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Date: 2002/05/06 19:19:54, Link 128.111.106.148
Author: niiicholas
testing, testing, 1 2 3...

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

Quote
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...

nic

Date: 2002/05/17 02:35:38, Link 128.111.106.148
Author: niiicholas
Howdy,

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):

Quote

"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



Guidelines:

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,

nic
niiicholas@yahoo.com

Date: 2002/05/17 21:43:08, Link 128.111.106.148
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


Quote

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 128.111.106.148
Author: niiicholas
Hi,

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.

nic



Date: 2002/05/17 22:09:17, Link 128.111.106.148
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: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6685059&dopt=Abstract

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: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=2169613

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: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3454300&dopt=Abstract

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: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3938299&dopt=Abstract

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: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2102616&dopt=Abstract

Doolittle, R. F. (1992). “A detailed consideration of a principal domain of vertebrate fibrinogen and its relatives.” Protein Science, 1(12): 1563-1577. Link: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1304888&dopt=Abstract

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: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1339026&dopt=Abstract

*Doolittle, R. F. (1993). “The Evolution of Vertebrate Blood Coagulation - a Case of Yin and Yang.” Thrombosis and Haemostasis, V70(N1): 24-28. Link: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8236110&dopt=Abstract

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: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3483343&dopt=Abstract

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: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9524761&dopt=Abstract

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: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2310387&dopt=Abstract

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: http://www.jstor.org/journals/00368075.html

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: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1549566&dopt=Abstract

Patthy, L. (1985). “Evolution of the Proteases of Blood Coagulation and Fibrinolysis by Assembly from Modules.” Cell, 41(3): 657-664. Link: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3891096&dopt=Abstract

Patthy, L. (1990). “Evolution of blood coagulation and fibrinolysis.” Blood Coagulation and Fibrinolysis, 1(2): 153-166. Link: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2130927&dopt=Abstract

Patthy, L. (1990). “Evolutionary Assembly of Blood Coagulation Proteins.” Seminars in Thrombosis and Hemostasis, 16(3): 245-259. Link: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2237446&dopt=Abstract

Patthy, L. (1999). “Genome evolution and the evolution of exon-shuffling—a review.” Gene, 238(1): 103-114. Link: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10570989&dopt=Abstract

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: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=2315305

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: http://www.jbc.org/cgi/content/full/274/11/7153

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 128.111.106.148
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="news:talk.origins" target="_blank">the talk.origins 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:

Quote

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 128.111.106.148
Author: niiicholas
Some good discussion and links on a bio.com article discussing the homology between a blood-clotting protein and a cone-snail venom protein (!!!) was posted on this II thread.

nic



Date: 2002/05/24 20:25:51, Link 128.111.106.148
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:

Quote

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:

Quote

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:

Quote

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:

Quote

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:

Quote

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.

nic

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

Quote

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. iinuma@med.nagoya-cu.ac.jp

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:

Quote

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:

Quote

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?

nic


*** 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:

http://iidb.org/ubb....759&p=2

On p. 86, Behe writes,

Quote

”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,

http://www.millerandlevine.com/km/evol/design2/article.html

...writes:

Quote

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 128.111.106.148
Author: niiicholas
A recent post on talk.origins by Dunk discussing some recent (2002) literature, with quotes:

Here is the google link

nic

Date: 2002/05/24 22:27:00, Link 128.111.106.148
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
http://www.amazon.com/exec/obidos/ASIN/0684834936/

Behe and the Blood Clotting Cascade (1997)
T.O. POTM on blood-clotting pointing out the sequence patterns
http://www.talkorigins.org/origins/postmonth/feb97.html

A Delicate Balance
by Russell F. Doolittle
http://bostonreview.mit.edu/br22.1/doolittle.html
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)
http://www.arn.org/docs/behe/mb_brrespbr.htm

Finding Darwin's God, Miller (1999)
Amazon.com link
http://www.amazon.com/exec/obidos/ASIN/0060930497/

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
http://www.discovery.org/viewDB/index.php3?program=CRSC%20Responses&command=view&id=442

Design on the Defensive, (Fall (?) 2000)
Ken Miller's page responding to Behe's review of Miller's book
http://biocrs.biomed.brown.edu/Darwin/DI/Design.html

(Ken Miller evolution page: http://www.millerandlevine.com/km/evol/index.html)

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: http://www.millerandlevine.com/km/evol/DI/Clotting.html
...linked from Miller's 'Design on the Defensive' (http://www.millerandlevine.com/km/evol/DI/Design.html)

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: http://www.millerandlevine.com/km/evol/DI/clot/Clotting.html

Comments on Ken Miller's Reply to My Essays (Behe, January 2001)
A response to Ken Miller, but blood-clotting isn't mentioned.
http://www.discovery.org/viewDB/index.php3?program=CRSC%20Responses&command=view&id=579


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 128.111.106.148
Author: niiicholas
Quote
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:

http://www.millerandlevine.com/km/evol/wells-april-2002.html

nic



Date: 2002/05/24 23:28:42, Link 128.111.106.148
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 www.doesgodexist.org, by Robert Harsh

nic

Date: 2002/05/24 23:51:37, Link 128.111.106.148
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:

Quote

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:

Quote

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.

nic

Date: 2002/05/25 00:35:53, Link 128.111.106.148
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.

Link: http://www.philoonline.org/library/shanks_4_1.htm

Regarding blood-clotting & specificity, they write:

Quote

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:

Quote

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.

nic

Date: 2002/05/26 00:55:42, Link 198.81.17.59
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):

Quote

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).

Quote

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:

Quote

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


Here is their conclusion FYI:

Quote

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.

Conclusions

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 128.111.106.148
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.

Quote

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

Abstract  



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

[38] Nisbet E.G. and Sleep N.H. (2001) The habitat and nature of early life.
Nature, 409:1083-1091. Cited by

[39] Olsen G.J. et al. (1994) The winds of (evolutionary) change: breathing new life into microbiology.
J. Bacteriol., 176:1-6. MEDLINE Cited by

[40] Gupta R.S. et al. (1999) Evolutionary relationships among photosynthetic prokaryotes (Heliobacterium chlorum, Chloroflexus aurantiacus, cyanobacteria, Chlorobium tepidum and proteobacteria): implications regarding the origin of photosynthesis.
Mol. Microbiol., 32:893-906. MEDLINE Cited by

[41] Xiong J. et al. (1998) Tracking molecular evolution of photosynthesis by characterization of a major photosynthesis gene cluster from Heliobacillus mobilis.
Proc. Natl. Acad. Sci. U. S. A., 95:14851-14856. Full text MEDLINE Cited by

[42] Xiong J. et al. (2000) Molecular evidence for the early evolution of photosynthesis.
Science, 289:1724-1730. Full text MEDLINE Cited by

[43] Blankenship R.E. (2001) Molecular evidence for the evolution of photosynthesis.
Trends Plant Sci., 6:4-6. Full text Cited by

[44] Castresana J. et al. (1994) Evolution of cytochrome oxidase, an enzyme older than atmospheric oxygen.
EMBO J., 13:2516-2525. MEDLINE Cited by

[45] Mulkidjanian A.Y. and Junge W. (1997) On the origin of photosynthesis as inferred from sequence analysis.
Photosynth. Res., 51:27-42.

[46] Nisbet E.G. et al. (1995) Origins of photosynthesis.
Nature, 373:479-480.

Date: 2002/05/29 23:30:40, Link 128.111.106.148
Author: niiicholas
Hi,

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'.

Quote

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.

nic

Date: 2002/05/30 00:02:55, Link 128.111.106.148
Author: niiicholas
Hi,

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:

Quote

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

...as 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.

nic

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:

Quote

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:

Quote

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:

Quote

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:

Quote

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. mlong@midway.uchicago.edu

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,
nic

Date: 2002/05/30 00:51:24, Link 128.111.106.148
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
http://link.springer.de/link/service/journals/00239/tocs/t1053004.html

Quote

Articles
261-268
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

269-281
David H. Ardell, Guy Sella
On the Evolution of Redundancy in Genetic Codes
Article in: PDF | HTML-Frames

282-289
Yoshikazu Nakamura
Molecular Mimicry Between Protein and tRNA
Article in: PDF | HTML-Frames

290-298
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

299-313
Robin D. Knight, Laura F. Landweber, Michael Yarus
How Mitochondria Redefine the Code
Article in: PDF | HTML-Frames

314-326
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.

nic

Date: 2002/05/30 01:14:38, Link 128.111.106.148
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:

Quote

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:

Quote

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:

Quote

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 128.111.106.148
Author: niiicholas
Reviewing this 1993 article by Paul Nelson and Jonathan Wells:

Quote

Is Common Descent an Axiom of Biology?

http://www.arn.org/docs/nelson/pn_darwinianparadigm061593.htm

[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:

Quote

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:

Quote

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:

Quote

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 128.111.106.148
Author: niiicholas
Howdy,

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):

Quote

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!

Nic



Date: 2002/05/31 01:31:35, Link 128.111.106.148
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

http://www.pnas.org/cgi/content/full/94/8/3485

Quote

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:



Quote

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.


(source)

Thanks, nic



Date: 2002/05/31 01:44:19, Link 128.111.106.148
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

http://www.sciencemag.org/cgi/content/full/282/5386/115

Quote

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 128.111.106.148
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 128.111.106.148
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):

Quote

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:

http://research.amnh.org/vertpaleo/dinobird.html

E.g.:





Date: 2002/06/11 01:24:42, Link 128.111.106.148
Author: niiicholas
Found this key Darwin quote on the ISCID forum:

Chapter 6 of Origin of Species

Here is the link:
http://www.talkorigins.org/faqs/origin/chapter6.html

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?

Quote

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 128.111.106.148
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:

Quote

link

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. giovanni.lavorgna@hsr.it

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:

Quote

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 128.111.106.148
Author: niiicholas
Following the tangent of the evolution of repeats *within* protein sequences:

Quote

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.

http://www.idealibrary.com/servlet/citation/1047-8477/134/117

pubmed

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

CONCLUSIONS
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.,
1997).

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:

Quote

Knotty Pine and Corroding Coins: John Bracht

link

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...

nic

Date: 2002/09/21 13:06:12, Link 198.81.16.151
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.

nic



Date: 2002/09/21 13:15:43, Link 198.81.16.151
Author: niiicholas
An initial list of Wells utterances on moths and tree trunks:

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


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


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


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


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

Quote
4) In the 1980's, several researchers showed independently that peppered moths do not rest on tree trunks in the wild.
[Jonathan Wells, http://www.calvin.edu/archive/evolution/199903/0348.html ]


Quote
BUT EVERYONE, INCLUDING MAJERUS, HAS KNOWN SINCE THE 1980'S THAT PEPPERED MOTHS DO NOT REST ON TREE TRUNKS IN THE WILD
[Calvin debate, http://www.calvin.edu/archive/evolution/199903/0348.html ]


(courtsey KC)

Date: 2002/09/21 13:26:13, Link 198.81.16.151
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 amazon.com

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

Quote
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 198.81.16.152
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:

Quote

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:
http://www.talkorigins.org/faqs/wells/#mothmaj )

Fracks response to the traps claim:

Quote

[Frack, "RE: My last word":
http://www.calvin.edu/archive/evolution/199904/0207.html ]

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.

nic



Date: 2002/09/22 23:37:02, Link 198.81.17.171
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.

Quote

http://www.sciencemag.org/content/vol297/issue5583/#books  
Science 297, 940-941 (2002)

EVOLUTION:
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.

References

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: Geometrid@aol.com




Date: 2002/09/24 03:36:07, Link 198.81.16.51
Author: niiicholas
Another review (or rebuttal of positive Hooper reviews, actually) on Intelligent Design Update yahoogroup:

http://groups.yahoo.com/group/IntelligentDesignUpdate/message/112

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

nic

Date: 2002/09/24 03:44:53, Link 198.81.16.51
Author: niiicholas
Quote (niiicholas @ Sep. 24 2002,03:36)

Online letters on the Salon.com review of Hooper:

http://www.salon.com/books/letters/2002/09/20/moths/index1.html

The Wells FAQ is referenced :-)

Date: 2002/09/24 04:48:34, Link 198.81.16.24
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

nic

Date: 2002/09/26 00:13:06, Link 172.191.200.144
Author: niiicholas
Here is another Wells gaffe:

Quote

(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.

[ http://www.calvin.edu/archive/evolution/199903/0348.html ]


Michael Majerus took the trouble to respond to this himself:

Quote

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.

[ http://www.calvin.edu/archive/evolution/199904/0103.html ]


yersinia

Date: 2002/10/01 13:47:50, Link 198.81.26.142
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.

Quote

http://www.pnas.org/cgi/content/abstract/202149599v1

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:

Quote

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 198.81.26.142
Author: niiicholas
Here's a different one:

http://www.pnas.org/cgi/content/abstract/152445399v1

Quote

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 12.225.105.174
Author: niiicholas
Similar to the prokaryotic flagella thread.

Introductory material:

http://www.wikipedia.org/wiki/Flagellum
(don't confuse eukaryotic cilia/flagella with prokaryotic flagella)


http://www.wikipedia.org/wiki/Evolution_of_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 198.81.26.142
Author: niiicholas
Might as well add these as I'm discussing them over at EvC:
http://www.evcforum.net/ubb/Forum10/HTML/000029.html


On the evolution of PCP degradation:

Quote

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. copley@cires.colorado.edu

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 172.191.11.209
Author: niiicholas
This is a "data accumulation" thread for me (and anyone else interested in Croizat) to learn the basics.

To start off:

http://zoo.bio.ufpr.br/diptera/bz023/leon.htm

Quote

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.
Abstract:
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:

http://www.ento.psu.edu/home....ate.htm

Date: 2002/12/02 19:12:32, Link 172.191.11.209
Author: niiicholas
http://gsa.confex.com/gsa/2002AM/finalprogram/abstract_37210.htm

Quote

THE EMERGENCE OF VICARIANCE BIOGEOGRAPHY: FROM WEGENER TO CROIZAT AND THE CLADISTS
HALLAM, Anthony, School of Earth Sciences, Univ of Birmingham, Edgbaston, Birmingham B15 2TT United Kingdom, A.Hallam@bham.ac.uk.

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:

http://www.msu.edu/course/zol/370/lindell/10-10-02,%20method.html

Date: 2002/12/03 23:13:15, Link 172.172.193.79
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.

http://www.millerandlevine.com/km/evol/design1/article.html

Date: 2002/12/07 15:23:08, Link 152.163.188.164
Author: niiicholas
bump

Date: 2002/12/08 00:10:21, Link 152.163.188.164
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:

Quote

http://www.ncbi.nlm.nih.gov/entrez....9678675

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 152.163.188.164
Author: niiicholas
Here's a good example of a debate that rapidly focused on the ambiguities in the defn of IC:

http://iidb.org/ubb....1759&p=

...other examples welcome.

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

Date: 2002/12/08 14:34:57, Link 152.163.188.164
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"?

--
Dene

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 128.111.106.15
Author: niiicholas
Interesting.  Here's another one by the same folks:

Quote

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 128.111.106.15
Author: niiicholas
Philosopher/Historian of science, who has authored a PhD and several articles on Kettlewell's work, has weighed in against Jonathan Wells:

Quote

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. david.rudge@wmich.edu

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:
http://vms.cc.wmich.edu/~rudged/index.html

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:
http://www.ed.psu.edu/CI/journals/2001aets/01file1.asp

Rudge's current and upcoming articles are listed here:
http://homepages.wmich.edu/~rudged/vita.html#refereed_journal_articles



Date: 2002/12/12 21:44:25, Link 128.111.106.15
Author: niiicholas
Other Biston researcher webpages:

Bruce Grant
http://faculty.wm.edu/bsgran/

Michael Majerus
http://www.gen.cam.ac.uk/dept/majerus.html

Books by Majerus:
amazon.com link

Date: 2002/12/13 01:13:29, Link 128.111.106.15
Author: niiicholas
And in the "duplicated genes aren't necessarily selectively neutral, dammit" category:

(bold added)
Quote

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. fkondras@ncbi.nlm.nih.gov

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.


[...]

Discussion:

[...]
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...)

nic

(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 128.111.106.15
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 128.111.106.15
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.

E.g.:

PubMed
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi

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.

GUIDE:
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


HINT:
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:

Quote

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. lazarillo@bioscience.utah.edu

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:

Quote

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]

[etc.]


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:

Quote

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]

[etc.]

Date: 2002/12/13 02:14:51, Link 128.111.106.15
Author: niiicholas
PubMed Central:

http://www.pubmedcentral.nih.gov/

...is 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:
http://www.pubmedcentral.nih.gov/

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 http://www.pnas.org )

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
http://jbiol.com/content/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:

http://www.ncbi.nlm.nih.gov/entrez/journals/loftext_noprov.html


nic

PS: Another important journal:

Evolution
Archives back to 1996:
http://lsvl.la.asu.edu/evolution/contents.html

From 2000 on:
http://evol.allenpress.com/

Current issue:
http://evol.allenpress.com/evolonline/?request=get-current-issue

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

Date: 2002/12/13 03:35:04, Link 128.111.106.15
Author: niiicholas
History of mousetraps:

http://www.uh.edu/engines/epi1163.htm

Quote

"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: http://www.lightlink.com/bbm/wmouse.html.



Clipart

The Conventional Snap Trap

Date: 2002/12/13 03:41:18, Link 128.111.106.15
Author: niiicholas
The History of the Mousetrap
http://inventors.about.com/library/inventors/blmousetrap.htm

http://inventors.about.com/library/inventors/blmousetrap2.htm

Some patented mousetraps:










Date: 2002/12/17 15:28:17, Link 128.111.106.15
Author: niiicholas
Quote

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 128.111.106.15
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 128.111.106.15
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:

Quote

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 128.111.106.15
Author: niiicholas
In the "nonmotile appendages can have a dispersal-related function despite being nonmotile" category:

Quote

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 198.81.26.142
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.

http://www.nationalreview.com/comment/comment-west121702.asp

This guy oughta read the Icons FAQs:
http://www.talkorigins.org/faqs/wells/
http://www.ncseweb.org/icons/
http://www.nmsr.org/iconanti.htm

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.

Quote

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 198.81.26.142
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

http://www.stephenjaygould.org/ctrl/archive/thomas_wedge.html

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 198.81.26.142
Author: niiicholas
Atrazine degradation pathways appear to have arisen recently:

This lab studies 'em:
http://www.cbs.umn.edu/bpti/mice/faculty/wacket1.htm


...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.
http://jb.asm.org/cgi/content/full/180/7/1951

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.
http://aem.asm.org/cgi/content/full/64/6/2323


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.
http://aem.asm.org/cgi/content/full/64/1/178

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).

Quote

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 172.172.59.216
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.

http://www.arn.org/ubb/ultimatebb.php?ubb=get_topic;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.

Quote

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 128.111.106.15
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:

Quote

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:

Quote

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:

Quote

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.

Introduction

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 1.14.13.50) 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 128.111.106.15
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

http://www.breakpoint.org/Breakpo....yth.htm

Date: 2002/12/20 01:10:56, Link 128.111.106.15
Author: niiicholas
Intelligent Design jargon explained!
By Casey Luskin
http://www.ideacenter.org/idjargon.htm

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 128.111.106.15
Author: niiicholas
This was posted on the DI website.  

Quote

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:
http://www.talkorigins.org/faqs/wells/default.htm#mothgrant

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.

ICONS OF EVOLUTION?
Why much of what Jonathan Wells writes about evolution is wrong
by Alan D. Gishlick
http://www.ncseweb.org/icons/



Date: 2002/12/20 20:53:02, Link 198.81.26.142
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 198.81.26.142
Author: niiicholas
Over at the ID network's response to the AAAS resolution:

[url=http://www.intelligentdesignnetwork.org/ResponseToAAAS.htm#Reason 6 text]Here if the internal spaces don't muck it up[/url]

...it is written:

Quote

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 198.81.26.142
    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:
    http://www.talkorigins.org/faqs/horses/horse_evol.html#part2

    ...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:
    http://www.talkorigins.org/faqs/wells/#horses


    Another resource:

    Also the UC Museum of Paleontology Online:
    http://www.ucmp.berkeley.edu/

    Teachers e-volution forum:
    http://www.ucmp.berkeley.edu/education/evoforum/

    Date: 2002/12/21 16:50:30, Link 198.81.26.142
    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 198.81.26.142
    Author: niiicholas
    Over on this ARN thread,

    http://www.arn.org/ubb/ultimatebb.php?ubb=get_topic;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 12.225.105.174
    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:

    [img]http://www.pnas.org/content/vol99/issue3/images/medium/pq0224771001.gif[/[img]

    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,

    Quote

    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.

    Refs:

    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)

    Quote

    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 12.225.105.174
    Author: niiicholas
    Wow.  This just goes to show that everything is relative.

    Date: 2002/12/24 02:39:32, Link 12.225.105.174
    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 12.225.105.174
    Author: niiicholas
    In the "yes, IDists have in fact argued that IC precludes the existence of precursors with other functions" category:

    Quote

    NO FOREBEARS
    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 12.225.105.174
    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:

    Quote

    source

    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:

    Quote

    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...

    Quote

    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.

    yersinia

    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 12.225.105.174
    Author: niiicholas
    Quote

    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.

    Quote

    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.  

    Quote

    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.

    Quote

    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.

    Quote

    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:




    Quote

    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:

    quote:
    --------------------------------------------------------------------------------
    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 12.225.105.174
    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:

    Source: http://www.sciencedaily.com/releases/2002/12/021226071202.htm


    T.o. discussion: here

    Quote

    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 12.225.105.174
    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:

    Quote

    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:

    Quote

    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 12.225.105.174
    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 12.225.105.174
    Author: niiicholas
    In the "cytoskeletal protein homologs found in prokaryotes" category:

    Quote

    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.
    Carballido-López


    "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.

    References:

    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 12.225.105.174
    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 12.225.105.174
    Author: niiicholas
    Regarding Google, Dunk has a very good post here.

    Quote

    (Go to http://groups.google.com/ )

    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
    20021231093815.02096.00000093@mb-cl.aol.com

    You must store the google groups prefix in a convinient place.

    It is:
    http://groups.google.com/groups?&selm=

    Next, append the ID to the prefix: (be sure you don't leave a space
    after the '='.

    http://groups.google.com/groups?....aol.com

    Voila!

    Dunk


    E.g., Dunk's post is:
    http://groups.google.com/groups?....ink.net

    nic

    PS: If you surf with Internet Explorer, don't forget about the Google Search Toolbar (*very* cool):

    http://toolbar.google.com/

    Date: 2002/12/31 17:37:05, Link 12.225.105.174
    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:

    Quote

    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.

    [...]

    Discussion  
     
    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 198.81.26.142
    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.

    nic

    Date: 2003/01/07 21:20:14, Link 128.111.106.15
    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:

    Quote

    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. a.m.poole@massey.ac.nz

    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:

    Quote

    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 68.6.113.238
    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 128.111.106.15
    Author: niiicholas
    Originally posted here.

    Quote

    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":

    Quote

    Evidence
    Introduction

    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

    EMBARRASSING QUESTIONS FOR THE EVOLUTIONISTS
    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.

    [...]



    [Bibliography]

    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 128.111.106.15
    Author: niiicholas
    Hey,

    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:

    http://www.arn.org/ubb/ultimatebb.php?ubb=get_topic;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
    =========
    Quote
    Originally posted by Geoff:
    [qb]...
    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.

    Regards,

    Geoff[/qb]
    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):

     
    Quote
    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:    ,
     ,
    and
     .  

    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 68.6.113.238
    Author: niiicholas
    Bump as this thread is being cited on ISCID:

    http://www.iscid.org/ubbcgi....279&p=2

    In the "origin of new information in the evolution of humans" category:

    Quote

    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:

    Quote

    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?

    Nick



    Date: 2003/01/18 23:54:17, Link 128.111.106.15
    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:

    Quote

    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.


    nic



    Date: 2003/01/19 00:48:17, Link 128.111.106.15
    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:

    Quote

    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.

    RBH


    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,
    nic


    [edit: cross-posted to II evo board:

    Vagueness and Explanatory Constraints
    http://www.iidb.org/vbb/showthread.php?s=&postid=791441#post791441

    ]



    Date: 2003/01/19 04:19:00, Link 128.111.106.15
    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:

    Quote

    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 68.6.113.238
    Author: niiicholas
    Some good stuff I found and posted in response to Nelson Alonzo here:

    http://www.arn.org/ubb/ultimatebb.php?ubb=get_topic;f=13;t=000576;p=3

    Quote

    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).

     
    Quote

    http://www.abo.fi/isb/students/anssi.malinen.html

    STRUCTURAL STUDIES OF PROTON TRANSLOCATING PYROPHOSPHATASE
    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.
    Quote

    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).