parent nest's fungus (and, BTW, don't they have a special 'chamber' in their heads in which they transport their sample?), there should be multiple cultivars.
    You aren't the first to have thought of this. Ulrich Mueller also finds this idea a bit suspect, and he has proposed that what originally happened was a fungus exploiting the ant for dispersal.  Ants of many kinds commonly pick stuff up in their infrabuccal chamber (the ‘special chamber' of which you speak), mostly stuff that they've filtered from food, and dump it out when it's full.  The symbiosis may have arisen as a result of the fungus getting picked up and dispersed by ants.  This is interesting, because it is a fungal-centered hypothesis.  Most explanations are ant-centered, and IMHO have come off as a bit weird.

    4. The evidence for common descent and natural selection in the ant/fungus/mold/bacteria system.

    One compelling reason to look for evolutionary processes as explanations for the ant/fungus/mold/bacteria relationship is that there is a great deal of evidence for common descent and for Darwinian evolution in these organisms.  Here it is, in no particular order:

    • Geography.  Attines and their cultivars are restricted to the new world tropics.  The estimated age of the symbiosis is 50 million years, which is after the break-up of Gondwana and the isolation of South America.  Given limited across-water dispersal (Attine queens are heavy and clumsy fliers, if you've seen them fly...), the agreement of date and location are supportive of common descent.  It is also relevant that the ant groups that come out as sister to the attines are also South American.  In contrast, many ant groups whose estimated ages (from phylogenies that were calibrated with fossils) are older than break-up of Gondwana are found in both the old and the new worlds. These include army/driver ants and elongate twig ants.  Does design theory have anything to say about the geographic distribution of the ant/fungus system?
    • Large scale phylogenetic congruence between ants, cultivars, and Escovopsis. This is the subject of the Jan 2003 Science article that sparked the NY Times commentary.  I strongly recommend that you read the paper:
      Ancient Tripartite Coevolution in the Attine Ant-Microbe Symbiosis
      Here is the abstract:      
      Currie CR, et al.2003. Ancient tripartite coevolution in the attine ant-microbe symbiosis. Science 299:386-388.
      The symbiosis between fungus-growing ants and the fungi they cultivate for food has been shaped by 50 million years of coevolution. Phylogenetic analyses indicate that this long coevolutionary history includes a third symbiont lineage: specialized microfungal parasites of the ants' fungus gardens. At ancient levels, the phylogenies of the three symbionts are perfectly congruent, revealing that the ant-microbe symbiosis is the product of tripartite coevolution between the farming ants, their cultivars, and the garden parasites. At recent phylogenetic levels, coevolution has been punctuated by occasional host-switching by the parasite, thus intensifying continuous coadaptation between symbionts in a tripartite arms race.
      Two congruent phylogenies is good evidence for common descent, but three pretty much clinches it.  I suppose that it is true that congruence could also reflect an intelligent design process as well (probably one integrated with descent), but since no mechanisms exist for how or when or to what effect such design might take place they are of little immediate use to researchers.
    • Complexity and specialization of the attines correlates with phylogeny, as expected under co-evolution and common descent. The oldest lineages of Attines have the smallest nests, a single worker morphological caste, the least specialized foraging habits, and the least prevalence of Escovopsis in their nests. They also have the highest rate of fungal swapping.  The most recent lineages of attines, have enormous colonies, with a dozen or so morphologically different worker castes (the largest workers are orders of magnitude larger than the smallest workers), multiple fungus gardens, highly specialized foraging habits, and the highest prevalence of Escovopsis.  And the lineages that are of intermediate age, such as Trachymyrmex+Sericomyrmex, are somewhere in between. This pattern makes sense under common descent.
    • Present day attine colonies have some life-history features with the signature of natural selection.  Most notable, sex investment ratios.  A ton has been written on how the differing Darwinian "goals" of queens and workers in ant colonies play out in manipulations of population sex investment ratio, such that species with particular mating systems should produce different sex ratios.  Attines, with some exceptions, fall into the generally predicted pattern of monandrous species investing very heavily in females. It's a bit too complicated to explain here, but I find the evidence compelling and you can read more about it in this book:

      Social Evolution in Ants

      In the past, I've also written threads on ARN about sex ratios and evolution, here:
      Successful predictions of evolutionary theory


    There.  Now I'm done.



    Date: 2003/02/24 20:27:35, Link
    Author: niiicholas
    The creos have taken up Behe's banner on this one.

    Mostly good for the pics, and a JBS Haldane quote that I would like to follow up:

    Design in Living Organisms: Motors
    by Jonathan Sarfati
    Creation Ex Nihilo Technical Journal 12(1):3–5, 1998


    Would any evidence convince evolutionists?
    The famous British evolutionist (and communist) J.B.S. Haldane claimed in 1949 that evolution could never produce ‘various mechanisms, such as the wheel and magnet, which would be useless till fairly perfect.’10 Therefore such machines in organisms would, in his opinion, prove evolution false. These molecular motors have indeed fulfilled one of Haldane’s criteria. Also, turtles11 and monarch butterflies12 which use magnetic sensors for navigation fulfil Haldane’s other criterion. I wonder whether Haldane would have had a change of heart if he had been alive to see these discoveries. Many evolutionists rule out intelligent design a priori, so the evidence, overwhelming as it is, would probably have no effect.

    10. Dewar, D., Davies, L.M. and Haldane, J.B.S., 1949. Is Evolution a Myth? A Debate between D. Dewar and L.M. Davies vs. J.B.S. Haldane, Watts & Co. Ltd / Paternoster Press, London, p. 90.

    Date: 2003/02/27 19:45:43, Link
    Author: niiicholas
    IDEA club (/center) responds to Project Steve in their page:

    Scientists and other Intellectuals that Doubt Darwinism and other Naturalistic Theories of Origins
    An incomplete and continually updated list

    I hadn't seen this page before, but Casey Luskin (and perhaps others...) compiled all the various lists of creationist scientists, DI list-signers, etc.  This is actually a useful service as we can see how many Steves there are in all the lists put together (note that the net is quite wide, being very much international and non-biology specific).

    At the end Luskin says there's 9 Steves in the list.  For your enjoyment, here they are (the list is in subsections but the numbers are cumulative as different lists are appended):


    14. STEPHEN MEYER (Ph.D. in History & Philosophy of Science University of Cambridge), currently professor of philosophy at Whitworth College.

    43. STEPHEN FAWL, Ph.D. Chemistry, Napa Valley College

    106. Steven Austin, PhD Geology (Pennsylvania State University). See his biography.

    229. Stephen Brocott, Ph.D. Organometallic Chemistry (University of Western Australia). Listed on the Institute for Creation Research Creation Scientists Page.

    237. Stephen Taylor, Ph.D. Electrical Engineering (University of Liverpool). Listed on the Institute for Creation Research Creation Scientists Page.

    347. Stephen W. Deckard (Ed.D. Univesity of Sarasota), Assistant Professor of Education. See his bio on the Answers in Genesis website.

    349. Stephen Grocott, Industrial Chemist (Ph.D. (1981), University of Western Australia in the field of organometallic chemistry of optically active metal complexes), Adjunct Professor of Chemistry at an Australian University. Member of Royal Australian Chemical Institute and American Chemical Society. See his bio on the Answers in Genesis website.

    398. Stephen Huxley, Ph.D., Professor of Information and Decision Modeling at the University of San Francisco as seen in his involvement with the IDEA 2002 Conference at USF.

    454. Steven Gollmer, Ph.D., Associate Professor of Physics, Cedarville College

    In case you weren't counting:

    Number of (probable) YECs: 5

    Number of biologists = 0.  Organometallic chemistry is as close as they get...


    Date: 2003/03/02 21:03:25, Link
    Author: niiicholas
    On the subject of how a proto-flagellum would be positioned on the cell surface, it occurred to me awhile ago that it wouldn't matter if the cell was spherical shaped (coccus).

    E.g. like this bacterium:  

    Zaar A, Fuchs G, Golecki JR, Overmann J.
    Arch Microbiol 2003 Mar;179(3):174-83
    A new purple sulfur bacterium isolated from a littoral microbial mat, Thiorhodococcus drewsii sp. nov.

    A new strain of purple sulfur bacterium was isolated from a marine microbial mat sampled in Great Sippewissett Salt Marsh at the Atlantic coast (Woods Hole, Mass., USA). Single cells of strain AZ1 were coccus-shaped, highly motile by means of a single flagellum, and did not contain gas vesicles. Intracellular membranes were of the vesicular type. However, additional concentric membrane structures were present. The photosynthetic pigments were bacteriochlorophyll a and carotenoids of the normal spirilloxanthin series, with rhodopin as the dominant carotenoid. Hydrogen sulfide (up to 11 mM), sulfur, thiosulfate, and molecular hydrogen were used as electron donors during anaerobic phototrophic growth. During growth on sulfide, elemental sulfur globules were transiently stored inside the cells. Strain AZ1 is much more versatile than most other Chromatiaceae with respect to electron donor and organic substrates. In the presence of CO(2), it is capable of assimilating C(1)-C(5) fatty acids, alcohols, and intermediates of the tricarboxylic acid cycle. Strain AZ1 could also grow photoorganotrophically with acetate as the sole photosynthetic electron donor. Chemotrophic growth in the dark under microoxic conditions was not detected. Optimum growth occurred at pH 6.5-6.7, 30-35 degrees C, >/=50 micro mol quanta m(-2) s(-1), and 2.4-2.6% NaCl. The DNA base composition was 64.5 mol% G+C. Comparative sequence analysis of the 16S rRNA gene confirmed that the isolate is a member of the family Chromatiaceae. Sequence similarity to the most closely related species, Thiorhodococcus minor DSMZ 11518(T), was 97.8%; however, the value for DNA-DNA hybridization between both strains was only 20%. Because of the low genetic similarity and since strain AZ1 physiologically differs considerably from all other members of the Chromatiaceae, including Trc. minor, the new isolate is described as a new species of the genus Thiorhodococcus, Thiorhodococcus drewsii sp. nov.

    This is aside from the question of whether flagellum positioning is needed even in your average cell, e.g. it seems that E. coli does just fine by having several randomly-placed (or perhaps random but spaced-apart) peritrichous flagella.

    A page describing the various ways flagella are distributed on bacteria.

    Date: 2003/03/02 21:49:25, Link
    Author: niiicholas
    Links/material on this topic that refute various common antievolutionist distortions of the topic:

    II Evo forum thread


    Date: 2003/03/09 20:01:34, Link
    Author: niiicholas
    Jarrell and others have written a detailed review of prok. motility.  Very useful article.  


    Microbiology 2003 Feb;149(Pt 2):295-304
    Prokaryotic motility structures.

    Bardy SL, Ng SY, Jarrell KF.

    Department of Microbiology and Immunology, Queen's University, Kingston, ON, Canada K7L 3N6.

    Prokaryotes use a wide variety of structures to facilitate motility. The majority of research to date has focused on swimming motility and the molecular architecture of the bacterial flagellum. While intriguing questions remain, especially concerning the specialized export system involved in flagellum assembly, for the most part the structural components and their location within the flagellum and function are now known. The same cannot be said of the other apparati including archaeal flagella, type IV pili, the junctional pore, ratchet structure and the contractile cytoskeleton used by a variety of organisms for motility. In these cases, many of the structural components have yet to be identified and the mechanism of action that results in motility is often still poorly understood. Research on the bacterial flagellum has greatly aided our understanding of not only motility but also protein secretion and genetic regulation systems. Continued study and understanding of all prokaryotic motility structures will provide a wealth of knowledge that is sure to extend beyond the bounds of prokaryotic movement.

    PMID: 12624192 [PubMed - in process]


    - They say the archaeal flagellum is powered by a proton gradient.  This contradicts my earlier thought which was that it was ATP-powered.  However, they cite no demonstration of the power source.  I would keep the question in mind, but here is what they say:

    "The other major subdivision of prokaryotes is the domain Archaea. Members are motile via a structure that appears to be fundamentally distinct from the bacterial counterpart in composition and, likely, assembly (Thomas et al., 2001). The archaeal flagellum is a rotary structure, driven by a proton gradient, and it is thinner than typical bacterial flagella."

    - A more detailed review of spirochete flagella which are weird.

    - A nice review of current knowledge on the archaeal flagellum proteins, several identified similarities/homologies to type IV pilins...

    - The archaeal flagellum probably/usually has hook and filament proteins, and they find at least a bit of evidence that the difference between the two is not so great:

    "In archaea, there are always multiple (2–6) flagellin genes present (Sulfolobus solfataricus appears to be an exception). Thus far the only components of the archaeal flagellum identified are the flagellins themselves, where it appears that the multiple flagellins are all present as structural components of the assembled flagellum. Recent work indicated that the hook protein might in fact be a minor flagellin, FlaB3 in the case of Methanococcus voltae (Bardy et al., 2002) (Fig. 4)."

    - Type IV pili movies (twitching motility etc.):
    Type IV pili movies

    - Ratchet structure review; it would be nice to know the genes involved, particularly if there is any rotary motion involved...

    - Here's a whole new kind of motility, the contractile cytoskeleton (in a prokaryote)

    Spiroplasma melliferum is one of the smallest free-living organisms on earth with a genome size about half that of E. coli. Surprisingly, this bacterium is motile, though nonflagellated, and it lacks any genes analogous to ones involved in flagellation as well as known gliding genes. This organism lacks a cell wall but has a membrane-bound internal cytoskeleton, composed primarily of a unique 59 kDa protein, which is thought to act as a linear motor, in contrast to the rotary motor of the flagellum (Trachtenberg, 1998) (Fig. 9). The cytoskeleton is attached to the cytoplasmic membrane, possibly through one or more of the approximately seven proteins that co-purify with it. The cytoskeleton is involved in motility due to its linear contraction and its close interaction with the cytoplasmic membrane (Trachtenberg & Gilad, 2001). The cytoskeleton exists as a seven fibril ribbon that extends the length of the cell. A conformational switch in the monomer leads to length changes: because of the strong interconnectiveness of the cytoskeleton subunits, changes in any part of the fibril are transmitted to neighbours and ultimately to the attached membrane. Though poorly studied at present, this motility structure represents a truly novel approach to motility using what appears to be a much smaller complement of genes than that required for flagellation. Identification of the roles of the cytoskeleton co-purifying proteins will be a major advance in the elucidation of this motility structure."

    Conclusion: not much on evolution but good overview review.

    While motility is commonplace among the prokaryotes, it is important to note the variety of structures responsible for motility. These structures vary depending not only on the organism in question, but also on the particular environment. Study of the bacterial flagellum has provided insights into many aspects of prokaryotic cellular activities including genetics and regulation, physiology, environmental sensing, protein secretion and assembly of complex structures. Continued study of all prokaryotic motility structures will provide knowledge that is likely to reach far beyond the topic of motility.

    Date: 2003/03/13 14:54:32, Link
    Author: niiicholas
    Charlie D. has expressed the problems with Mike Gene's frontloading in about the most succinct way, ever, I think:;f=13;t=000644

    Originally posted by Mike Gene:
    The key is always to remember how ID critics view ID proponents - ID proponents are either stupid, ignorant, deluded, or evil. The ID critics argue with me not to understand my views, or even objectively compare views, but because they are looking for ways to rationalize my existence. Someway, somehow, I must be fitted into the precast stereotypes. That's their only interest in these debates (that is, when they are not politicking).

    Talk about projecting and sterotyping, Mike! LOL.

    Personally, I think your theories have muddled considerably in the past few months. As such, they may seem to you they "explain" more things, but in fact to me they are far less interesting.

    Right now, your hypothesized designers seem to me completely schizophrenic. On one side, they seem like totally anal micromanagers: they gave their colonizing bacteria supersophisticated micromachines made up of (altogether) probably hundreds of complex proteins, to do things like syntesizing more proteins, degrading proteins through the ubiquitin system, replicating DNA and correcting replication errors, generating energy, etc etc, even allowing them to swim.

    On the other side, the same alien bioengineers were supposedly complete laissez-faire evolutionists, providing bacteria with a minimalist compendium of protein domains (to the point of purposefully avoiding hydrophobic aminoacids!;), and a front-loaded genetic system that would introduce mutations at high frequency in these very simple protein domains to allow them to later develop more complex domains, so that those bacteria could evolve freely in a fully darwinain fashion.

    So bacteria were both very simple, and programmed to evolve, and very complex, with all sorts of unevolvable, rigid micromachines. They had very simple protein domains and a system to mutate them at high frequency, and very complex proteins, with fully formed domains, in which changes in domain structure almost invariably kill the original function. Extreme mutability and error correction. On the one side the bioengineers spent countless alien-hours designing a system for bacteria to swim, and on the other their evolvable bacteria evolved probably a half dozen equally efficient motility systems on their own, thanks to their evolvability.

    Whenever the evolution of something seems hard to figure out, it's because that something was designed; whenever it seems pretty straightfoward, it's because it was designed to evolve. Basically, your model right now it's not just indistinguishable from evolutionary theory, it's indistinguishable from pretty much anything. Pardon our lack of enthusiasm, if you know what I mean.
    The non-teleologist also wants the teleologist to prove the impossible, namely, demonstrate that non-teleological processes couldn't produce some aspect of biotic reality.

    Wrong, at least as far as I am concerned. I just want evidence that teleology can generate any aspect of current biotic reality. We have plenty of positive evidence of the existence and power of non-teleologic processes - none of teleology. It's up to the teleologicians to show there's something there, other than smoke and mirrors.


    Date: 2003/03/15 01:37:14, Link
    Author: niiicholas



    But none of what you wrote (or linked to) contradicts what I said above. There is no evidence of a pre-PPi synthase, and no evidence that the ATP synthesis molecular machine can be reduced to one component. The synthesis of ATP is a lot more than just inorganic phosphate.
    IIRC the ATPase doesn't synthesize the entirety of ATP, it just adds or removes energized phosphates -- Adenosine Triphophsate toe Diphosphate and back.


    Rather like what the remarkably simple, 1-component (dimer) PPase does with phosphates:

    Hmm, might not be working, look here:

    ...and both are coupled to H+ gradients, and use the same basic fold, what a coincidence!  It just looks like all of that rotating complexity may be useful and efficiency-increasing add-on rather than an absolutely necessary part of primitive cellular energetics.


    Since the synthesis of diphosphate can be reduced to one subunit, I would say that it is simpler than ATP synthesis, but I wonder if a prediction not unlike the TTSS can be formed, in that it came after or evolved from ATP synthase rather than to it.
    You are entitled to your prediction.  Regarding TTSS, I am holding out for:

    1) TTSS with nonvirulence, nonflagellar functions, and
    2) Basal homologs of the TTSS.

    These are predictions that only further data can resolve, however.  In general, you'll forgive me for sticking with Baltscheffsky until some IDist (1) acknowledges his existence and (2) explains how they don't greatly weaken the ID argument based on the F1F0 ATPase.

    Date: 2003/03/15 02:05:37, Link
    Author: niiicholas
    Some ISCID threads on this:

    Topic: Is the DNA code universality strong evidence for evolution?;f=6;t=000316

    Topic: Common descent;f=6;t=000056

    Date: 2003/03/15 04:56:51, Link
    Author: niiicholas
    Free online article comparing PPases and F1F0-ATPases:


    FEBS Lett 1999 Sep 3;457(3):527-33
    H(+)-PPases: a tightly membrane-bound family

    Baltscheffsky M, Schultz A, Baltscheffsky H.

    Department of Biochemistry, Arrhenius Laboratories, Stockholm University, S-106 91, Stockholm, Sweden.

    The earliest known H(+)-PPase (proton-pumping inorganic pyrophosphatase), the integrally membrane-bound H(+)-PPi synthase (proton-pumping inorganic pyrophosphate synthase) from Rhodospirillum rubrum, is still the only alternative to H(+)-ATP synthase in biological electron transport phosphorylation. Cloning of several higher plant vacuolar H(+)-PPase genes has led to the recognition that the corresponding proteins form a family of extremely similar proton-pumping enzymes. The bacterial H(+)-PPi synthase and two algal vacuolar H(+)-PPases are homologous with this family, as deduced from their cloned genes. The prokaryotic and algal homologues differ more than the H(+)-PPases from higher plants, facilitating recognition of functionally significant entities. Primary structures of H(+)-PPases are reviewed and compared with H(+)-ATPases and soluble PPases.

    Date: 2003/03/21 00:31:33, Link
    Author: niiicholas
    Well, as predicted, the people who actually know something about peppered moths are much more critical of Judith Hooper's book Of Moths and Men.  All I'm waiting for now is a review from M.E.N. Majerus.

    David Rudge, Untitled book review of Judith Hooper's Of Moths and Men, Journal of the History of Biology, Spring 2003, pp. 207-209


    Judith Hooper, Of Moths and Men: An Evolutionary Tale: Intrigue, Tragedy and the Peppered Moth (New York: W.W. Norton; London: Fourth Estate, 2002), xx + 377 pp., illus., $26.95.

    [note weird inversion of "Of Moths and Men" in first sentence.  Guess the journal editor is a bit overworked...]

    Of Men and Moths is a popularized account of Bernard Kettlewell’s investigations of the phenomenon of industrial melanism, the rapid rise in frequency of dark forms of many moth species downwind of manufacturing centers that occurred as an apparent consequence of large-scale air pollution associated with the industrial revolution. Kettlewell’s experiments are widely cited as demonstrating that this change is due to natural selection, and, in particular, the selective advantage of dark coloration against birds in sootdarkened environments. Hooper accuses Kettlewell of committing fraud and members of E.B. Ford’s Oxford School of Ecological Genetics of conspiring to hide details of outstanding problems surrounding the phenomenon to advance their own pan-selectionist agenda. The book concludes by reviewing how the career of a lone dissenter, Ted Sargent, was derailed as a result of his heresy. The subtitle is apt, but not for reasons the author intends. The intrigue surrounding this book rests in making sense of why someone with Hooper’s gift for science writing would stoop to the trumped-up fiction of scientific fraud to sell a book; the tragedy is the pernicious effects this book will have on biology education and the history of science community.

    While Kettlewell was highly regarded as a naturalist, his colleagues had less respect for him as a scientist. It is also fair to say that the phenomenon is more complicated than textbooks would have us believe and that several of the techniques and assumptions Kettlewell used have been called into question. Hooper’s evidence that Kettlewell committed fraud, a claim neither historians nor any of the numerous researchers on industrial melanism who have attempted to extend Kettlewell’s work have *ever* made, is an apparent discrepancy in his 1953 recapture results. Calling attention to the fact that the figures went up the day Ford wrote a letter sympathizing with Kettlewell’s results thus far, Hooper alleges that as a result of exhaustion, sickness, alcohol, tobacco, and his own insecurities, Kettlewell resorted to falsifying his data to placate Ford. Using historical meteorological records, she considers and triumphantly rejects one alternative explanation. There are many other reasons for why the recapture figures might have risen (for example, on this day Kettlewell began using three times as many moths). Significantly, not even Ted Sargent, one of Kettlewell’s most vocal critics who Hooper interviews, agrees with Hooper’s claim that Kettlewell committed fraud (p. 255).

    The portrayals of Kettlewell’s and Ford’s scientific work are distorted by Hooper’s obvious agenda and littered with interpretive errors (see B. Grant, “Sour Grapes of Wrath,” Science 297 [2002]: 940–941). Much of the book is devoted to spreading gossip. While some use of anecdotes is warranted to humanize the story, the emphasis on details of their private lives results in caricatures that make the respect and affection their colleagues had for Kettlewell and Ford (both privately and publicly) a complete mystery. The relevance of these anecdotes to Hooper’s accusations is also unclear. Repeated references to Ford’s reputation as a misogynist, his homosexuality, his mysterious young ward, and the sordid circumstances surrounding the suicide of Kettlewell’s daughter suggest that, in lieu of evidence, Hooper has resorted to dredging up every bit of dirt she could find on Kettlewell and Ford to coax the reader into believing they were capable of committing fraud.

    Hooper’s second thesis is more problematic. She alleges that researchers on industrial melanism have conspired to hide outstanding problems and ostracize those who dare to question the standard story. This elite group centered in Britain supposedly have the power to jeopardize Ted Sargent’s candidacy for tenure at Amherst in the U.S., yet curiously cannot prevent the publication of articles that raise questions about the standard account. Surely the primary source of Sargent’s tenure problems has to do with the excessive stress science departments place on external funding, a concern his British colleagues no doubt share.

    Sadly this book will undoubtedly be used by creationists and intelligent design theorists in their ongoing assault on the teaching of evolution. The several outstanding interpretive problems surrounding the phenomenon of industrial melanism and Kettlewell’s work do not imply it should be removed from textbooks and indeed may augment its value for the teaching of science (see D.W. Rudge, “Does Being Wrong Make Kettlewell Wrong for Science Teaching?” Journal of Biological Education 35 [2000]: 5–11). The most pernicious effect of this book however, will be upon the history of science community. It is a warning to scientists of what can happen to the memories of you and your loved ones if your papers fall into the wrong hands.

    David Wÿss Rudge

    David Rudge links for those interested in his other work:

    Dave Rudge's Home Page

    Rev Biol Trop 2002 Mar;50(1):1-7

    Cryptic designs on the peppered moth.

    Rudge DW.

    Department of Biological Sciences, Institute for Science Education, Western Michigan University, 3134 Wood Hall, Kalamazoo, MI 49008-5410, USA.

    In a provocative recent book, Jonathan Wells (2000) decries what he discerns as a systematic pattern in how introductory biology textbooks "blatantly misrepresent" ten routinely cited examples offered as evidence for evolution. Each of these examples, according to Wells, is fraught with interpretive problems and, as such, textbooks that continue to use them should at the very least be accompanied by warning labels. The following essay critiques his reasoning with reference to one of these examples, the phenomenon of industrial melanism. After criticizing Wells's specific argument, the essay draws several conclusions about the nature of science lost in his account.

    Date: 2003/03/21 01:32:44, Link
    Author: niiicholas
    A coupla recent flag-related articles, my summaries of evo-interesting bits in [].


    Proc Natl Acad Sci U S A 2003 Mar 18;100(6):3027-30
    Type III secretion systems and bacterial flagella: Insights into their function from structural similarities.

    Blocker A, Komoriya K, Aizawa S.

    Sir W. Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom; and Department of Biosciences, Teikyo University, Utsunomiya 320-8551, Japan.

    Type III secretion systems and bacterial flagella are broadly compared at the level of their genetic structure, morphology, regulation, and function, integrating structural information, to provide an overview of how they might function at a molecular level.


    [More homologies to flagellar proteins than the standard ~9 or so: ]

    Old and New Sequence Homologies.

    TTS apparatuses are encoded by 25 genes (4), nearly all essential for function. About 10 TTSS proteins are similar in sequence or membrane topology to cytoplasmic or inner membrane proteins of flagellar hook-basal bodies (HBBs; refs. 5 and 6). Others show no significant sequence homology. However, they show "functional conservation" because when knocked out, they lead to similar phenotypes in assembly or function of the apparatuses. By matching biochemical characteristics and biological information about each protein (see Supporting Text, which is published as supporting information on the PNAS web site,, we propose the functional homologs shown in Fig. 1.

    Morphological Similarities.

    A part of the TTS machinery, the "needle complex" (NC) resembles HBBs (6, 7). NCs comprise a 10 × 60-nm external needle inserted within a 30-nm (in diameter) cylinder traversing both bacterial membranes and the peptidoglycan. The Shigella secreton has an additional "bulb," 45 × 25 nm, on the cytoplasmic side of the inner membrane, similar to the flagellar C-ring (refs. 8 and 9; Fig. 1). NCs are traversed by a 2- to 3-nm channel (10), which exists also within the entire bacterial flagellum (11). Flagellin may transit partially unfolded (12) through this channel to its tip, where it refolds and inserts into the growing filament (13, 14). Effectors from plant pathogen TTSSs are also secreted from the distal tip of their TTS machineries (15). During assembly of flagella in vivo, a cap is added before each transition to a new part of the flagellum so new subunits, which would otherwise diffuse away, can be inserted directly under the cap (16). NC components, including the needle component MxiH/PrgI, have been identified (17, 18). No cap has been identified in any TTSS. Morphological divergence between TTSSs is discussed in Supporting Text.


    What are the energizers of posttranslational and cotranslational secretion?
    The flagellar ATPase FliI is required for export of all flagellar proteins except the outer membrane components (5). Without it only the inner membrane and cytoplasmic components are assembled. Mutants in homologous TTSS ATPases display analogous phenotypes (65). Does cotranslational secretion occur by docking of the ribosome to the cytoplasmic part of the TTS machine like cotranslational export across the membrane of the endoplasmic reticulum? An empty flagellar C-ring could only accommodate two ribosomes, the protein channels of which could not directly dock to the HBB without a gap being left. Therefore, cotranslational secretion is probably also driven by the ATPase and hence indirect.

    How is energy transduced by the export motor during secretion?
    The ATPases interact with cytoplasmic components of TTSSs or flagella but the function(s) of these interactions are mostly unidentified (66, 67). The biological cycle of the enzyme is unknown and its localization is debated [cytosolic or membrane-bound (69)?]. How might these ATPases catalyze processive protein export? Spa47 (the Shigella FliI homolog) shares 33% amino acid identity with the -subunit of F1-ATPase. Proteins with >30% sequence identity have a high probability of sharing similar structures (69). Active F1-ATPase is a heterohexamer consisting of alternating - and -subunits with a -subunit inserted in a central channel where it rotates during the catalytic cycle (70). No equivalent of the -subunit of F1-ATPases is found within flagellar or TTSS-encoding operons, so we assume that the type III export motor is a homohexamer. When modeled on the F1 structure, Spa47 fits at the inner membrane base of our NC structure (Fig. 3). It would contain a central channel aligned with the one found within the NC and of similar diameter to it, through which the proteins could be secreted (see Supporting Text).

    [It would be very interesting if the FliI ATPase really was a homohexamer like the F1 subunits in the F1F0 ATPase.  Not determinative of anything I suppose but it would make Rizzotti's model a bit more likely]



    Our understanding of TTSSs was applied to obtain an MHC class I response against a heterologous translocated protein (75). TTSSs are targets for new antimicrobial drugs. Work on type IV secretion systems in other Gram-negative pathogens shows that they, too, can perform host cell contact-mediated protein translocation (76). Type IV secretion apparatuses resemble bacterial conjugation systems, which function differently from TTSSs. The sec-dependent secretion pathway of Gram-positive bacteria also seems capable of polarized protein translocation into host cells (77). These may be examples of convergent evolution.


    Mol Cell Probes 2003 Feb;17(1):25-32
    Detection of type III secretion genes as a general indicator of bacterial virulence.

    Stuber K, Frey J, Burnens AP, Kuhnert P.

    Institute of Veterinary Bacteriology, University of Bern, Langgassstrasse 122, CH-3012, Bern, Switzerland

    Type III secretion systems of Gram-negative bacteria are specific export machineries for virulence factors which allow their translocation to eukaryotic cells. Since they correlate with bacterial pathogenicity, their presence is used as a general indicator of bacterial virulence. By comparing the genetic relationship of the major type III secretion systems we found the family of genes encoding the inner-membrane channel proteins represented by the Yersinia enterocolitica lcrD (synonym yscV) and its homologous genes from other species an ideal component for establishing a general detection approach for type III secretion systems. Based on the genes of the lcrD family we developed gene probes for Gram-negative human, animal and plant pathogens. The probes comprise lcrD from Y. enterocolitica, sepA from enteropathogenic Escherichia coli, invA from Salmonella typhimurium, mxiA from Shigella sonnei, as well as hrcV from Erwinia amylovora. In addition we included as a control probe the flhA gene from E. coli K-12 to validate our approach. FlhA is part of the flagellar export apparatus which shows a high degree of similarity with type III secretions systems, but is not involved in pathogenicity. The probes were evaluated by screening a series of pathogenic as well as non-pathogenic bacteria. The probes detected type III secretion in pathogens where such systems were either known or were expected to be present, whereas no positive hybridization signals could be found in non-pathogenic Gram-negative bacteria. Gram-positive bacteria were devoid of known type III secretion systems. No interference due to the genetic similarity between the type III secretion system and the flagellar export apparatus was observed. However, potential type III secretion systems could be detected in bacteria where no such systems have been described yet. The presented approach provides therefore a useful tool for the assessment of the virulence potential of bacterial isolates of human, animal and plant origin. Moreover, it is a powerful means for a first safety assessment of poorly characterized strains intended to be used in biotechnological applications.

    [short version: no evidence of basal Type III secretion systems, but then this technique would probably only detect T3SS within the flagellum-derived-virulence-system "clade" anyhow...

    Note that e.g. gram-positive bacteria have regular flagella, so when the authors say "Gram-positive bacteria were devoid of known type III secretion systems" they are not including flagella.]

    Trends Cell Biol 2003 Mar;13(3):114-21
    Rotary protein motors.

    Oster G, Wang H.

    Depts Molecular and Cellular Biology and ESPM, College of Natural Resources, University of California, 94720, Berkeley, CA, USA

    THREE PROTEIN MOTORS HAVE BEEN UNAMBIGUOUSLY IDENTIFIED AS ROTARY ENGINES: the bacterial flagellar motor and the two motors that constitute ATP synthase (F(0)F(1) ATPase). Of these, the bacterial flagellar motor and F(0) motors derive their energy from a transmembrane ion-motive force, whereas the F(1) motor is driven by ATP hydrolysis. Here, we review the current understanding of how these protein motors convert their energy supply into a rotary torque.

    [*two* motors in the F1F0 ATPase?  This is a different interpretation.  Anyhoo, no full-text access to this one for me.


    J Mol Biol 2003 Mar 21;327(2):453-63
    Ion-coupling Determinants of Na(+)-driven and H(+)-driven Flagellar Motors.

    Asai Y, Yakushi T, Kawagishi I, Homma M.

    Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa-Ku, 464-8602, Nagoya, Japan

    The bacterial flagellar motor is a tiny molecular machine that uses a transmembrane flux of H(+) or Na(+) ions to drive flagellar rotation. In proton-driven motors, the membrane proteins MotA and MotB interact via their transmembrane regions to form a proton channel. The sodium-driven motors that power the polar flagellum of Vibrio species contain homologs of MotA and MotB, called PomA and PomB. They require the unique proteins MotX and MotY. In this study, we investigated how ion selectivity is determined in proton and sodium motors. We found that Escherichia coli MotA/B restore motility in DeltapomAB Vibrio alginolyticus. Most hypermotile segregants isolated from this weakly motile strain contain mutations in motB. We constructed proteins in which segments of MotB were fused to complementary portions of PomB. A chimera joining the N terminus of PomB to the periplasmic C terminus of MotB (PotB7(E)) functioned with PomA as the stator of a sodium motor, with or without MotX/Y. This stator (PomA/PotB7(E)) supported sodium-driven motility in motA or motB E.coli cells, and the swimming speed was even higher than with the original stator of E.coli MotA/B. We conclude that the cytoplasmic and transmembrane domains of PomA/B are sufficient for sodium-driven motility. However, MotA expressed with a B subunit containing the N terminus of MotB fused to the periplasmic domain of PomB (MomB7(E)) supported sodium-driven motility in a MotX/Y-dependent fashion. Thus, although the periplasmic domain of PomB is not necessary for sodium-driven motility in a PomA/B motor, it can convert a MotA/B proton motor into a sodium motor.

    [interesting bit of mixing and matching]

    Date: 2003/03/21 03:03:24, Link
    Author: niiicholas
    If anyone has text access and could send me the pdf of the previous article I'd be grateful.  I did a google search but no one has put it on the web yet.


    I did turn this up, though, dunno how I missed it before:

    A Scenario for the Evolution of Hemostasis
    by Kevin O'Brien


    A Scenario for the Evolution of Hemostasis
    by Kevin O'Brien

    This is a revised version of an article that originally appeared in the newsgroup. It was composed in response to the following challenge:

    Let's start with the clotting system. Tell us all how the IC core, consisting of fibrinogen, prothrombin, Stuart factor, and accelerin, could have evolved.

    It is granted that prothrombin and the Stuart factor may have evolved from a common ancestor A by duplication and divergence, if A was autocatalytic.

    References specific to have been removed and slight editorial changes have been made. - Richard Harter, editor.



    I've often thought that such an article could be written, I just didn't know who would do it.  But someone has.

    I recommend we attempt to get some version of this on if theyeti et al. consider it reasonable and if we can get permission (its a t.o. poster, I don't think that would be a problem).  

    It would need a fair bit more editing though...

    Date: 2003/03/25 20:49:43, Link
    Author: niiicholas
    EMBO Reports 4, 3, 235 (2003)

    A rather uncritical review:

    Gabby Dover  

    Gabby Dover is at the University of Leicester, UK, and is author of Dear Mr Darwin: Letters on the Evolution of Life and Human Nature (2000).

    Of Moths And Men: An Evolutionary Tale
    by Judith Hooper
    W. W. Norton & Co., New York, USA
    377, $26.95
    ISBN 0 393 05121 8

    Date: 2003/03/29 16:15:44, Link
    Author: niiicholas
    Here is a thread with some striking pics on human tails and natural variation in the tailbone:

    Baby with tail 'reincarnation of Hindu god'


    Date: 2003/03/29 17:43:32, Link
    Author: niiicholas
    A recent post of mine that I rather like:

    (follows some discussion of eye evolution)

    Topic: Distinguishing Mechanisms of Co-option, started by John Bracht

    John writes,


    This is the question I am trying to get at in this thread: how do we know that Darwinian co-option events really occurred by a non-intelligent mechanism? My experience is that there is no "test" that Darwinian thinkers apply to co-option events; rather they simply look at protein similarities and use that as "evidence" for their view. My point is that a design-driven co-option event would look exactly the same from our vantage point and hence the Darwinian comparison-of-similarity approach doesn't really test different mechanisms that might have been responsible for a given system.

    This is the problem with the "vague designer" hypothesis -- an uncharacterized designer could, for all we know, do things however the heck he wants.  The "vague designer" hypothesis can "explain" not only observations supporting standard evolutionary biology but also any other set of observations.

    Darwin had a similar problem: once he had convinced someone that the special creation "poof" model was untenable, a common response was to retreat to a vaguer position such as "the plan of Creation" or whatnot.  There are some great Darwin quotes somewhere on just how scientifically useless such statements are, unfortunately I can only find one at the moment:


    It is so easy to hide our ignorance under such expressions as the “plan of creation,” “unity of design,” &c., and to think that we give an explanation when we only restate a fact. (OoS)

    To get a little more specific, consider one major difference between human intelligent design and "design" as seen in biology.  Human designs -- such as transistors, computers, radios, plastics, GPS systems, etc., etc., -- get invented in one place and then transplanted wholesale into a multiude of other "lineages" -- cars, boats, planes, rockets, etc.  In biology, on the other hand, the transmittance of designs through lineages appears to be strictly limited to that allowed by known processes of heredity, namely:

    1) Lineal descent (parents to children, species to descendent species).  This is the major one.

    2) or, sometimes, lateral gene transfer (although this seems to be limited to fairly simple systems that can fit on plasmids and subject to a number of other constraints, e.g. rare in things like metazoans with protected germline cells).

    In other words, in human design you see an invention originate and then get basically simultaneously integrated across a wide range of "lineages".  In biological design the invention sits in whatever lineage it originated in (small groups of genes on mobile genetic elements being the exception, with a known and observed natural mechanism).

    The fact that putative instances of cooption (the "same" structure being used for different functions) appear to follow the above pattern to a tee seems to me to be a perfect example of John's request regarding:

    how do we know that Darwinian co-option events really occurred by a non-intelligent mechanism?

    There is no reason for us to expect a designer to constrain design-transmittance to the processes of heredity; and yet we see such constraints, as we would expect based on common descent (= the continous operation of everday heredity).

    However, a typical response that I've seen is to invoke front-loading, or "maybe the designer constrained himself to work within lineages for some reason", or "the designer might work in mysterious ways", or some other backup defense in order to save design from the falsification given in the above argument.  And this gets us back to Darwin's point about how vague designer-talk is scientifically vacuous and actually does no explaining at all.

    In summary, you need at least a somewhat specific model of the designer (this does *not* require foreknowledge, just like any proposed hypothesis does not require foreknowledge) in order to have something with scientific tractability.  If ID stays in the "vague" category -- then it will never rise above the level of other such vague ideas ("an immaterial innate force causes design").


    PS: Another similar test is that:

    1) Evolved cooptions will always have the "purpose" of increasing the reproduction of the genes of the organism carrying the new adaptation, but

    2) There is no reason to expect such from IDed cooptions, indeed in human designs the designs are always meant to serve the purposes of the designer.

    This is also, IMO, a good test, but again the IDist can escape by post-hoc appeals to a designer that mimics evolution for some reason.  In doing so they escape the frying pan of falsification but fall into the fire of scientific vacuousness.

    Date: 2003/03/31 22:14:27, Link
    Author: niiicholas
    New TCS article gives us the short version of current euk. phylogeny & who may and may not be primitively non-ciliated:


    J Mol Evol 2003 Apr;56(4):387-96
    Molecular phylogeny of centrohelid heliozoa, a novel lineage of bikont eukaryotes that arose by ciliary loss.

    Cavalier-Smith T, Chao EE.

    Recent molecular and cellular evidence indicates that eukaryotes comprise three major lineages: the probably ancestrally uniciliate protozoan phylum Amoebozoa; the ancestrally posteriorly uniciliate opisthokont clade (animals, Choanozoa, and fungi); and a very diverse ancestrally biciliate clade, the bikonts-plants, chromalveolates, and excavate and rhizarian Protozoa. As Heliozoa are the only eukaryote phylum not yet placed on molecular sequence trees, we have sequenced the 18S rRNA genes of three centrohelid heliozoa, Raphidiophrys ambigua, Heterophrys marina, and Chlamydaster sterni, to investigate their phylogenetic position. Phylogenetic analysis by distance and maximum likelihood methods allowing for intersite rate variation and invariable sites confirms that centrohelid heliozoa are a robust clade that does not fall within any other phyla. In particular, they are decisively very distant from the heterokont pedinellid chromists, at one time thought to be related to heliozoa, and lack the unique heterokont signature sequence. They also appear not to be specifically related to either Amoebozoa or Radiolaria, with which they have sometimes been classified, so it is desirable to retain Heliozoa as a separate protozoan phylum. Even though centrohelids have no cilia or centrioles, the centrohelid clade branches among the bikont eukaryotes, but there is no strong bootstrap support for any particular position. Distance trees usually place centrohelids as sisters to haptophytes, whereas parsimony puts them as sisters to red algae, but there is no reason to think that either position is correct; both have very low bootstrap support. Quartet puzzling places them with fairly low support as sisters to the apusozoan zooflagellate Ancyromonas. As Ancyromonas is the only other eukaryote that shares the character combination of flat plate-like mitochondrial cristae and kinetocyst-type extrusomes with centrohelids, this position is biologically plausible, but because of weak support and conflict between trees it might not be correct. Irrespective of their precise position, our trees (together with previous evidence that Chlamydaster sterni has the derived dihydrofolate reductase/thymidylate synthetase gene fusion unique to bikonts) indicate that centrohelid heliozoa are ancestrally derived from a bikont flagellate by the loss of cilia. The centroplast that nucleates their axonemal microtubules is therefore almost certainly homologous with the centrosome of ciliated eukaryotes and should simply be called a centrosome.


    Recent reappraisal of the basal radiation of eukaryotes argues that all eukaryotes belong to one of three major lineages: Amoebozoa, opisthokonts, and bikonts (Cavalier-Smith 2002a). Opisthokonts comprise the kingdoms Animalia and Fungi and the protozoan phylum Choanozoa (Cavalier-Smith 1987) and are the best-established multikingdom clade on the eukaryotic tree (Baldauf 1999; Baldauf et al. 2000; Cavalier-Smith 1998b, 2002a; Cavalier-Smith and Chao 2003; Patterson 1999; Stechmann and Cavalier-Smith 2002). Opisthokonts are characterized by a single posterior cilium with two centrioles, radiating singlet centrosomal microtubules, flat mitochondrial cristae, an insertion in EF-1, characteristic indels in enolase, and a very rare base-pair change in 18S rRNA (Cavalier-Smith and Chao 2003). Bikonts have only recently been recognized as a clade ancestrally with two divergent centrioles and cilia, at least two dissimilar microtubular centriolar roots, and often ciliary and centriolar root transformation spread over two cell cycles (Cavalier-Smith 2002a). The probable holophyly of the bikonts has been strikingly supported by the discovery that they share a derived gene fusion between dihydrofolate reductase and thymidylate synthetase (Stechmann and Cavalier-Smith 2002). The demonstration that the centrohelid heliozoan Chlamydaster sterni also has this fusion (Stechmann and Cavalier-Smith 2002) strongly indicates that it must have had a biciliate ancestry also and lost both cilia and centrioles. In agreement with this, we find no evidence for a grouping of Heliozoa with Amoebozoa, the only protozoan phylum for which a nonciliated ancestry remains open, given our present understanding of the position of the eukaryote root (Stechmann and Cavalier-Smith 2002).

    Date: 2003/03/31 22:22:48, Link
    Author: niiicholas
    Note that while flagella do not apparently make use of a secretin as the outer membrane pore, type III virulence systems do.  And furthermore, the outer membrane ring of the flagellum *is* secreted by a type II rather than Type III virulence system, an interesting similarity.

    Other points here:
    - 6+ secretion systems in one critter

    - both type II and type III SS have virulent and non-virulent uses


    Secretins of Pseudomonas aeruginosa: large holes in the outer membrane
    Wilbert Bitter1

    Abstract  Pseudomonas aeruginosa produces a large number of exoproteins, ranging from the ADP-ribosyltransferases exotoxin A and ExoS to degradative enzymes, such as elastase and chitinase. As it is a gram-negative bacterium, P. aeruginosa must be able to transport these exoproteins across both membranes of the cell envelope. In addition, also proteins that are part of cellular appendages, such as type IV pili and flagella, have to cross the cell envelope. Whereas the majority of the proteins transported across the inner membrane are dependent on the Sec channel, the systems for translocation across the outer membrane seem to be more diverse. Gram-negative bacteria have invented a number of different strategies during the course of evolution to achieve this goal. Although these transport machineries seem to be radically different, many of them actually depend on a member of the secretin protein family for their function. Recent results show that secretins form a large complex in the outer membrane, which constitutes the actual translocation channel. Understanding the working mechanism of this protein translocation channel could open up new strategies to target molecular machineries at the heart of many important virulence factors.
    Keywords  Secretin - Outer membrane - Exoprotein - Pseudomonas aeruginosa - Pili


    Secreted proteins of Pseudomonas aeruginosa
    Gram-negative bacteria are efficiently protected against many harmful compounds in the environment by the presence of a second membrane, the outer membrane, which functions as a molecular sieve because of the presence of both specific and general pore-forming proteins (Hancock 1997). These porins form channels in the outer membrane through which small hydrophilic molecules with a molecular mass up to 250 Dalton can diffuse. However, gram-negative bacteria also have to transport a range of macromolecules across the outer membrane. Today, at least 19 different soluble exoproteins are known to be secreted by P. aeruginosa (Table 1). Most of these soluble exoproteins, such as exotoxin A, S, U and Y, elastase, staphylolytic protease, lipase and phospholipase C, are well-known virulence factors (Sandkvist 2001a; Cornelis and Van Gijsegem 2000), whereas others are at least suspected to be involved in virulence. This means that, among the gram-negative bacteria, P. aeruginosa is one of the most active secreting species. Proteins that are part of cellular appendages also have to be transported across the outer membrane. These compounds include the subunits that compose the flagella and the type IV pili. Both these appendages are used for binding and motility in P. aeruginosa and are essential for pathogenicity (Hahn 1997). Adhesins and surface-associated enzymes may also belong to this category.
    All the proteins and protein structures described above have to be secreted through outer membrane channel(s). The opening of these channels will have to be strictly regulated in order to retain proper functioning of the outer membrane as a molecular sieve. In the last decade, it has become clear that there are multiple outer membrane channels and transport machineries for the translocation of proteins across this second membrane. If one only considers the soluble exoproteins, already six different pathways have been identified: the type I pathway (Andersen et al. 2000); the type II pathway (Filloux et al. 1998); the type III or contact secretion pathway (Cornelis and Van Gijsegem 2000); the type IV pathway (Christie 2001); the autotransporter pathway (Henderson et al. 1998); and the two-partner secretion pathway (Jacob-Dubuisson et al. 2001). Apart from the type IV secretion pathway, all of these different systems are used (Table 1) or are at least present in P. aeruginosa. In addition, chitinase is probably secreted via a novel pathway (Folders et al. 2001). Although there are many different transport systems, one family of outer membrane proteins has been shown to be particularly useful for P. aeruginosa, the secretins. Members of this family are involved in two of the secretion systems described above: the type II and the type III secretion pathways. These two systems seem to be completely different: the type III system mediates the secretion of virulence factors directly from the cytoplasm into eukaryotic target cells and is homologous to the flagellar assembly system, whereas the type II system secretes folded proteins from the periplasm into the surrounding and is highly homologous to the type IV pili biogenesis machinery. The only common denominator between these systems is the outer membrane component, which belongs to the secretin family (Genin and Boucher 1994). Secretin family members are also used for the biogenesis of type IV pili (Mattick et al. 1996), but not in flagella synthesis. In addition, secretins are involved in other processes, such as the biosynthesis of another class of pili (Skerker and Shapiro 2000) and the biogenesis of filamentous phage particles (Linderoth et al. 1997). These phages, such as Pseudomonas phage Pf3 and Escherichia coli phages M13 and f1, are continuously produced by infected bacterial cells without disrupting the integrity of the bacterial cell. Again, only the outer membrane component of this machinery shows homology with the other secretin-dependent secretion systems described above. Finally, in several other gram-negative bacteria, such as Haemophilus influenza and Neisseria species, secretin family members have been implicated in the process of natural competence, i.e. the uptake of DNA from the environment (Dubnau 1999). However, this dependence can be explained by the fact that, in these cases, type IV pili are involved in competence and secretin family members are essential components in the biosynthesis of this class of pili.

    These data show that secretins are involved in many different processes in Proteobacteria. Recently, genome sequencing projects have demonstrated that secretins can also be found in a wide variety of other bacterial species, including such diverse species as Chlamydia trachomatis, Deinococcus radiodurans, and even the deep-branching species Aquifex aeolicus. This means that the use of secretins for outer membrane transport is widespread among the bacteria and that some of these new secretins could very well be involved in transport processes that have not been characterised thus far. What makes the secretin family members such useful proteins to be employed in protein transport? Part of the answer is probably related to the functional unit of secretins: the oligomeric complex.

    Date: 2003/03/31 22:46:04, Link
    Author: niiicholas
    Since this came up again with the discussion with Nelson Alonso on the ISCID thread, I just came across a review of a recent workshop on evolutionary immunology.  I quote the bit about the origin of recombining receptors:


    Dev Comp Immunol 2003 Apr;27(4):263-71
    Workshop report: evolutionary immunobiology--new approaches, new paradigms.

    Du Pasquier L, Smith LC.


    3. The boundary between invertebrates and vertebrates
    Those working on innate immunity and who are impressed by the efficiency of these defense mechanisms frequently ask, "why did vertebrates acquire an adaptive immune system that was based on somatic rearrangement?" The multiplicity and diversity of the innate systems described above may provide the beginnings of an answer to this question. If an animal like Drosophila, which lives for a relatively short time, requires many germ line encoded innate mechanisms to survive, how many mechanisms will be required for the survival of long lived species? At some point during metazoan evolution, an increase in the number of genes devoted to innate immunity would have been required. Rather than an amplification of genetic material devoted to immune defenses becoming detrimental, the introduction of a somatic mechanism to generate a repertoire of recognition structures resulted in an economy or at least a status quo in the amount of the genome that was devoted to immune responsiveness. At the same time a somatic mechanism providing in fact a `kit' to generate one's repertoire by oneself would probably be favored by species producing few offspring where the value of a single individual would be very important. Therefore it would not be that surprising that phyla other than vertebrates have invented (by means that could be different from those of the vertebrates) a somatic way of increasing the diversity of their receptors (e.g. see the above mentioned possibilities of alternate RNA processing and splicing). Today, one of the striking paradoxes of the evolution of the combinatorial immune system is that RAG homologues appear to be totally lacking in the lower deuterostomes and in all non-deuterostome metazoans. This suggests a rapid evolutionary emergence and phylogenetic restriction for the capacity to generate specific inducible immunity in higher vertebrates. This implies that the introduction of the rearranging machinery occurred in a gene encoding a receptor that was already committed to expression in a lymphocyte-like cell, and perhaps involved in innate immune defense mechanisms. Therefore, to understand this major evolutionary step, a search is under way for the origin of the lymphocyte lineage and for an Ig superfamily (IgSf) gene target which may be similar to a T-cell receptor or an immunoglobulin gene. The animals used in these searches include modern members of classes that preceded the gnathostomes in evolution.

    Michele Anderson (Pasadena) presented information on transcription factors involved in hematopoiesis and the definition of lymphoid lineages. If diversity was a master theme during this workshop, conservation of patterns was another and not only for the Toll cascade. A good example is the conservation of patterns (in structure, function and pathways) of transcription factors. Anderson discussed her investigations of skates, lampreys, amphioxus and sea urchins, and searches for homologues of transcription factors important in hematopoiesis. She has been monitoring the Ikaros/Aiolos/Helios family, PU.1, and GATA-1/2/3 families of transcription factors, all of which include essential or important factors in lymphoid development. In the clear nose skate (Raja eglanteria, a species that is also suitable for developmental studies), the existence of EBF, GATA3, members of the Ikaros family, and PU.1, are all consistent with the finding of Ig and TCR genes expressed at this level of vertebrate phylogeny. Expression of the transcription factor, Spi-C, appeared to be specific to the spleen and therefore, may be involved with B cell development. It was assumed that multiple members of each transcription factor family found in the elasmobranchs arose by gene duplication from a less complex population of progenitor genes. In invertebrates the number of homologues found so far fits with this hypothesis: fewer in the invertebrates and increased gene family sizes in higher vertebrates. For example, PU.1 and Spi-C are not found in the Drosophila genome, while one member of the PU.1 family is found in the lamprey, even though no classical adaptive immune system has been characterized in this species. Based on the sequence of the lamprey GATA gene, it appears to encode a pre-duplication molecule with GATA 2/3 features. The existence of PU.1 and GATA-1/2/3 family transcription factors in the lamprey, a jawless vertebrate, suggests that the stage was set for lineage-specific expression of certain antigen receptors just prior to the introduction of RAG-1 and RAG-2 in the earliest jawed vertebrates. Anderson stressed the importance of the cis-acting elements that control the expression of the duplicated GATA genes and orient them in different patterns of expression. She also warned us about terminology in this field and about the difficulty of identifying orthologues. The workshop participants discussed and agreed upon the need for a strong gene ontology if highly diverse systems are to be compared fruitfully.

    Still within the context of transcription factors, Jack Marchalonis (Tucson) described the lamprey vitamin D receptor (VDR), a ligand-specific transcription factor that is a member of the Nuclear Receptor Superfamily (NRS), which has been cloned from `protospleen' cDNA of the larval stage. In mammals, the VDR is a transcription factor that mediates the actions of its ligand, vitamin D, and can promote monocyte/macrophage differentiation and inhibit proliferation and cytokine production by activated T lymphocytes. These functions make the VDR relevant and interesting for innate immunity. Like VDRs of jawed vertebrates, the lamprey molecule consists of two C4-type zinc fingers, and both DNA-binding segments and ligand-binding segments show significant conservation across species. Cladograms of the NRS family, using the ecdysone receptor of insects as an outgroup (a distantly related member of this gene family) indicated that the lamprey VDR clustered unambiguously with the other vertebrate VDRs and constituted the basal member of the group.

    Marchalonis (Tucson) also commented on the complete characterization of the RAG1/RAG2 gene cluster in the sandbar shark and the evolutionary and functional implications of this analysis. The ancestors of the sharks were apparently the first vertebrates in phylogeny to have acquired RAG genes which have been highly conserved during evolution both in terms of sequence and gene organization. In common with other vertebrate species, the shark RAG2 coding region lacks introns and is closely linked in opposite orientation to the RAG1 gene. The intergenic region (~10 kb) is comparable in length to that of tetrapods. About 40% of the spacer consists of SINE and LINE fragments homologous to those found in other sharks, reptiles and birds.

    (the bit about the regulation of lamprey receptors is key...)

    In the conclusion the old theme of change-of-function is emphasized:


    At the heart of it, we are attempting to understand the dynamics of complex systems by comparative methods. For example, are there common threads in the metabolic machinery from one system to another? Clearly there must be, as one of the themes of this conference was the adaptation of pre-existing molecules and metabolic pathways to new functions. Likewise, are there common features of the immune (or other metabolic) system that can be extracted and used to understand more fully the evolution of immunity and organisms? This field has become known as phylogenomics. Further, the response of an organism to environmental change is equivalent in concept to immune responses to invading organisms. Does it really matter whether the environmental challenge is a pathogen or an elevation in temperature? The organism will respond to environmental changes that alter metabolic functions. The application of genomic tools to the study of ecosystems, ecogenomics, is an emerging discipline dedicated to this end and owes much to developments in immunology. We are very familiar with the common features in ecosystems of primary producers, herbivores, carnivores and decomposers which circumscribes the flow of energy and mass through the system. In phylogenetics, there are accepted hierarchies in vertebrate groups, and some invertebrates as well, which are assumed to reflect the ancestor–descendent relationships (i.e. flow of genetic material over time). However, similar unifying principles and classification schemes are completely lacking in studies of cellular mechanisms except where individual components are concerned (e.g. the TCA cycle). Hence, the concepts developed in a systems approach to immune function can cut across a wide range of biological studies and mathematical tools are needed to exploit these data.

    ...this last bit seems to be saying that understanding the evolution of a complex system is much easy when you have a good phylogenetic understanding of the system (as with the immune system) than when you don't (e.g. most of Behe's IC systems, which originated in single-celled organisms).

    Date: 2003/03/31 22:49:44, Link
    Author: niiicholas
    In the "here is part of what non-rearranging receptors do" category:


    Vet Immunol Immunopathol 2003 Jan 10;91(1):1-12
    TOLL-like receptors linking innate and adaptive immune response.

    Werling D, Jungi TW.

    Institute of Veterinary Virology, University of Berne, Langgass-Str. 122, CH-3012 Bern, Switzerland.

    Invading pathogens are controlled by the innate and adaptive arms of the immune system. Adaptive immunity, which is mediated by B and T lymphocytes, recognises pathogens by rearranged high affinity receptors. However, the establishment of adaptive immunity is often not rapid enough to eradicate microorganisms as it involves cell proliferation, gene activation and protein synthesis. More rapid defense mechanisms are provided by innate immunity, which recognises invading pathogens by germ-line-encoded pattern recognition receptors (PRR). Recent evidence shows that this recognition can mainly be attributed to the family of TOLL-like receptors (TLR). Binding of pathogen-associated molecular patterns (PAMP) to TLR induces the production of reactive oxygen and nitrogen intermediates (ROI and RNI), pro-inflammatory cytokines, and up-regulates expression of co-stimulatory molecules, subsequently initiating the adaptive immunity. In this review, we will summarize the discovery and the critical roles of the TLR family in host defense, briefly allude to signaling mechanisms mediating the response to TLR ligands, and will provide an update on current knowledge regarding the ligand specificity of these receptors and their role in immunity of domestic animals, particularly cattle.

    Date: 2003/03/31 23:29:49, Link
    Author: niiicholas
    Wow, thanks for the info Erik.

    I think that the variability of the coccyx is interesting as it is just the kind of thing that CD mentions a bunch of times in OoS -- that structures that have lost utility become more variable...

    Date: 2003/04/04 21:26:21, Link
    Author: niiicholas
    Good little one that Ian Musgrave posted at t.o. in rebuttal to a creo reiterating Behe's argument regarding Ken Miller's citation of Barry Hall's work on lactose metabolism:


    G'Day All
    Address altered to avoid spam, delete RemoveInsert

    On Thu, 3 Apr 2003 17:59:50 +0000 (UTC), (Sean Pitman M.D.) wrote:

    >Evolving Rube Goldberg Machines

    [enormous snip]
    >But what if the E. coli had
    >not been so fortunate as to have this spare tire gene?  What would
    >have happened then?  Hall wondered about this himself.  He then
    >deleted the spare tire gene as well as the lacZ genes.  Would there be
    >lactase evolution now?

    See Matsumura I, Ellington AD. In vitro evolution of
    beta-glucuronidase into a beta-galactosidase proceeds through
    non-specific intermediates. J Mol Biol. 2001 Jan 12;305(2):331-9)
    where they have evolved a beta glactosidase from an enzyme other than
    the "spare tyre". I believe I have directed you to this paper before.

    link to thread

    Da paper:


    Matsumura I, Ellington AD. In vitro evolution of
    beta-glucuronidase into a beta-galactosidase proceeds through
    non-specific intermediates.
    J Mol Biol. 2001 Jan 12;305(2):331-9

    The Escherichia coli beta-glucuronidase (GUS) was evolved in vitro to catalyze the hydrolysis of a beta-galactoside substrate 500 times more efficiently (k(cat)/K(m)) than the wild-type, with a 52 million-fold inversion in specificity. The amino acid substitutions that recurred among 32 clones isolated in three rounds of DNA shuffling and screening were mapped to the active site. The functional consequences of these mutations were investigated by introducing them individually or in combination into otherwise wild-type gusA genes. The kinetic behavior of the purified mutant proteins in reactions with a series of substrate analogues show that four mutations account for the changes in substrate specificity, and that they are synergistic. An evolutionary intermediate, unlike the wild-type and evolved forms, exhibits broadened specificity for substrates dissimilar to either glucuronides or galactosides. These results are consistent with the "patchwork" hypothesis, which postulates that modern enzymes diverged from ancestors with broad specificity.

    Date: 2003/04/04 23:21:16, Link
    Author: niiicholas

    Date: 2003/04/04 23:50:11, Link
    Author: niiicholas
    As Commentary has once again indulged Berlinski's meanderings around evolutionary theory (they never appear to run out of purple ink for his prose), I am starting a thread to discuss him, accumulate links, etc., perhaps eventually have a FAQ.

    Eye-evolution specific, or general picking of nits, as there are many to pick with Berlinski and he sure loves doing it to the Darwinists...

    First, background links on Berlinski and his writings:

  • In the ID-files section of AE.
  • The Discovery Institute bio and articles list.

    Recent articles under discussion:
  • Has Darwin Met His Match? David Berlinski, Commentary, December 1, 2002
    (Berlinski on ID and evolution; full-text must be purchased, but his section on the eye is hosted by the DI under The Vexing Eye)

  • The many letters in response to Berlinski were originally online here at Commentary's website but now are not (although you can purchase them here). However, we do have:

  • The subset of responses from DI fellows
  • Some of the critics' responses online at Talk.Reason

    And then:
  • A Scientific Scandal
    (Commentary.  April 1, 2003: On the 1994 paper by Nilsson and Pelger on eye evolution, and the usage thereof.  Online at the DI with a few typos and weirdly-formatted equations)

    Older articles:
  • Keeping an Eye on Evolution
    (Berlinski reviews Dawkins Climbing Mount Improbable and comments on eye evolution at length) (also hosted by the DI)

    And the famous:
  • The Deniable Darwin
  • Denying Darwin: David Berlinski and Critics

  • Date: 2003/04/05 00:33:05, Link
    Author: niiicholas
    There are some great t.o. posts on Berlinski that never got turned into FAQs:

    Here is the link to the google search, see the part-by-part critique "Response to Berlinski" by Paul J. Gans replying to "A Deniable Darwin".

    If you scroll down a bit you even find some Berlinski posts from 1996 where various t.o. regulars hand him his head on topics like molecular evolution.

    Date: 2003/04/05 00:55:52, Link
    Author: niiicholas
    Here is the Berlinski-relevant bit of my recent t.o. post:

    A mistaken popularization, even fairly widely repeated, does not amount to "scientific fraud" as Berlinski alledges.  Further, it should be noted that some sites follow the paper closely, e.g. good ol' Don Lindsay's site from 1998 is fine and worth recommending to people.

    Nilsson ('s lab?) describes this 1994 paper as "theoretical modelling", with full computer simulations in the "something we will do" category:

    Research in the Nilsson lab

    A long standing question has been how variation and selection can produce an imaging eye. We have previously approached this question by theoretical modelling (Nilsson and Pelger, 1994: A pessimistic estimate of the time required for an eye to evolve. Proc R Soc Lond B 256: 53-58) which demonstrate that even with rather weak selection, the structures of a focused camera type eye can evolve in less than half a million generations. We now continue this line of research by computer simulations of eye evolution. These simulations are made to accurately mimic a realistic genetic control, and involves selection from populations of partially mutated offspring. The project has three principal aims: 1, to understand the conditions and criteria that select the fundamental optical types of eye (compound and simple etc) during early eye evolution; 2, to better understand the fine tuning of eyes to special visual requirements and habitat conditions; 3, to provide an insight into the mechanisms of genetic control required for evolution in general and eyes in particular. (Dan-Eric Nilsson, Lars Gislén)

    ...however, I strongly doubt that the calculations that they performed to determine eye acuity (their measure of eye "goodness") were done by hand.  The paper repeatedly speaks of functions, curves, etc. which, in order to plot them, would always be done with a computer. Therefore it was a computer model of a sort, although not what I would call "a stochastic computer simulation" which is what Dawkins was implying had occurred (he did not use those exact words, mind you).

    I think that people have a kind of mystical notion about computer models, that if the model is "more complex than I can understand" then it is equivalent to "they modelled the world in all necessary detail inside the computer!!".  This is particularly true if someone presents a nice animation as the output.   This is not the case.  All computer models are gross simplifications, and IMO there is no particular hard-and-fast distinction between a theoretical model where calculations are done with a computer and a computer simulation where there is some attempt to perform a simulation with random inputs and explicit time-steps.  It is, to plagiarize from Darwin, a difference of degree, not of kind.

    "Mere calculations" computer models, e.g. the kind that can be done in a spreadsheet, have a very valid place.  E.g. for a class I once simulated atmospheric temperature profiles in various latitudinal zones (a 2-D climate model) in Excel.  You can reproduce some important features of the atmosphere using this kind of simple model (and in fact modern Global Climate Models are in part just a repetition of this kind of model in 3D).

    So, to sum up my assessment of Berlinski:

    How very remarkable all this is--inasmuch as there are no computer models mentioned, cited, or contained in Nilsson and Pelger's paper;


    inasmuch as Dan-Erik Nilsson denies having based his work on any computer simulations;

    The DI reports that Nilsson says this, here:

    "Evolution" Series Claim on Eye Evolution More Fiction than Fact

    ...but there is no indication that the complexities of defining "computer model" were discussed.

    inasmuch as Nilsson and Pelger never state that their task was to "set up computer models of evolving eyes" for any reason whatsoever;

    ...well, Nilsson says that he is doing just that now.

    inasmuch as Nilsson and Pelger assume but do not prove the existence of "a smooth gradient of change, from flat skin to full camera eye, such that every intermediate is an improvement";

    Here I strongly disagree.  This is exactly one of the things that they documented IMO: that at least at the morphological level, just such a continuum exists, given the starting point.  Only small quantitative variations in "cell" position, thickness, density, etc. are required.

    and inasmuch as the original light-sensitive patch in Nilsson and Pelger's paper was never allowed to undergo "localized random mutations of its refractive index."

    This is true as far as I can tell; however we *know* that variation + selection results in the kinds of gradual "microevolutionary" changes that Nilsson & Pelger were modelling in their paper.  The only changes they invoked in their model were of the finch-beak-size variation type: small and quantitative.  This is pretty much the point of their paper.

    And how very remarkable again--inasmuch as there are no computer "screens" mentioned or cited by Nilsson and Pelger, no indication that their illustrations were computer-generated, and no evidence that they ever provided anyone with a real-time simulation of their paper where one could observe, "almost like a conjuring trick," the "swift and decisive" results of a process that they also happen to have designed.

    True, but this gets us back to what a naive view of a "computer model" Berlinski's depiction is.  Still, Dawkins shouldn't have implied that such existed.

    (But: Didn't the "Evolution" special have a section wherein Nilsson or somebody constructed a *physical* model of their eye evolution scenario, where various stages could be enacted, variations tried, and the resulting "vision" actually seen?  I remember someone gradually inflating a lens or something at any rate, and the picture moving from blurry to being focused.)

    And yet again how very remarkable--inasmuch as Nilsson and Pelger's "computer-simulation model" did not home in unerringly on Mattiessen's ratio, Nilsson and Pelger having done all the homing themselves and thus sparing their model the trouble.

    Tis true, there was no "homing" in the form of a search algorithm --however, they did demonstrate progressive advantage for eye shapes approaching Mattieseen's ratio.  The relative advantage can be calculated, which is what they did.

    Each and every one of these very remarkable asseverations can be explained as the result of carelessness only if" one first indicts their author for gross incompetence.

    Mistakes happen.  I can think of more than a few that Berlinski has made, and yet he is the one declaring the central theory of modern biology to be no better than ID (which he now considers similarly unsupported).

    BTW, it appears that someone has kindly put an HTML version of the Nilsson article online here (there is no pdf that I am aware of anywhere):

    A pessimistic estimate...
    (unfortunately there are no graphics included, and a few typos/format issues)

    FINAL QUESTIONS. Why, in the nine years since their work appeared, have Nilsson and Pelger never dissociated themselves from claims about their work that they know are unfounded?

    They probably did, somewhere.  It is not the duty of authors to chase down every representation of their work, particularly *in other countries*.  It might surprise Berlinski but not every country has the United States' hangup with evolution.

    This may not exactly be dishonest, but it hardly elicits admiration. More seriously, what of the various masters of indignation, those who are usually so quick to denounce critics of Darwin's theory as carrying out the devil's work? Eugenie Scott, Barbara Forrest, Lawrence Krauss, Robert T. Pennock, Philip Kitcher, Kelly Smith, Daniel Dennett, Paul Gross, Ken Miller, Steven Pinker--they are all warm from combat. Why have they never found reason to bring up the matter of the mammalian eye and the computer simulation that does not exist?

    What, are they obligated to dig through every popular science book, look up the original literature on every single topic and determine the degree of accuracy of representation?  This can be done but it is not a small matter.  I suspect that Berlinski's evolution-related works would not fare well.  For instance:

    Commentary, Vol. 101, June 1996 No. 6 The Deniable Darwin


    Unflagging Success Darwin conceived of evolution in terms of small variations among organisms, variations which by a process of accretion allow one species to change continuously into another. This suggests a view in which living creatures are spread out smoothly over the great manifold of biological possibilities, like colors merging imperceptibly in a color chart.

    Life, however, is absolutely nothing like this. Wherever one looks there is singularity, quirkiness, oddness, defiant individuality, and just plain weirdness. The male redback spider (Latrodectus hasselti), for example, is often consumed during copulation. Such is sexual cannibalism -- the result, biologists have long assumed, of "predatory females overcoming the defenses of weaker males." But it now appears that among Latrodectus basselti, the male is complicit in his own consumption. Having achieved intromission, this schnook performs a characteristic somersault, placing his abdomen directly over his partner's mouth. Such is sexual suicide-awfulness taken to a higher power.2

    It might seem that sexual suicide confers no advantage on the spider, the male passing from ecstasy to extinction in the course of one and the same act. But spiders willing to pay for love are apparently favored by female spiders (no surprise, there); and female spiders with whom they mate, entomologists claim, are less likely to mate again. The male spider perishes; his preposterous line persists.

    This explanation resolves one question only at the cost of inviting another: why such bizarre behavior? In no other Latrodectus species does the male perform that obliging somersault, offering his partner the oblation of his life as well as his love. Are there general principles that specify sexual suicide among this species, but that forbid sexual suicide elsewhere? If so, what are they?

    Once asked, such questions tend to multiply like party guests. If evolutionary theory cannot answer them, what, then, is its use? Why is the Pitcher plant carnivorous, but not the thorn bush, and why does the Pacific salmon require fresh water to spawn, but not the Chilean sea bass? Why has the British thrush learned to hammer snails upon rocks, but not the British blackbird, which often starves to death in the midst of plenty? Why did the firefly discover bioluminescence, but not the wasp or the warrior ant; why do the bees do their dance, but not the spider or the flies; and why are women, but not cats, born without the sleek tails that would make them even more alluring than they already are?

    Why? Yes, why? The question, simple, clear, intellectually respectable, was put to the Nobel laureate George Wald. "Various organisms try various things," he finally answered, his words functioning as a verbal shrug, "they keep what works and discard the rest."

    But suppose the manifold of life were to be given a good solid yank, so that the Chilean sea bass but not the Pacific salmon required fresh water to spawn, or that ants but not fireflies flickered enticingly at twilight, or that women but not cats were born with lush tails. What then? An inversion of life's fundamental facts would, I suspect, present evolutionary biologists with few difficulties. Various organisms try various things. This idea is adapted to any contingency whatsoever, an interesting example of a Darwinian mechanism in the development of Darwinian thought itself.

    A comparison with geology is instructive. No geological theory makes it possible to specify precisely a particular mountain's shape; but the underlying process of upthrust and crumbling is well understood, and geologists can specify something like a mountain's generic shape. This provides geological theory with a firm connection to reality. A mountain arranging itself in the shape of the letter "A" is not a physically possible object; it is excluded by geological theory.

    The theory of evolution, by contrast, is incapable of ruling anything out of court. That job must be done by nature. But a theory that can confront any contingency with unflagging success cannot be falsified. Its control of the facts is an illusion.


    I don't have answers to all of these questions, but just as an amateur I can provide some.  Unfortunately Berlinski never saw fit to look any of these up, and none of his DI fellows have bothered to correct him since the article came out in 1996.  Roughly in order:

    1) Male-eating is a subset of the widespread practice (in arthropods) of males offering up nutrient "gifts" to females for the purposes of (1) obtaining copulation and (2) prolonging copulation and preventing other males from copulating.  And it is not true that the males always get eaten -- some of them will run for their lives at the first hint of hostility.  This is only my hazy summary, but there is a massive literature on the topic.  See e.g.:

    Choe, Jae C., Crespi, Bernard J.  The Evolution of Mating Systems in Insects and Arachnids.  Cambridge, 1997.

    ...I would like to see a theory other than evolution devote the kind of attention and scientific sophistication that evolutionary theory has brought to the issue. What evolution predicts is that there will be a selective benefit for whatever apparently crazy behavior one sees (assuming it is a species-wide trait that easily could/should be something else).  And apparently entomologists have confirmed that this is the case in the spider that Berlinski cites, even though he seems not to appreciate the significance of the fact.

    2) "Why is the pitcher plant carnivorous, but not the thorn bush?"

    If Berlinski had bothered to get up off his tush and go to the library to consult the literature -- which after all is what libraries are for -- he wouldn't have been so mystified.  In a 1989 article by Thomas Givnish (of the Dept. of Botany, University of Wisconsin) entitled "Ecology and Evolution of Carnivorous Plants," Berlinski's question is anticipated and answered.  I have included translation of the scientific jargon [in square brackets like this] for non-nerds in the audience.

    Insofar as plants essentially trade carbohydrates [carbon compounds -- aka sugars -- generated from photosynthesis] for nutrients from animals or microbes in nitrogen fixation and ant-fed myrmecophily [ant-plant mutually beneficial relationships], the question naturally arises as to whether the same cost-benefit considerations and expected pattern of distribution apply to species with these associations as to carnivorous plants.  With regard to nitrogen fixation, the answer is probably a qualified yes.  Sunny, moist, nitrogen-poor conditions are most likely to favor nitrogen-fixing symbioses, as they do carnivores. However, the conditions favoring these two groups should differ in three important respects.  First, because highly anaerobic [oxygen-deprived, as in bogs] conditions in the soil are inimical to nitrogen fixation in root nodules (Pate, 1986), nitrogen-fixing symbioses are more likely to occur in well-drained or seasonally arid sites than carnivores.  Second, legumes and other nitrogen-fixing plants seem to be most competitive on sites that are relatively rich in other limiting nutrients, especially phosphorus (e.g., see Tilman, 1982); carnivores might be expected to have an advantage in soils that lack any nutrient that is abundant in prey carcasses [nitrogen can be fixed from the atmosphere, but phosphorus and other nutrients cannot be].  Third, nitrogen fixation always entails the use of nitrate reductase, and thus, of molybdenum; nitrogen-fixing symbioses should thus be excluded from molybdenum-poor soils, as they indeed are (Pate, 1986).  This same exclusion should apply only to those carnivores that obligately produce nitrate reductase [that is, few to none of them --NT].  (Givnesh 1989, p. 282, emphasis added)

    In other words, the main answer to Berlinski's question is that nitrogen fixation doesn't work in the oxygen-poor muck of stagnant bogs, which gives the advantage to plants with an alternative means of acquiring nitrogen, namely carnivory.  The secondary answer to Berlinski's question is that nitrogen fixing plants still need to get their trace nutrients (such as phosphorous) from the soil, and have the special requirement of molybdenum, so that in places where these nutrients are absent carnivorous plants have a further advantage.

    Givnesh, T. J. (1989). Ecology and Evolution of Carnivorous Plants. Plant-Animal Interactions. W. G. Abrahamon. New York, McGraw-Hill Book Company: 243-290.

    3) "[w]hy does the Pacific salmon require fresh water to spawn, but not the Chilean sea bass?"

    I have no idea.  Salmon are however related to a number of freshwater fish like trout.  Are seabass?  Is there an icthyologist in the audience?  Did Berlinski ever consult one?

    4) "Why has the British thrush learned to hammer snails upon rocks, but not the British blackbird, which often starves to death in the midst of plenty?"

    I doubt that this even occurs as a regular matter.  Why did Berlinski never provide a citation?  I expect that the specialization of bird species on different foods would however be an important thing to consider.

    5) "Why did the firefly discover bioluminescence, but not the wasp or the warrior ant."

    Last I checked, wasps and ants were colonial social species where the queen is fertilized by one or a few males, IIRC just once before a long period of hive-making.  Fireflies are, I expect, totally different.  There are however chapters on both groups in Choe & Crespi (1996).

    6) "why do the bees do their dance, but not the spider or the flies"

    Well, gee, maybe because bees are colonial honey gatherers that live or die as a hive, and need to communicate the good nectar sources, while flies and spiders do nothing of the sort.

    7) "why are women, but not cats, born without the sleek tails that would make them even more alluring than they already are?"

    Berlinski is speaking for himself regarding attaction to tails, but the topic was recently discussed on t.o.:

    Code Sample

    > >And oh, another "little question".  Why did humans lose their tails?
    > Now, that's the question. Actually, the tails in that line were
    > already lost in the last common ancestors of all apes [gibbons and
    > great apes all lack (external) tails].
    > Note that among Old World monkeys, there are groups like the
    > genus Macaca with both long-tailed and almost tailless species.
    > What might be a selective advantage for taillessness? It occurs to me
    > that in an animal like an early ape [or a macaque] that doesn't use
    > the tail for anything much, it's just something that can get injured,
    > such as bitten in a fight and infected.  
    > >It seems like a good long strong tail could have supplied balance for
    > >walking on two legs.
    > But it was already too late by then. Our ape ancestors already
    > lacked tails.
    > cheers.

    The pattern may be running on top of branches vs. brachiating (hanging
    underneath them).  For the former, a tail is handy for balance, for
    the latter it's not.  Once a primate gets big enough it switches to
    brachiation and (several times indepedently, apparently), the tail is
    reduced or lost.

    Great apes

    Some macaques (see above, I don't know much about them)

    Large lemurs -- e.g., the largest extant lemur, Indri indri, has but a
    stubby little tail.  I believe the larger (up to gorilla-sized)
    extinct subfossil lemurs also have no tails.

    ...maybe others.  These aren't primates, but do tree sloths have
    significant tails?

    ...and I can add:


    "With an increase in body size, a critical point is reached where a potentially unstable system will inevitably lead to overbalancing (fig. 3.21).

    Figure 3.21 Caption: ...with increase in body size the ratio [of branch size to body size] becomes critical and overbalancing can occur; ...suspension provides one solution."

    (Napier JR, and Napier, PH. The natural history of the primates, MIT Press, Cambridge, 1997, p. 44, )

    ...and note that humans are descended from large, brachiating -- and not coincidentally, tailless -- apes.

    Berlinski's comparison of geology to evolution is more apt than he knows.  He can see how geology gives good overall explanations of mountains, if not every detail -- but for some reason he can't see that evolution does the same with organisms.  Evolution predicts correlation of traits with the environment.  Berlinski never looks at the environment (physical and ecological) in which his particular traits of interest occur, so he doesn't understand why they occur.[/quote]

    Returning to Berlinski's original article in this thread:

    And what should we call such a state of affairs? I suggest that scientific fraud will do as well as any other term.

    If Dawkins' mistake is fraud, then Berlinski's multiple and repeated mistakes amount to a far ranging conspiracy (perhaps, a conspiracy to keep himself from understanding biology).  I suggest that pronouncing on biology, without first knowing any, is the greater sin.

    This anti-Berlinski rant has been developing in my head for some time. Thanks to Sunday morning for allowing its expression...


    Date: 2003/04/05 01:05:24, Link
    Author: niiicholas
    Hmm.  Perhaps we should have a FAQ, "20 questions with David Berlinski" where all of his various questions are answered, and then we ask him some questions of our own.

    Add such things to this thread if they occur to you.

    Date: 2003/04/05 01:55:45, Link
    Author: niiicholas
    Here is a bit of startling naivete from Berlinski's latest ("A Scientific Scandal").  I may send this bit as a letter to commentary or somthing.


    Let us agree that in the development of an eye, an initial light-sensitive patch in a given organism becomes invaginated over time. Such a change requires a corresponding structural change to the organism's anatomy. If nothing else, the development of an eye requires the formation of an eye socket--hardly a minor matter in biological terms. Is it really the case that an organism otherwise adapted to its environment would discover that the costs involved in the reconstruction of its skull are nicely balanced by what would initially be a very modest improvement in sensitivity to light? I can imagine the argument going either way, but surely an argument is needed.

    While Berlinski should be congradulated for pointing out Dawkins' inaccurate popularization of Nilsson and Pelger's article on eye evolution as a stochastic computer simulation (it was actually a mathematical model), Berlinski should remove the plank from his own (discussion of the) eye.  In "A Scientific Scandal" he asserts that one of the problems for eye evolution that Nilsson and Pelger did not consider was how the skull would be "reconstructed" to include eye sockets.

    But as any decent student who has taken high school biology would know (at least as long as evolution was not expunged due to creationist political armtwisting), eyes evolved before bones!  Cephalochordates, the closest invertebrate relatives of vertebrates, have primitive eyes but no bones.  In fact, based on genetic evidence many biologists now think that vertebrate eyes share a common ancestral eyespot with insect eyes, the common ancestor being a perhaps millimeter-long, nearly transparent but eyespot-equipped worm.

    Unfortunately, it is a typical creationist strawman to envision eye evolution as occurring on some kind of mythical eyeless fish with a fully-formed skull, brain, etc.  On the contrary, biologists (who actually know some biology) know that all manner of gradations of eye complexity exist in extant organisms, from creatures with an "eye" consisting of a single photoreceptor cell, through all of the various stages that Nilsson and Pelger depict, to the "advanced" camera eyes of mammals and cephalpods.  Sometimes the whole sequence from eyespot to advanced eye with lens can be seen in a single group (e.g. snails), yet another thing which Berlinski would have known if he'd followed the reference that Nilsson and Pelger gave to the actual classic work on eye evolution, a monster 56 page article by Salvini-Plawen and Mayr in the journal Evolutionary Biology (volume 10, 1977) that reviewed hundreds of papers on eyes across the animal kingdom, entitled "On the evolution of photoreceptors and eyes".  Complex eyes with lenses have even evolved in single-celled dinoflagellates, which have no brains, blood vessels, or numerous other features Berlinski is concerned about.

    Berlinski on the other hand has a brain as well as eyes, but apparently does not see when it comes to biology.  He is not a creationist but he certainly seems to hang out with them and uncritically repeats many of their arguments, unaware of the biological facts which contradict them.  If Berlinski is going to declare as bunk the central organizing theory of biology, he should be taking the matter up with biologists in the professional literature, rather than in forums like Commentary, wherein elementary questions like "which came first, skulls or eyes?" can be botched and yet still get published.

    Date: 2003/04/05 02:47:35, Link
    Author: niiicholas
    BTW, Nilsson is interviewed in the PBS "Evolution" series, and the segment is online here:

    Evolution of the Eye  

    Zoologist Dan-Erik Nilsson demonstrates how the complex human eye could have evolved through natural selection acting on small variations. Starting with a simple patch of light sensitive cells, Nilsson's model "evolves" until a clear image is produced. Examples of organisms that still use the intermediary forms of vision are also shown. From Evolution: "Darwin's Dangerous Idea."

    Salient points:

    (1) "Computer model" or "computer simulation" is never mentioned, all anyone talks about is Nilsson's "calculations".  So the whole DI stink about this starting in 2001 was really about Dawkins, because the video represents Nilsson's work accurately.

    (2) Nilsson does show a physical model he has constructed which allows one to "see" what the eye would "see" at various stages in the eye sequence.

    Date: 2003/04/05 02:56:54, Link
    Author: niiicholas
    Section of Futuyma's textbook on the evolution of complex features.

    Features the snail eye continuum from Salvini-Plaw and Mayr:

    Date: 2003/04/05 11:07:10, Link
    Author: niiicholas
    Other Nilsson papers (Web of Science search):

    TRENDS NEUROSCI 13 (2): 55-64 FEB 1990

    BIOSCIENCE 39 (5): 298-307 MAY 1989

    P ROY SOC LOND B BIO 217 (1207): 177-& 1983

    Also see the PubMed search.

    Regarding Nilsson and Pelger 1994, Web of Science reveals that it has been cited 32 times in their database.  It would be instructive I think to see how many papers actually characterize the paper as a stochastic simulation.  For instance, Thornhill and Ussery 2000 ("A classification of possible routes of Darwinian evolution," J THEOR BIOL 203 (2): 111-116  ISI PubMed) write:


    (b) Parallel direct Darwinian evolution. This means approximately synchronous changes in more than one component, so that modification to other components always occurs before the total modification to any one component has become significant. For example, in the evolution of the eye of Nautilus, and of the vertebrate eye if this passed through a Nautilus-like stage (Land & Fernald, 1992), it would be necessary for the evolution of the retina to be approximately synchronous with that of the pinhole eye. The retina is accessible via smallsteps from a single photosensitive cell, with increments of photosensitivity, and the pinhole eye is likewise accessible from a minor concavity, with incremental advantages initially in physical protection and then in focusing (Nilsson & Pelger, 1994). However, neither component would function without the other, and, furthermore, the retina would be exposed to damage if not enclosed.

    ...which seems pretty reasonable to me.

    Date: 2003/04/05 11:18:43, Link
    Author: niiicholas
    Here's another gem from Berlinski 2003.  Berlinski lists a larger number of problems that he has with the paper.  One of them is that Nilsson and Pelger don't give any details about how they calculated optical acuity:


    Nilsson and Pelger treat a biological organ as a physical system, one that is subject to the laws of theoretical optics. There is nothing amiss in that. But while theoretical optics justifies a qualitative relationship between visual acuity on the one hand and invagination, aperture constriction, and lens formation on the other, the relationships that Nilsson and Pelger specify are tightly quantitative. Numbers make an appearance in each of their graphs: the result, it is claimed, of certain elaborate calculations. But no details are given either in their paper or in its bibliography. The calculations to which they allude remain out of sight, if not out of mind.

    The graphics he is referring to are Figure 1a, 1b, and 1c (attached).


    Figure 1. Strategies for improving spatial resolution in an evolving eye. (a) An originally flat light-sensitive patch, or retina, is gradually invaginated (solid line) to form a pit whose distal aperture keeps the size of the original patch. The optical resolution is calculated as the inverse of the field of view of a point in the centre of the retina. At various points on the curve, the deepening of the pit is interrupted and all morphological change is instead spent on constriction of the aperture (broken lines). Calculations are made for aperture constriction to start when the pit depth, P. is 0.1, 0.5, 1.0 and 1.5 times the original width of the patch. (b) Optimisation of lenses aperture. Continuations of the dashed P = 1 curve in (a), but with photon noise taken into account with equation (1). The three curves are calculated for ambient intensities (I) separated by two log units. The upper curve is thus for an intensity 10000 times higher than that for the lower curve. The intensity is in units normalised to the nodal distance (pit depth): photons per nodal distance squared per second per steradian. The unconventional use of nodal distance instead of micrometres in the unit allows the three curves to be interpreted as eyes differing in size by a factor of 10. assuming constant intensity, the upper curve is thus for an eye with h is 100 times larger than that for the lower curve.

    There is an optimum aperture size, indicated vertical lines, beyond which resolution (maximum resolvable spatial frequency) cannot be improved without a lens. © The optical resolution plotted as a function of the gradual appearance of a graded-index lens. The spherical lens is assumed to fill the aperture, and to be 2.55 lens radii away from the retina (e.g. as in fish eyes (Fernald 1990). The central refractive index of the lens is plotted on the horizontal axis. From this value the refractive index is assumed to follow a smooth gradient down to 1.35 at the peripheral margin. The calculation demonstrates that optical resolution continuously improves prom no lens at all to the focused condition where the central refractive index is 1.59. The maximum resolution in the focused Condition will be limited by both photon noise, as in (b), and by diffraction in the lens aperture, but none of these limitations are significant within the range plotted. The vertical axis of all three graphs (a) © was made logarithmic to allow for comparisons of relative improvement. A doubling of performance is thus always given by the same vertical distance.

    Date: 2003/04/05 11:41:53, Link
    Author: niiicholas
    Berlinski claims,


    Numbers make an appearance in each of their graphs: the result, it is claimed, of certain elaborate calculations. But no details are given either in their paper or in its bibliography.

    But did he actually read the paper?  Nilsson and Pelger in fact spend a paragraph explaining the calculation of each graph.

    For Figure 1a, they say:


    We let the evolutionary sequence start with a patch of light-sensitive cells, which is backed and surrounded by dark pigment, and we expose this structure to selection favouring spatial resolution. We assume that the patch is circular, and that selection does not alter the total width of the structures. The latter assumption is necessary to isolate the design changes from general alterations of the size of the organ. There are two ways by which spatial resolution can be gradually introduced: (i) by forming a central depression in the light sensitive patch; and (ii) by a constriction of the surrounding pigment epithelium Both these morphological changes reduce the angle through which the individual light-sensitive cells receive light. The relative effects that depression and constriction have on the eye's optical resolution is compared in figure 1a. Initially, deepening of the pit is by far the most efficient strategy, but when the pit depth equals the width (P= 1 in figure 1a), aperture constriction becomes more efficient than continued deepening of the pit. We would thus expect selection first to favour depression and imagination of the light-sensitive patch, and then gradually change to favour constriction of the aperture During this process a pigmented-pit eye is first formed which continues gradually to turn into a pinhole eye (see Nilsson 1990).

    Looks like Nilsson 1990 (see reference above) might be the place to see how this was calculated.  Is Nilsson required to repeat all his previous work in every new article, for the benefit of people like Berlinski?

    For Figure 1b, Nilsson and Pelger write,

    As the aperture constricts, the optical image becomes increasingly well resolved, but constriction of the aperture also causes the image to become gradually dimmer, and hence noisier. It is the random. nature of photon capture that causes a statistical noise in the image. When the image intensity decreases, the photon noise increases in relative magnitude, and the low contrast of fine image details gradually drowns in the noise. If we assume that the retinal receptive field, delta[ro]ret and the optical blur spot, delta[ro]lens, are identical Gaussians, with half-widths being the angle subtended by the' aperture at a central point in the retina (this effectively means that the retinal sampling density is assumed always to match the resolution of the optical image), then we can use the theory of Snyder (1979) and Warrant & McIntyre (1993) to obtain the maximum detectable spatial frequency, vmax  as:

    vmax = (0.375P/A) [ln (0.746A2 /I)]^½

    where A is the diameter of the aperture, P is the posterior nodal distance, or pit depth and I is the light intensity in normalized units of 'photons per nodal distance squared per second per steradian'. We can now use this relation to plot resolution against aperture diameter (figure 1b). For a given ambient intensity and eye size there is an optimum aperture size where noise and optical blur are balanced in the image. A large eye or high light intensity makes for an optimum aperture which is small compared with the nodal distance. When the aperture has reached the diameter which is optimal for the intensity at which the eye is used, there can be no further improvement of resolution unless a lens is introduced.

    Look at that, an equation, with these references to the theory cited:

    Snyder, A. W. 1979 Physics of vision in compound eyes. In Handbook of sensory physiology, vol. vii/6A, led. H.-J. Autrum, pp. 225-313. Berlin: Springer.

    Warrant, E.J. & McIntyre, P. D. 1993 Arthropod eye design and the physical limits to spatial resolving power., Prog. Neurobiol. 40, 413-461.

    Did Berlinski really look up these references and not find the relevant theory?

    For Figure 1c, Nilsson and Pelger write,


    In a lensless eye, a distant point source is imaged as a blurred spot which has the size of the imaging aperture. A positive lens in the aperture will converge light such that the blur spot shrinks, without decreasing the brightness of the image. Most biological lenses are not optically homogeneous, as man-made lenses normally are (Fernald 1990; Nilsson 1990; Land & Fernald 1992). In fact, a smooth gradient of refractive index, like that in fish or cephalopod lenses, offers a superior design principle for making lenses: the optical system can be made more compact, and aberrations can be reduced considerably (Pumphrey 1961). A graded-index lens can be introduced gradually as a local increase of refractive index. As the focal length becomes shorter, the blur spot on the retina will become smaller. The effect this has on resolution was calculated by, using the theory of Fletcher et al. 1954) for an ideal graded-index lens (figure 1c). Even the weakest lens is better than no lens at all, so we call be confident that selection for increased resolution will favour such a development all the way. from no lens at all to a lens powerful enough to focus a sharp image on the retina (figure 1c).

    Hmm, they say the optical theory is in:

    Fletcher, A., Murphy, R. & Young, A. 1954. Solutions two optical problems. Proc. R. Soc. Lond. [Physical Series] A223, 216-222

    ...which would, I expect, have some equations in it.  Did Berlinski really look this up? If not, how can he say,

    But no details are given either in their paper or in its bibliography.

    (leaving aside the equation that they do include, which sure seems like details to me)

    Date: 2003/04/05 23:21:11, Link
    Author: niiicholas
    Yet another kind of bacterial motility:


    Mol Microbiol 2003 Feb;47(3):671-97

    The bacterial linear motor of Spiroplasma melliferum BC3: from single molecules to swimming cells.

    Spiroplasma melliferum BC3 are wall-less bacteria with internal cytoskeletons. Spiroplasma, Mycoplasma and Acholeplasma belong to the Mollicutes, which represent the smallest, simplest and minimal free-living and self-replicating forms of life. The Mollicutes are motile and chemotactic. Spiroplasma cells are, in addition, helical in shape. Based on data merging, obtained by video dark-field light microscopy of live, swimming helical Spiroplasma cells and by cryoelectron microscopy, unravelling the subcellular structure and molecular organization of the cytoskeleton, we propose a functional model in which the cytoskeleton also acts as a bacterial linear motor enabling and controlling both dynamic helicity and swimming. The cytoskeleton is a flat, monolayered ribbon constructed from seven contractile fibrils (generators) capable of changing their length differentially in a co-ordinated manner. The individual, flat, paired fibrils can be viewed as chains of tetramers approximately 100 A in diameter composed of 59 kDa monomers. The cytoskeletal ribbon is attached to the inner surface of the cell membrane (but is not an integral part of it) and follows the shortest helical line on the coiled cellular tube. We show that Spiroplasma cells can be regarded, at least in some states, as near-perfect dynamic helical tubes. Thus, the analysis of experimental data is reduced to a geometrical problem. The proposed model is based on simple structural elements and functional assumptions: rigid circular rings are threaded on a flexible, helical centreline. The rings maintain their circularity and normality to the centreline at all helical states. An array of peripheral, equidistant axial lines forms a regular cylindrical grid (membrane), by crossing the lines bounding the rings. The axial and peripheral spacing correspond to the tetramer diameter and fibril width (100 A) respectively. Based on electron microscopy data, we assign seven of the axial grid lines in the model to function as contractile generators. The generators are clustered along the shortest helical paths on the cellular coil. In the model, the shortest generator coincides with the shortest helical line. The rest, progressively longer, six generators follow to the right or to the left of the shortest generator in order to generate the maximal range of lengths. A rubbery membrane is stretched over (or represented by) the three-dimensional grid to form a continuous tube. Co-ordinated, differential length changes of the generators induce the membranal cylinder to coil and uncoil reversibly. The switch of helical sense requires equalization of the generators' length, forming a straight cylindrical tube with straight generators. The helical parameters of the cell population, obtained by light microscopy, constitute several subpopulations related, most probably, to cell size and age. The range of molecular dimensions in the active cytoskeleton inferred from light microscopy and modelling agrees with data obtained by direct measurements of subunit images on electron micrographs, scanning transmission electron microscopy (STEM) and diffraction analysis of isolated ribbons. Swimming motility and chemotactic responses are carried out by one or a combination of the following: (i) reciprocating helical extension and compression ('breathing';); (ii) propagation of a deformation (kink) along the helical path; (iii) propagation of a reversal of the helical sense along the cell body; and (iv) irregular flexing and twitching, which is functionally equivalent to standard bacterial tumbling. Here, we analyse in detail only the first case (from which all the rest are derived), including switching of the helical sense.

    Omigod!  Yes another nonflagellar swimming system!!  That designer sure was a busybody!


    My cursory thoughts:

    1) This page on spiroplasma:
    ...says that sprioplasmas are related to gram-positive bacteria, and have no cell wall, have a cytoskeleton and membranes with cholesterol.  This all seems to go along fairly well with Cavalier-Smith's proposed scheme for the evolution of eukaryotes as something like:

    gram-negative --> gram-positive --> early divergence from archaeabacteria --> eukaryotes

    ...even if this doesn't pan out it is an interesting bit of (vague) convergence.

    2) I don't really even understand how the spiroplasma swimming works so speculating on evolution is pointless, however it sounds rather more like what Lynn Margulis thought spirochetes worked like when she proposed the spirochete-->eukaryotic cilium hypothesis.  I doubt that spiroplasma-->cilium has any prospects either but it is interesting.

    3) Even so, the more ways there are to swim, the more it seems that Dembski has drawn the target around the arrow with the flagellum.


    It was suggested that this is vaguely like spirochetes, but not really IMO.

    Periplasmic flagella of spirochaetes

    Perhaps the most unusual case of bacterial flagellation is
    that of the spirochaetes. Here flagella are located in the
    periplasm between the outer membrane sheath and cell
    cylinder, subterminally attached to one end of the cell
    cylinder (Fig. 3). The number of periplasmic flagella and
    whether the flagella overlap at the centre of the cell varies among species (Li et al., 2000a). The flagella function by rotating within the periplasmic space. Unlike some other bacteria in which flagellation depends on environmental changes, the spirochaete periplasmic flagella are expressed throughout the cell’s life-cycle and are believed to have vital skeletal and motility functions (Li et al., 2000b; Motaleb et al., 2000). Due to their continuous presence, the complex regulatory controls observed for motility gene expression in many bacteria seem to be absent in at least certain spirochaetes.


    Titanospirillum velox: A huge, speedy, sulfur-storing spirillum from Ebro Delta microbial mats

    paper online at

    Date: 2003/04/06 00:06:05, Link
    Author: niiicholas

    NISBET, E. G., Dept. of Geology, Royal Holloway, Univ. of London, Egham TW20 0EX United Kingdom,

    Oxygenic photosynthesis, coupled tightly with nitrogen fixation, is the manager of the modern atmosphere. When and how did this begin? Carbon isotopes imply that rubisco has controlled the global distribution of carbon in the atmosphere-ocean system for at least 3.5Ga, selectively fractionating carbon into the biosphere from an abundant atmospheric reservoir. Modern biochemical reactions of carbon capture (including nitrogen fixation) already operated very productively by then. Anoxygenic photosynthesis may substantially predate oxygenic. The first life was most likely non-photosynthetic, existing on the redox contrast between the atmosphere-ocean and the mantle.

    The biochemistry of key housekeeping enzymes may suggest evolutionary history. Many are metal proteins, especially with Fe-S clusters, including some key proteins in photosynthesis. Nitrogenase uses Fe-Mo, urease uses Ni. The oxygen-evolving complex is Mn-based. Such clues suggest photosynthesis began in and around hydrothermal systems, possibly originally as an accessory, facultative, process. .Support comes from the role of heat shock proteins, essential for assembly of rubisco. A possible speculation is that Haem may have come from an alkaline system, perhaps around ultramafic volcanism.

    Perhaps infrared thermotaxis, in a hydrothermally supported organism, allowed the start of anoxygenic photosynthesis, followed by the development of oxygenic photosynthesis in a symbiotic chimaera in a microbial mat. With the evolution of cyanobacteria, capable not only of anoxygenic and oxygenic photosynthesis, but also nitrogen fixation, life could escape the hydrothermal ghetto and occupy the planet. Walker-world intervals (air more reduced than sediment) may have occurred, perhaps many times, but after 3.5Ga, Earth has probably in general had relatively oxidised air, though without abundant free molecular oxygen until the Proterozoic.

    Date: 2003/04/06 13:13:29, Link
    Author: niiicholas
    Here is a good one:


    Code Sample

    Glenn <> wrote in message news:<>...
    > Steven J. wrote:
    > -- [snip]
    > > The "design hypothesis" need not protect itself from falsification by
    > > continually incorporating _ad hoc_ hypotheses.  It has the mother of
    > > all _ad hoc_ hypotheses built into it from the beginning: the identity
    > > (by which ID propenents mean not merely the name, but the motives,
    > > methods, and abilities of the Designer) are said to be irrelevant to
    > > and inaccessible by science.
    > EH?? The "identity" of a designer is not necessary, nor are the
    > abilities required to be known to detect design in structures.
    > And you said yourself that mechanisms are not needed as long as there is
    > evidence of an event(s).
    > You'll have to do a little better than that, Steven.
    Let me restate my position.  One recognizes "design" not by
    identifying "irreducibly complexity" or "specified complexity," but by
    recognizing similarities to things known to be designed, in structure,
    composition and methods of construction, and purpose.  To take Paley's
    famous watch example, he could tell that the watch has gears and
    springs, because he recognized them as members of known classes of
    manufactured items.  He recognized that it told time, because he
    already had the concept of telling time.  Whether he understood either
    how these gears and springs told time, or how they were manufactured,
    is another question.  At the low extreme of complexity, one recognizes
    the crudest stone tools of early hominids because they show the sorts
    of chips we recognize as the results of human manipulation.  Design is
    recognized by analogy with the work of known and observed designers.

    This applies, of course, to SETI as well -- the search for
    extraterrestrial intelligence depends crucially on the assumption that
    ETIs would design in similar ways and for similar purposes to those of
    humans.  One could, I suppose, hypothesize a Designer of radically
    different capabilities, methods, and goals; if one had a sufficiently
    detailed hypothesis, one could predict what sort of results one should
    expect of that design.  That is, one must *recognize* the
    specifications of the complexity.  IDers argue, on the one hand, that
    living things are obviously designed for their functions.  But when
    examples of seemingly bad or just eccentric design (what Designer
    would use one basic wing design for all birds, flying or nonflying,
    and another for all bats, of all sizes?) are adduced, they retort that
    we can't know the purposes of the Designer.  Well, if we can't know
    them, we can't very well marvel at how wonderfully the design
    accomplishes them, can we?

    Now, ID proponents argue that SCI can be recognized because no natural
    mechanism can produce it, and intelligence can, even if we can't be
    sure what exactly the specification is.  But even to the extent that
    currently known regularities of nature, operating alone or in
    combination in currently known ways, can't explain a phenomenon, all
    that shows is that some currently unknown mechanism (whether employed
    by an intelligent Agent, or purely nonteleological) produced it.
    Without an exhaustive knowledge of all nonteleological regularities of
    nature, and all their possible combinations, we can't rule out the
    possibility of unknown, natural, unintelligent causes.  Nor, of
    course, can we rule out intelligent causes of sorts (e.g.
    intelligences no more interested in our morals, welfare, or worship
    than we would be in that of bacteria in a petri dish) that would not
    greatly interest most ID supporters.
    > > That is, they have no idea how their proposed explanation is supposed
    > > to work, or what sort of systems the Designer should be expected to
    > > design, or to refrain from designing.  They've no foggiest idea
    > > whether the Designer should give every creation identical
    > > cytochrome-c, or arrange variants in a nested hiearchy, or arrange
    > > variants in a pattern clearly NOT a nested hierarchy.  Because of
    > > this, they can't explain why anything in nature is the way it is,
    > > rather than some other imaginable way.
    > All I know is that I'm not taking your word for this.
    *shrug*  Take the IDers' own word for it.  In Phillip Johnson's
    _Darwin on Trial_ , Behe's _Darwin's Black Box_, and quite a few other
    books, the author deals with some variant of the "panda's thumb"
    argument that the sort of design we see in living things is *not* the
    sort of design we would expect from any observed sort of intelligent
    designer.  The response is invariably that this is a theological, not
    scientific, position -- that we aren't entitled to any assumptions
    about how the Designer would work.  But if we aren't entitled to any
    assumptions about how the Designer would work, we surely can't make
    any predictions about what design will and will not look like.
    Therefore we can't tell design from the results of unknown, but
    unintelligent, causes -- or, indeed, from the results of known
    unintelligent causes (maybe the Designer crafts each snowflake
    individually and intelligently -- how would we ever know otherwise?).
    > >
    > > ID theory predicts *nothing* except that there will be aspects of
    > > biological complexity and diversity not explicable by current theories
    > > -- and these gaps will be seized upon as places to stuff a "Designer
    > > of the gaps."
    > >
    > Unlike what Ho and Sanders claim "But a real synthesis should begin
    > by identifying conflicting elements in the theory, rather than in
    > accommodating contradictions as quickly as they arise."
    Very unlike that, indeed.  ID does not seize on newly identified
    mechanisms with which to explain this or that aspect of design.  Its
    flaws do not include finding one purpose or technique for design, and
    using it to explain the bacterial flagellum, while seizing on a
    different sort of design for a completely different purpose to explain
    the immune system.  It does not seek mechanisms or explanations for
    anything at all, or make predictions detailed enough that it needs to
    rescue them with _ad hoc_ explanations.  Rather, it simply argues that
    this, and that, and some other thing can't be explained in perfect
    detail by current models, so "theDesignerdidit" (in some unspecified
    manner, at some unspecified time, for some unspecified purpose) is
    somehow a superior explanation.

    -- Steven J.

    ...coudla written it myself, although I didn't.

    Date: 2003/04/08 23:41:28, Link
    Author: niiicholas
    [note, the thread title is wrong as Glenn points out, it should be "Wiker".  I am officially dumb.]

    Just came across this:

    Does Science Point to God?
    The Intelligent Design Revolution
    By Benjamin D. Wiker
    Crisis Magazine

    Crisis link

    DI link

    Date: 2003/04/08 23:54:59, Link
    Author: niiicholas
    Here's a great little tidbit:


    ID theory affirms the universe to be 15 billion years old (more or less) and endorses the generally accepted account of the wonderful unfolding of stellar and planetary evolution, but it makes clear that it is the original and inherent fine-tuning that allows the unfolding to occur. ID proponents look at the wonderful and wonderfully strange history of life the same way. They do not deny many of the marvelous things that Darwinism has uncovered, and so an ID account of biology would include much of what Darwinists have discovered. What they question, however, is the Darwinian assertion that such things are explicable solely as the result of purposeless, unguided mechanisms. Just as stellar (and hence planetary) evolution requires finely tuned parameters written into nature in order to bring about all the necessary material conditions for life, so also biological evolution will require finely tuned parameters written into nature. ID critics overlook the obvious. Since biological evolution depends on stellar evolution—where else would all the necessary chemical elements to make those incredibly complex molecules come from?—the necessity of fine-tuning for biological evolution has already been proven. Even now, Darwinism cannot claim to be designer-free.

    But ID proponents suspect that the necessity for biological fine-tuning is more immediately and intimately necessary for evolution, and that means an investigation of the mechanism proposed by Darwin to eliminate design completely from biology. If the elimination of design in biology was wrongheaded, then the mechanism by which Darwin tried to exclude it must somehow be faulty or incomplete. To that mechanism we must now turn.

    A classic example of:

    The fact that the laws of the universe are perfect for life is evidence for a Designer. The fact that the laws of the universe can't produce life is evidence for a Designer.

    (from The Quixotic Message

    Date: 2003/04/09 00:01:56, Link
    Author: niiicholas

    The Design Revolution in Biology

    To understand the design revolution as it applies to biology, we need to step back a bit from the heat and dust currently being generated by ID/anti-ID arguments about evolution and look more closely at evolutionary theory itself. Contrary to popular belief, the notion of evolution was not discovered by Charles Darwin. As I argue in Moral Darwinism, evolution is an inference from a larger theoretical framework, a particular kind of materialism, the historical roots of which can be traced all the way back to the ancient Greek philosopher Epicurus (d. 270 b.c.). In fact, about 50 years before the birth of Christ, the Roman Epicurean Lucretius provided the first extended evolutionary account in the fifth book of his philosophic poem, De Rerum Natura (On the Nature of Things). All who think Darwin discovered evolution are amazed when they read it.

    The poem is online here: is not the kind of thing however one can absorb in a speed-read so I refrain judgement.

    Anyone know of any informed commentary on Lucretius' poem?  Ah here's one.  So far this seems to support Whitaker's contention:


    De Rerum Natura, Lucretius' great poem interpreting and extolling Epicurean thought, comprises six books in all. Each book is ordered into self-contained sections, designed to develop and drive home a major set of ideas. The first book begins with a joyous (and presumably metaphorical) hymn to Venus, and then presents an introduction to atomic theory. The universe is explained as consisting of an infinite number of atoms, small, indivisible, eternal particles, moving in a space infinite in extent, and periodically uniting into compounds. The second book explains Epicurean ethics and the infamous "atomic swerve". (This is widely considered to represent the chief weakness of Epicurean thought. In an attempt to rescue a sovereign human will from the determinism of Democritus, he postulated the strange notion of uncaused swerves in streams of atoms.) The third book returns to the more lasting insights of Epicurus. It covers the structure and essentially mortal and material nature of the soul, and the reasons why the premise of mind-body dualism is untenable. The fourth book discusses the Epicurean theory of perception and the role of sex in human behavior. The fifth provides an overview of the origin of the cosmos, of life, and of the development of civilization -- all within an evolutionary frame of reference. The sixth book offers a eulogy to Epicurus and to Athenian civilization in general, and ends with a dark story of calamitous happenings and forebodings about the future.

    Date: 2003/04/09 00:09:00, Link
    Author: niiicholas
    More is on the way in the future:


    Now What? Now Where?

    I have spent quite a few words trying to show that the ID movement is both larger than its well-publicized and strongly criticized attempts to question Darwinism and also that it is justified in publicly and strongly criticizing Darwinism. I believe that this analysis allows us to see the merit of the work done so far by ID proponents Michael Behe and William Dembski. Behe’s wonderful arguments about the irreducible complexity of biological structures (Darwin’s Black Box) show clearly that biological fine-tuning is a real problem for Darwinism precisely because of the discovery of the unfathomable complexity of even the smallest biological structures. Dembski (most recently, No Free Lunch) has declared war, so to speak, on the kind of irrational reliance on chance all too characteristic of Darwinism and seen all too clearly in Dawkins. Such reliance, we recall, is rooted in the desire to eliminate the design inference in biology, and Dembski’s arguments are essential to removing such irrational obstacles.

    Where is the ID revolution headed? Time will tell. But it’s a young movement, after all. As with all scientific and philosophical revolutions—so also with ID—one is not able to predict what this mode of scientific inquiry will discover.

    Of course, I have not answered all questions one might have about ID theory. Exactly how is it related to theology? To philosophy? To morality? Happily, the kind editors of this fine magazine have given me the opportunity to answer those questions in a future issue.

    Benjamin D. Wiker is a senior fellow at the Discovery Institute and the author of Moral Darwinism: How We Became Hedonists. He is a lecturer in theology and science at Franciscan University of Steubenville.

    Date: 2003/04/09 01:23:39, Link
    Author: niiicholas
    This comes up often in Ev/Cre debates, basically "where the press got it wrong".  I just discovered that there is whole journal devoted to the topic of science & the public:

    E.g. here's an interesting article:


    Newspaper coverage of maverick science: creating controversy through balancing

    James W Dearing
    Department of Communication, Michigan State University, East Lansing, MI 48824-1212, USA

    Abstract. How do journalists portray the ideas of maverick scientists to the general public? Are mavericks portrayed as credible scientific sources? Do the stories written by journalists function to merely translate maverick theories for nonscientific audiences, or do they more often transform those maverick theories into the realm of scientific controversies? This study hypothesized answers to these questions by analysing how journalists wrote about three maverick theories: (1) a 1990 earthquake prediction, (2) an alternative theory about the cause of AIDS, and (3) cold fusion. A content analysis of 393 news articles in 26 US newspapers and a mailed survey of the journalists who wrote those stories suggest that scientific theories which are believed to be credible by a minority of scientists may be lent credibility in mass media stories, even though the journalists themselves thought that the maverick scientists lacked credibility. Implications for the communication of risk through the mass media are discussed.

    Date: 2003/04/10 23:56:26, Link
    Author: niiicholas
    A few key papers on the origin of the innate immune system:


    Immunopharmacology 1999 May;42(1-3):107-20

    Complement systems in invertebrates. The ancient alternative and lectin pathways.

    Smith LC, Azumi K, Nonaka M.

    Department of Biological Sciences and Institute of Biomedical Sciences Graduate Program in Genetics, George Washington University, Washington, DC 20052, USA.

    The complement system in higher vertebrates is composed of about thirty proteins that function in three activation cascades and converge in a single terminal pathway. It is believed that these cascades, as they function in the higher vertebrates, evolved from a few ancestral genes through a combination of gene duplications and divergences plus pathway duplication (perhaps as a result of genome duplication). Evidence of this evolutionary history is based on sequence analysis of complement components from animals in the vertebrate lineage. There are fewer components and reduced or absent pathways in lower vertebrates compared to mammals. Modern examples of the putatively ancestral complement system have been identified in sea urchins and tunicates, members of the echinoderm phylum and the protochordate subphylum, which are sister groups to the vertebrates. Thus far, this simpler system is composed of homologues of C3, factor B, and mannose binding protein associated serine protease suggesting the presence of simpler alternative and lectin pathways. Additional components are predicted to be present. A complete analysis of this invertebrate defense system, which evolved before the invention of rearranging genes, will provide keys to the primitive beginnings of innate immunity in the deuterostome lineage of animals.


    Immunobiology 2002 Sep;205(4-5):340-54

    Which came first, the lectin/classical pathway or the alternative pathway of complement?

    Dodds AW.

    Department of Biochemistry, University of Oxford, UK.

    It is a widely accepted canon of immunology that the alternative pathway is more primitive and hence older in evolutionary terms than the lectin/classical pathway. This idea has been reinforced by the discovery of "C3" and "factor B" proteins in invertebrate species. However, it is clear that the gene duplications which gave rise to C3/C4/C5 and factor B/C2 occurred in the vertebrate lineage. Hence, the naming of the invertebrate proteins may be based on preconceptions rather than on solid structural or functional evidence. Lectins and associated MASP/C1r/C1s-like proteins have been found in invertebrates, while factor D, the defining component of an alternative pathway, has so far been found only in the bony fish and higher species. It is a principle of Darwinian evolution that complex systems develop through small sequential steps. It is possible to imagine such a series of steps for the evolution of a lectin pathway, involving as it does recognition of non-self. It is difficult to see how the alternative pathway, which lacks a recognition molecule, could have evolved without the prior development of control proteins to protect self from attack.

    Date: 2003/04/12 18:33:05, Link
    Author: niiicholas
    A highly entertaining new ISCID thread on the

    Intelligent Design of Immunity

    Date: 2003/04/13 17:51:01, Link
    Author: niiicholas
    I'm going to post some posts here for safekeeping on this thread:

    Nelson, what is this babble about an immune system producing "not enough specific antibodies to make a difference"????

    Way back on the other thread, charlie pointed out to you:


    Antibodies do not necessarily have single specificities. Indeed, the vast majority of our circulating immunoglobulins (the so-called "natural" antibodies) are low affinity, broad specificity antibodies directed towards common antigens (bacterial wall moieties, for instance).

    Antibodies become highly specific and gain high affinity only late during an antigen-specific immune response, through a process of mutation/selection called affinity maturation. This however has nothing to do with the VDJ recombination process we are discussing here, which takes place, irrespective of antigen, during B cell differentiation in the bone marrow.

    "Naive", newly generated B cells, as they emerge from the bone marrow, carry antibodies that are mostly of low affinity. For insatnce, the antibodies produced early during an immune response (which reflect the naive repertoire) bind antigen with a Kd in the 10^-5-10^-6 M range - compared that with the high affinity, "matured" antibodies of late immune responses, which have a Kd of 10^-8-10^-9 M. Most antibodies in the primary repertoire are also not very specific – in fact, polyspecific antibodies abound (which goes along with their low affinity for antigen). As an aside, the vast majority of antibodies in the primary repertoire do not in fact recognize anything at all, and the B cells that make them die after a while without ever seeing any "action" (one of the drawbacks of the darwinian approach of the adaptive immune system – high, widespread wastefulness for rare but exceptional returns).

    As for innate immunity receptors, again you are mistaken. While some of them do indeed have broad spectrum, many have quite subtle specificities, for instance TLR4 binds very specifically to the lipid A moiety of the very large bacterial lipolysaccharide (LPS) molecules. Their binding constants also actually compare quite well with those of most primary response antibodies (in the 10^-6-10^-7 M range).

    The fundamental difference between adaptive and innate immunity receptors is in fact neither in their affinity nor in their specificity, but in their logic. The adaptive immune system, using VDJ recombination, can generate an almost infinite variety of specificities, and thanks to clonal selection can pick any extremely rare, low affinity antibody molecule and turn it into close to a “magic bullet” (this however has again nothing to do with VDJ recombination). The innate immune system, on the other hand, can count on only a limited array of receptors, which must focus on a few abundant antigens (sometimes classes of antigens) commonly found on pathogens (often, like LPS, molecules that we ourselves do not produce); moreover, the binding of the ligand has to be good to start with, because these antigens cannot undergo mutation and selection processes.
    So we have the following facts:

    1) Many innate receptors have similar specificity to "naive" (first-generation lymphocyte) recombinant antibodies.  Most of the antibodies in your and my blood, right now, are therefore "not specific enough to make a difference".  According to you.

    2) Specificity is not produced just by having cells that mysteriously produce lots of specific antibodies, it is produced by the selective replication of those very few lymphocytes that happen to match whatever the antigen is.  Further somatic mutation and selection is what produces many copies of the very few antibody phenotypes that are "specific enough to make a difference".

    3) Therefore at no point are huge numbers of diverse, "single specificity" antibodies produced.

    So speaking crudely, phylogenetically, we have this sequence of organisms:

    (a) invertebrates, with many non-rearranging receptors of moderate specificity (similar to the specificity of "naive" antibodies)

    (b) cartilagenous fish, which add diverse rearranging receptors of moderate specificity, genes in VDJ VDJ VDJ arrangement

    © "lower" vertebrates, which have diverse rearranging receptors of moderate specificity in a VVVV DDDD JJJJ-type arrangement

    (d) mammals, like lower vertebrates except that a few of the rearranging receptors, which happen to match the antigen, get replicated and gradually improve from moderate specificity to high specificity via somatic mutation & selection.

    (charlie can refine the above if I garbled things)

    And yet, Nelson, you've been proclaiming for endless pages that there is some sort of requirement somewhere to produce large numbers high-specificity antibodies with different specificities.

    Please, Nelson, can you help us out here?

    charlie said,


    It can't, anymore that a human system can get a V1 fused to a V2 in its Ig clusters. V segments have RSSs only on their 3', and they all have the same spacers (for steric reasons related to RAG structure, recombination only occurs between RSSs that vave different sized spacers), so that recombination cannot occur. What can occur is a V from one shark cluster recombining with a D in another.

    Thanks, that's what I was trying to explain when I wrote,


    But it wouldn't make a difference anyway, because RAG figures out where to cut based on RSS (IS in above diagram), and these sequences would get copied along with the V, D or J segments as they get duplicated [...]

    Yet another supposed reason for the unevolvability of VDJ recombination hits the dust!!  It's like shooting skeet.  

    All Nelson has left is that:

    (1) the exact non-rearranging ancestor receptor has not yet been identified, and (2) that he thinks a transposon insertion, a well-known natural event that is happening all the time (it causes some cancers for instance) is "non-Darwinian" and for some mysterious reason therefore an intelligent intervention.

    Regarding (1), even though (a) Ig domains are common, (b) we know that non-rearranging receptors would work because we have a bunch of them, and © due to selection for immune system diversity sequence homology will decay very fast.

    To emphasize the Ig domain point:

    ...all those circles are Ig(-like) domains.

    Regarding (2), there are a multitude of transposon types and events; there is no need to postulate intelligent intervention in order to explain a transposon inserting into a non-rearranging receptor.  Plus, there is the published literature and experiments which the immunologists view as having tested and strengthened the hypothesis.

    Date: 2003/04/14 01:38:47, Link
    Author: niiicholas
    Well, famed antievolutionist demagogue Phil Johnson took the opportunity to try to spread his message to the Boy Scouts.  Speaking as an Eagle Scout I find the whole thing intensly annoying, but that's another story.



    Phillip Johnson on Boy Scouts and Evolution ...

    In the March 2003 issue of Touchstone magazine (Vol. 16, No. 2), leading "Intelligent Design" spokesman Phillip Jonhson writes "If it is important to the Boy Scouts that their members be and remain believers in God, then they need to make some effort to protect the
    boys under their care from the predictable effects of the teaching of evolution, that 'universal acid,' to use Daniel Dennett's classic phrase, which has dissolved the religious faith of so many. Perhaps there should be a merit badge for understanding the evolution controversy, including knowledge of the truth about the Haeckel
    embryo drawings, the Cambrian explosion, and the peppered moth story .... For now, the law may allow the Boy Scouts to exclude atheists and homosexuals, but is it right for them to do so? That question will trouble the Scouts continually until the culture is persuaded again that God really is our creator rather than merely a
    product of the human imagination, and that he cares about what we do sufficiently to build a moral code into the bedrock of reality."


    There are a number of dumb things in this article, but it would have behooved PJ to actually do some reading on the history of the Boy Scouts before spouting off.  But this is PJ we're talking about, he's still repeating Wells' errors on the peppered moth etc...

    The Boy Scouts were founded by Robert Baden-Powell.  See here for an extensive webpage on him and the history of scouting:

    Now, Robert's father was:

    The Rev. Baden Powell, F.R.S.,  
    Savilian Professor of Geometry,
    Oxford University

    ...and he lived from 1796-1860.  "F.R.S." means "Fellow of the Royal Society", and yes, this means he was well aware of Darwin and his Origin of Species.  Baden-Powell senior even contributed a positive review:



    Professor Baden Powell wrote on mathematics, physics, theology and philosophy and fought for the principle acknowledging scientific advances were compatible with Christian religion. Following Darwin's "Origin of Species" in 1859, he contributed one of seven essays in "Essays and Reviews," 1860. This was violently attacked, and the authors denounced as being inspired by "the Evil One himself." "There was some expectation of him becoming a Bishop, before Essays and Reviews were published" (letter from his widow to her nephew 20.8.1909)

    Further down on the page we have:


    Science and Religion: Baden Powell and the Anglican Debate, 1800-1860 by Pietro Corsi was published by the Cambridge University Press in 1988. The publishers describe the context of this debate and the content of Corsi's research in the Cambridge University Press online catalogue:

    Science and Religion assesses the impact of social, political and intellectual change upon Anglican circles, with reference to Oxford University in the decades which followed the French Revolution and the Napoleonic wars. More particularly, the career of Baden Powell, father of the more famous founder of the Boy Scout movement, offers material for an important case-study in intellectual and political reorientation: his early militancy in right-wing Anglican movements slowly turned to a more tolerant attitude towards radical theological, philosophical and scientific trends. During the 1840s and 1850s, Baden Powell became a fearless proponent of new dialogues in transcendentalism in theology, positivism in philosophy, and pre-Darwinian evolutionary theories in biology. He was for instance the first prominent Anglican to express full support for Darwin’s Origin of Species. Analysis of his many publications, and of his interaction with such contemporaries as Richard Whately, John Henry and Francis Newman, Robert Chambers, William Benjamin Carpenter, George Henry Lewes and George Eliot, reveals hitherto unnoticed dimensions of mid-nineteenth-century British intellectual and social life.

    & here is quote of what Baden Powell senior had to say about Darwin:


    "Just a similar scepticism has been evinced by nearly all the first physiologists of the day, who have joined in rejecting the development theories of Lamarck and the Vestiges; and while they have strenuously maintained successive creations, have denied strenuously maintained successive creations, have denied and denounced the alleged production of organic life by Messrs. Crosse and Weekes, and stoutly maintained the impossibility of spontaneious generation, on the alleged ground of contradiction to experience. Yet it is now acknowledged under the high sanction of the name of Owen (British Association Address 1858), that 'creation' is only another name for our ignorance of the mode of production; and it has been the unanswered and unanswerable argument of another reasoner that new species must have originated either out of their inorganic elements, or out of previously organized forms; either development or spontaneous generation must be true: while a work has now appeared by a naturalist of the most acknowledged authority, Mr. Darwin's masterly volume on The Origin of Species by the law of 'natural selection,' - which now substantiates on undeniable grounds the very principle so long denounced by the first naturalist, - the origination of new species by natural causes: a work which must soon bring about an entire revolution of opinion in favour of the grand principle of the self-evolving powers of nature."


    And Darwin wrote in a letter:


    "Henslow [says he]... will go a very little way with us [in accepting the Darwinian theory of evolution], but brings up no real argument against going further. He also shudders at the eye! It is really curious (and perhaps is an argument in our favour) how differently different opposers view the subject... Baden Powell says he never read anything so conclusive as my statement about the eye!" (Darwin to Charles Lyell Feb. 15, 1860)

    Anyway, this is Baden Powell's father, not the founder of scouts himself.  Baden Powell jr. was a military man, not a scientist, and never said much about Darwin one way or the other, although:



        In Chapter 6 of his book Rovering To Success, Powell addressed "irreligion" and atheism.  He clearly opposed the attacks upon religion expressed by many atheists and the divisiveness it caused.  He believed that nature showed evidence of God and that religion was essential for happiness.  He marveled, as so many religionists have, at the amazing workings of the eye.  B-P wrote, "Ask Mr. Atheist who it was who invented and made that wonderful machine?"  

        Curiously, Charles Darwin, whose observations of nature led him to embrace agnosticism, also marveled at the complexity of the eye, though came to believe its development would be explained by natural selection.  Darwin actually acknowledged B-P's father in the introduction to The Origin of the Species and wrote in a letter, (Rev.) "Baden Powell says he never read anything so conclusive as my statement about the eye!"   Indeed, Darwin's theory had been embraced and defended by the senior Baden Powell; yet, the only reference B-P made to Darwin in his writings was to use him as an example to boys that even those who did poorly in school could become successful scientists.

    B-P's view of God was much more inclusive than most.  He always told the scouts that they needed to be tolerant and respectful of others' differing religious beliefs.  God, he said, is "a vast Spirit of Love that overlooks the minor differences of form and creed and denomination and which blesses every man who really tries to do his best, according to his lights, in His service."

        B-P's writings show a broad appreciation of culture and diversity and a deep desire to develop strong, moral character in the world's young men.  He staunchly maintained that chivalry and self-sacrifice were the basis of religion and this was necessary in scouting.

    Heh.  Here's the Darwin quote from B-P jr:


    "Is it not true that both Newton and Darwin, founders of the scientific method, were both regarded as blockheads by their school teachers?

    Hmm, I guess other people have made my connections before:


    Boy Scouts
    Letter to the Editor
    Los Angeles Times January 18, 1998.

    Re Jan. 13 letters concerning atheism and the Boy Scouts: Lord Baden-Powell, the founder of the Boy Scouts, once stated emphatically in response to the question of religion, a quotation of the philosopher Carlyle. "The religion of a man is not the creed he professes, but his life—what he acts upon and knows of life and his duty in it. A bad man who believes in a creed is no more religious than a good man who does not." Lord Baden-Powell’s father was a professor and a great friend and admirer of Charles Darwin, and at one time had been reported to the bishop of London for heretical preaching, and so he was acutely aware of the tyranny of religious zealots. I would point out that most Nazi troops in World War II were Lutherans or Roman Catholics and very probably none were atheistic Boy Scouts!

    --Alex Sheppard Reseda

    A discussion at a scouting forum:

    Date: 2003/04/30 18:28:04, Link
    Author: niiicholas
    The topic of so-called "junk" DNA (or, apparently disposable noncoding DNA, more neutrally) has come up endless times in various online debates.  Often, someone will find a new article indicating a function for some bit of DNA, and declare that the "junk" hypothesis is dead and that those evil materialists were blinded by their evil materialism for ever believing it.

    The situation is of course much  more complex, so link/post articles, posts (both sides), etc. in this thread.


    Date: 2003/04/30 18:43:15, Link
    Author: niiicholas
    Here is a post I wrote in response to Nelson Alonso:

    On Paul Nesselroade's current column


    Originally posted by Nelson Alonso:
    Key scientists agree they are now obliged to abandon the term "junk DNA".

    The large stretches of genetic material formerly known as "junk DNA" are now acknowledged to contain important instructions essential for life.
    Which is what lead to Dr. Eric Lander's statement about humans.
    [/QUOTE]Please, Nelson, this is some kind of company press release and gives no details about how what the function is.

    While you're at it you might try explaining the function of the DNA in near-identical sister species, where one species has 50%+ more than the other.
    Sorry this is a little vague. Can you give me a reference?[/QB][/QUOTE]Gee, you haven't heard of this kind of thing, yet you have made all kinds of authoritative pronouncements in this thread?  How surprising...

    For example:


    Molecular melodies in high and low C
    Daniel L. Hartl

    For 50 years now, one of the enigmas of molecular evolution has been the C-value paradox, which refers to the often massive, counterintuitive and seemingly arbitrary differences in genome size observed among eukaryotic organisms. For example, the genome of the fruitfly Drosophila melanogaster is 180 megabases (Mb), whereas that of the European brown grasshopper Podisma pedestris is 18,000 Mb. The difference in genome
    size of a factor of 100 is difficult to explain in view of the apparently similar levels of evolutionary, developmental and behavioural complexity of these organisms.

    The C-value paradox emerged from among the first applications of spectrophotometric analysis of nuclear DNA content1. The haploid DNA content of eukaryotic organisms ranges over a factor of 80,000. Some of the largest genomes are found among the lowliest of eukaryotes, such as the amoebae, and some of the smallest genomes are found among organisms with complex developmental
    and behavioural repertoires, such as Drosophila melanogaster. These discoveries were made before the elucidation of the molecular structure of DNA or its genetic coding function, so it is  understandable that massive differences in DNA content were difficult to interpret. In the subsequent two decades molecular biologists laid out the molecular mechanistic framework of life — replication, transcription, translation and mutation. But at the culmination of this period, the C-value paradox was as great a mystery as ever. Maybe the paradox lay within ourselves.
    What if our concepts of organismic complexity were backwards? Perhaps the lower forms actually do have more genes — maybe, in fact, “they require more genes to conduct their dreary affairs”2.

    DNA renaturation kinetics carried out on many eukaryotes showed that genomic DNA contains many moderately or highly repetitive sequences, the relative amounts of which can differ markedly from one species to the next3,4. Many of the differences in genome size can be attributed to differences in the abundance of these repetitive sequences, rather than to large differences in the nonrepetitive fraction of unique DNA, which
    includes the coding sequences5.

    (bolds added)

    Folks, *these* are the observations that led, and still lead, to the "junk DNA" suggestion.  Unless a junk DNA critic comes up with an explanation for why species A will have 100 times as much DNA as very similar species B, they haven't explained "junk DNA".  The question is (1) why are eukaryotic genomes primarily made up of repetitive sequences and (2) why can the amounts of these sequences vary so much within closely-related groups?

    IDists who talk about junk DNA with out bringing up the above observations front-and-center are not even talking about the actual issue.

    More quote:

    Large-scale genomic sequencing gives a quantitative picture. On the long arm of human chromosome 22 (REF. 6), only 39 per cent of the DNA sequence resides in annotated genes, including
    their introns, and only three per cent resides in the exons of the annotated genes; in contrast, about 42 per cent of the chromosome consists of tandem and interspersed repeats of various kinds, including 16.8 per cent Alu repeats, 9.7 per cent LINE 1 repeats, and 3.8 per cent LINE 2 repeats. On chromosome 21 the situation is similar, but with only 26.2 per cent of the DNA in annotated
    genes7. To a large extent the C-value paradox is due to the proliferation or diminution of repetitive elements.

    The players
    Some of the main mechanisms for change in genome size are shown in FIG. 1. We include chromosomal mechanisms, such as polyploidy and accessory chromosomes, even though these mechanisms are prominent only in certain lineages, particularly in plants.  In some lineages in which polyploidy does take place,most of the differences in genome
    size in different species are nevertheless due to other causes. For example, the fact that wheat (genome size 16,000 Mb) is hexaploid accounts for only about 8 per cent of its genome size relative to that of rice (genome size 430 Mb), because the wheat genomes contain large amounts of repetitive DNA that are not present in the rice genome.

    Figure 1 | Principal mechanisms for changes in genome size. In a large genome, such as the human
    genome, the protein-coding DNA is sparse and interspersed with non-coding DNA; at the scale shown here, coding DNA would be invisible. Except in some plant lineages, polyploidy is not a principal cause of variation in genome size. Insertions and deletions differ in size as well as in rate among species of organisms.
    Now, FWIW, I think there is some good evidence for "function" of a sort of "junk DNA" -- namely, the total amount of DNA in a cell correlates well with cell volume.  This would indicate that "junk DNA" serves a "skeletal" or "spacer" function, or alternatively that larger cells have less selection pressure for mutational deletions. This would be a function, but it is not very sexy and not sequence-dependent.  The article quoted above cites some of the literature for those who are interested:

    Nature Reviews Genetics article

    Here is the bit I'm talking about.  As you can see, there are a variety of "live" hypothesis among evolutionary biologists, both pro- and anti- "junk", even though they are supposedly all nasty materialists:



    FIGURE 1 focuses on the mutational mechanisms that can change genome size, but natural selection may act on the genetic variation created by mutation. With regard to selection for genome size, there is an extensive literature on potential adaptive functions of non-coding DNA, much of it related to correlations between genome size and cellular traits (notably nuclear volume) or organismic traits (notably developmental time)8. Amoebas, with among the largest genomes, also have among the largest cells; in describing an entamoebal infection in 1890,William Osler9 observed:

    “They are most extraordinary and striking creatures and take one’s breath away at first to
    see these big amoebae — 10–20 times the size of a leucocyte — crawling about in the pus.”

    Limitations of space preclude an extensive discussion here, but the varieties of adaptive hypotheses for the maintenance of non-coding DNA include the ‘skeletal DNA’hypothesis10, according to which non-coding DNA functions as part of the basic framework for the assembly of the nucleus and serves to regulate nuclear volume in relation  to cell volume; and the ‘buffering DNA’hypothesis 11, which posits that non-coding DNA buffers condensed chromatin from intracellular solutes, and uncondensed chromatin from nonspecific DNA binding by proteins and their ligands.

    Conversely, views of non-coding DNA as merely accumulated ‘junk DNA’12 or self-perpetuating ‘selfish DNA’13,14 stand against these adaptionist models of genome evolution. Recent evidence showing that non-coding DNA is subject to elimination comes from studies of cryptomonads and chlorarachneans15,16. In these organisms, the descendants of ancient symbioses, the nucleus of a former algal partner persists as a simplified ‘nucleomorph’, surrounded by a periplastid membrane; in different lineages, the nucleomorph has undergone a 200–1,000-fold  reduction in genome size with the elimination of virtually all of the non-coding DNA.

    Date: 2003/04/30 18:50:00, Link
    Author: niiicholas
    A good complement to a junk DNA FAQ would be a "mechanisms of mutation" FAQ, which I don't think exists anywhere.  People seem to treat mutation as some kind of magically process and therefore get mislead into all kinds of directed mutation, etc. stuff.

    Most stuff on the web appears to be either lecture outlines or very technical "my research is"-type pages.

    But there is some good stuff.  For example:

    Mutation, Mutagens, and DNA Repair


    Introduction: Definitions and mutation rates
    Types of Mutations
    Origins of Spontaneous Mutation
    DNA Repair Systems

    Date: 2003/05/05 17:50:36, Link
    Author: niiicholas
    Another Nelson debate:




    This is way off topic but you've made a number of assertions that needs to be addressed. For example, you say that I leave out various homologies. But in fact, I don't, the homologies you cite strengthen the fact that there exist mini-IC systems that would require unselectable steps for any evolutionary pathway.

    "Mini-IC systems?"  But I thought that IC meant that the *whole thing* was IC?  


    For example, with regard to MotAB, the motor complex in the flagellum requires 3 components, fliG, motA, and motB, and this is analogous to the ICness of ExbB, ExbD, and TonB.

    ExbB and ExbD act on TonB, IIRC there's another ExbBD pair homolog that acts on something else.  And motAB act on fliG in a similar fashion.  Which is why Kojima & Blair wrote in Biochemistry (2001, vol. 40, pp. 13041-50),

    The occurrence of significant conformational change in the stator has implications not only for the present-day mechanism but also for the evolution of the flagellar motor. A membrane complex that undergoes proton-driven conformational changes could perform useful work in contexts other than (and simpler than) the flagellar motor, and ancestral forms of the MotA/MotB complex might have arisen independently of any part of the rotor.

    Nelson continues,


    Still, there are more problems with regard to the logistical operations needed to be performed by a stochastic process in order to make this thing work from an ion channel, as Mike points out:

    Of all the ways to mutate an ion channel, the number of ways that would result in its interacting with the base of some filament is surely in the distinct minority. And of all the ways to mutate an ion channel that gloms onto a filament, the number of ways to mutate it such that rotation does not occur is probably much higher than the number of ways to elicit some rotation...

    None of this is disputed, but all it is saying is that "beneficial mutations are unlikely" which is no surprise to evolutionary biology.  All that is needed is one rare beneficial mutation amongst millions of ones that "don't work" and selection will pick it out.  And, FWIW, mutation experiments seem to indicate that there is a fair bit of flexibility where motor function is retained despite mutation in the MotB--rotor interface.


    This [mutation] allows some ion channel to glom onto the base of a filament and open its channel and expose the ion flow to the proto-rotor in such a way that a set of electrostatic interactions just happen to form and elicit significant rotation.

    This depends upon a particular model of the mechanism of flagellar rotation, which is an unsolved question (Hey! A place for the IDer to act in modern times!  Unless you're a nasty methodological naturalist...).  Based on the ExbBD homology, I would expect that the ion channel is essentially internal to the ExbBD system and that the energy resulting from H+ flow is transferred through the protein structure via conformational change to act on the flagellum base (or on TolB etc.) to do work at a distance.  Call it a prediction if you like.  The electrostatic model certainly is elegant, but based on ExbBD homologs being independent units doing "work at a distance" in several different systems, it seems unlikely.  Time will tell.

    The homology between FliI is said to only be homologous to the b subunit of the F-ATP synthase, not the whole 8 parts of the synthase, the whole thing requires all 8 parts to work.

    IIRC the 3 alpha and 3 beta subunits of the F1 ATPase are thought to be homologs of each other, with only the beta subunits retaining ATPase activity:

    The similarity of the beta subunit to FliI is something like 33% which is highly statistically significant, well above the ambiguous level:


    How might these ATPases catalyze processive protein export? Spa47 (the Shigella FliI homolog) shares 33% amino acid identity with the beta-subunit of F1-ATPase. Proteins with >30% sequence identity have a high probability of sharing similar structures (69). Active F1-ATPase is a heterohexamer consisting of alternating alpha- and beta-subunits with a gamma-subunit inserted in a central channel where it rotates during the catalytic cycle (70). No equivalent of the alpha-subunit of F1-ATPases is found within flagellar or TTSS-encoding operons, so we assume that the type III export motor is a homohexamer. When modeled on the F1 structure, Spa47 fits at the inner membrane base of our NC structure (Fig. 3). It would contain a central channel aligned with the one found within the NC and of similar diameter to it, through which the proteins could be secreted (see Supporting Text).

    Source: Blocker A, Komoriya K, Aizawa S. Proc Natl Acad Sci U S A 2003 Mar 18;100(6):3027-30. Type III secretion systems and bacterial flagella: Insights into their function from structural similarities.

    ...the assumption of homology seems to be confirmed by the fact that the resulting protein complex fits well into their model of T3SS structure.


    With respect to the possibility that the rod proteins were derived from each other, Mike Gene addresses this in his essay:

    It would seem there is no reason why the rod should be built around three proteins instead of simply one. Yet these three gene products are found in all flagella, dating back to the putative ancestral flagellum. This suggests one protein is not sufficient to form a functioning flagellar rod. Furthermore, the size of these proteins among these five distantly related bacteria has been held relatively constant (Fig 2), despite billions of years of experiencing very different selective pressures. It would seem some form of constraint or specification is at work, as natural selection will not tolerate too much deviation. And these size constraints map back to the last common ancestral flagellum, indistinguishable from the first flagellum.

    It seems highly unlikely that the different rod proteins have radically different functions.  Probably their retention has to do with starting and stopping the rod construction process, wherein it would be helpful to have a tightly-controlled starting and stopping points, but where simpler mechanisms could suffice at first, e.g. just generating a certain amount of one rod protein.

    All that is required to get from one rod protein to several is the sub-functionalization of gene copies, which you, Nelson, have enthusiastically endorsed in other threads.


    Gram positive bacteria don't need the L and P rings because they simply do not have an outer membrane. I think that it's as simple as that (well not really, Mike has hinted at how this can illuminate something about it's origin but hasn't discussed this yet).

    So, are they part of the IC system or not, and how many orders of magnitude difference in probability does this decision result in?


    I'm not familiar with a flagellum serving as an adhesion organelle, although I'm familiar with pili that do.

    An example (one of many) was cited in the original immune system thread.


    With that you continue to introduce more unselectable steps, the irreducible complexity of the folding of P Pilus, not to mention the sophisticated mechanisms, donor strand exchange and donor strand complementation. The pilus itself is made up of 5 parts, PapK PapA,PapE,PapK, and PapG. Furthermore, the pilus doesn't seem to be able to secrete proteins, and the biggest difference between flagella and pili is that flagella are built from the top to the bottom, whereas pili are built from the bottom to the top. The notion of a simple filament sticking to an export machine seems to vanish.

    Huh?  There are many kinds of pili, the term basically means "sticky-outy bit" as far as I can tell.  And it seems that basically every transport system tha