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Date: 2002/05/23 16:32:16, Link
Author: theyeti
Awhile back I had a discussion about the DI's wacko response to the PBS evolution series here.  Scroll down a few messages.  There are some links to some good recent papers in that thread.  The references are:

Trends in Biochemical Sciences 2001, 26:591-596

Proc Natl Acad Sci U S A 1995 Mar 92:2441-5

J. Biol. Chem., Vol. 276, Issue 10, 6881-6884, March 9, 2001

Proc. Natl. Acad. Sci. USA, Vol. 97, Issue 15, 8392-8396,       July 18, 2000

Annu. Rev. Biochem. 2000. 69:617-650.

theyeti

Date: 2002/05/28 09:54:22, Link
Author: theyeti
Niiicolas:
Quote

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]"?


Here are a few links from various places.

PBS Charged with "False Claim" on "Universal Genetic Code"  From ARN.  The title says it all...

A "Dying Theory" Fails Again  Miller's response.

Reply To Kenneth Miller On The Genetic Code.  The DI's wacky response to Miller.

DI Fails Again to "Crack" the Code.  Miller's second response.

That's it for the DI vs. Miller spat AFAIK.  A couple of others:

Is Common Descent an Axiom of Biology?  This one's by Nelson.  Scroll down a bit and you'll see his genetic code arguments.

Should We Stop Criticizing the Doctrine of Universal Common Ancestry?  By our dear friend Jonathan Wells.  He uses the genetic code argument, along with a number of other really bad ones.  I don't think that Wells does much more than assert his position, but this is a good article to keep handy next time someone says that Wells accepts common ancestry, though he's ambiguous as usual.

Date: 2002/05/30 12:59:58, Link
Author: theyeti
Quote
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.


That's got to be the stupidest argument I've ever seen.  If common descent is true, then there will be no empirical evidence against it.  What they're basically saying is "true theories can't be shown to be false empirically".  Why don't they just say that differing genetic codes are empirical evidence against common descent and be done with it?  How does it make sense to construct a thought experiment where we try to hold two contradictory notions at once, i.e., common descent is both true and shown to be false by the evidence?

Anyway, Nelson & Wells' contention that biologists dropped the "no viable intermediates" claim in order to protect common descent is demonstrably false.  It was dropped because it was shown to be wrong, empirically.  Not only does the example of ambiguous codes demonstrate this, but also the ability of researchers to alter the codes of living organisms.  Ironically, the DI aticle that responds to Miller alludes to this:

Quote
Experiments to change the identity of transfer RNA (tRNA)--another possible mechanism by which genetic codes might reassign codon “meanings”--have shown that the intermediate steps must be bridged by intelligent (directed) manipulation. In one such experiment, for instance, Margaret Saks, John Abelson, and colleagues at Caltech changed an E. coli arginine tRNA to specify a different amino acid, threonine. They accomplished this, however, only by supplying the bacterial cells (via a plasmid) with another copy of the wild-type threonine tRNA gene. This intelligently-directed intervention bridged the critical transition stage during which the arginine tRNA was being modified by mutations to specify threonine. [6]


Notice that they're trying to do with this experiment what they do with animal and plant breeding.  When mutation and selction are shown to be sufficient to cause substantial morphological change, they dismiss it outright because it was really just "intelligent design" even though it has nothing to do with ID as they conceive it.  And here, the ability of the code to change is dismissed because it was caused by "intelligent design", as if plasmid transfers never happen in the wild.    

Anyway, here are the refs for the papers cited:

6. Margaret E. Saks, Jeffrey R. Sampson, and John Abelson, “Evolution of a Transfer RNA Gene Through a Point Mutation in the Anticodon,” Science 279 (13 March 1998):1665-1670.

7. Jennifer Normanly, Richard C. Ogden, Suzanna J. Horvath & John Abelson, “Changing the identity of a transfer RNA,” Nature 321 (15 May 986):213-219.

I haven't read them as I don't have online access to either journal (though I might just get off my butt and walk the 100 yards to the library.)  I am interested in seeing how these papers compare to the DI quote-mining spin.

theyeti

P.S.  Just noticed that the DI has a typo in their reference for the Normanly et al paper.  It looks like it's from 1986, in which case they're using a reference that's much too old given that they're lots of recent ones.

Date: 2002/05/30 16:43:39, Link
Author: theyeti
Here's another well studied one:

The jingwei gene in Drosophila.

(quick side note:  you find most of these suckers in well studied organisms like Drosophila whose genome has been sequenced.  The particular significance of this is that we can trace the ancestry of the gene in question by looking at closely related species Drosophila, whose common ancestry is not even doubted by YECs.  Their only recourse here would be to claim that the gene had always existed and that every other species of Drosophila had lost the gene independently.  This would a) be extremely unparsimonious, given that it requires multiple parallelisms with no known non-random mechanism and b) force us to ignore all of the other evidence of recent origin.)  

Onto jingwei:

In a 1993 issue of Science, Manyuan Long, and CH Langley published their findings of a novel Drosophila gene, located on chromosome 3, that is found in sister species D. teissieri and D. yakuba and thus presumably first appeared in the common ancestor of both.  They dubbed this new gene jingwei (jwg).  The evidence that they uncovered, especially the lack of introns, suggested that the gene was derived from a retrotransposed mRNA from an alcohol dehydrogenase (adh) gene on chromosome 2.  Further results suggested that jwg is not a pseudogene as was first thought, but is rather a functional novel gene, though its exact function is still not clear.  The gene not only has specific RNA expression patterns, but has also undergone extensive evolution without suffering from any frameshift or nonsense mutations that are the hallmark of pseudogenes; the evidence strongly suggests that jwg has been under positve Darwinian selection.  Not only that, but Long and Langely’s results suggest that selection is playing a role throughout the origin of new genes, rather than being initially relaxed as was previously thought.
 
Perhaps the most interesting aspect of jwg is that its gene product is a chimera, meaning that it has function portions that are derived from different ancestral genes (aka gene fusion).  The C-terminal portion of jwg was almost certainly derived from the ancestral adh gene via retrotransposition, but that left the origin of the N-terminal exons still unexplained.  Did they come from non-coding upstream regions of DNA, or were they derived from parts of non-related functional genes?  Further study by Long et al. (1999) demonstrated that the N-terminal regions were the result of duplications of exons from a gene named yellow-emperor (ymp).  A follow-up study by Wang et al. (2000) showed that ymp is also a functional gene whose first three exons are the donor for the recruited portion of jwg.









Quote
Fig. 2.—Origin of the three novel proteins, YMP-1, YMP-2, and JGW, as a consequence of exon recombination. E1–E12 represent exons 1–12 of ymp (for the origin of YMP-1 and YMP-2); E1–E3, making up JGW, are the first three exons of ynd (Long and Langley 1993 ), a duplicate copy of ymp. The hatched boxes are the regions encoding protein sequences, with different patterns showing different peptide sequences. The open boxes represent untranslated regions (UTRs) of mRNAs (the open boxes on the left represent 5' UTRs; those on the right represent 3' UTRs)
{from Wang et al, 2000}

That's not the world's best image, but it gets across the general idea of how these new genes evolve.  Notice also that this graphically demonstrates the evolution of the yellow emperor genes as well.  As for jingwei, the basic idea is as follows, and I'd like to get it (and all other such examples) into a fancy colored graphic when possible (if anyone knows of a good program for this, let me know.)

Ald ---> retrotransposition ---> Jingwei Ct portion

YMP --> duplication of first three exons ---> exon shuffling ---> fusion of Jingwei Nt and Ct portions.


Refs:

Long M, Langley CH, Natural selection and the origin of jingwei, a chimeric processed functional gene in Drosophila.  Science 1993 Apr 2;260(5104):91-5
PubMed

Long M, Wang W, Zhang J., Origin of new genes and source for N-terminal domain of the chimerical gene, jingwei, in Drosophila.  Gene 1999 Sep 30;238(1):135-41
full text pdf

Luque T, Marfany G, Gonzalez-Duarte R., Characterization and molecular analysis of Adh retrosequences in species of the Drosophila obscura group.  Mol Biol Evol 1997 Dec;14(12):1316-25
PubMed

Wang W, Zhang J, Alvarez C, Llopart A, Long M., The origin of the Jingwei gene and the complex modular structure of its parental gene, yellow emperor, in Drosophila melanogaster.  Mol Biol Evol 2000 Sep;17(9):1294-301
full text



Date: 2002/05/31 00:21:26, Link
Author: theyeti
Here's the most recent one that I know of off hand:

PNAS, Vol. 99, Issue 7, 4448-4453, April 2, 2002

Origin of sphinx, a young chimeric RNA gene in Drosophila melanogaster

Quote
Non-protein-coding RNA genes play an important role in various biological processes. How new RNA genes originated and whether this process is controlled by similar evolutionary mechanisms for the origin of protein-coding genes remains unclear. A young chimeric RNA gene that we term sphinx (spx) provides the first insight into the early stage of evolution of RNA genes. spx originated as an insertion of a retroposed sequence of the ATP synthase chain F gene at the cytological region 60DB since the divergence of Drosophila melanogaster from its sibling species 2-3 million years ago. This retrosequence, which is located at 102F on the fourth chromosome, recruited a nearby exon and intron, thereby evolving a chimeric gene structure. This molecular process suggests that the mechanism of exon shuffling, which can generate protein-coding genes, also plays a role in the origin of RNA genes. The subsequent evolutionary process of spx has been associated with a high nucleotide substitution rate, possibly driven by a continuous positive Darwinian selection for a novel function, as is shown in its sex- and development-specific alternative splicing. To test whether spx has adapted to different environments, we investigated its population genetic structure in the unique "Evolution Canyon" in Israel, revealing a similar haplotype structure in spx, and thus similar evolutionary forces operating on spx between environments.


This is an RNA gene, and the role that RNAs play in terms of regulation is only now starting to be fully realized.  RNA genes can probably evolve by retrotransposition easier than protein coding genes can, since the characteristic 5' truncation is less likely to have a major effect, and there is no worry about frameshifts.  In the case of small RNAs, there should be no 5' truncation.  (Retrogenes and processed pseudogenes are caused when a reverse transcriptase creates a cDNA from a mature mRNA (or other RNA).  The reverse transcrpitase starts at the poly A tail and works its way 3'.  However, if the mRNA is of decent size, it usually falls off before finishing, resulting in a cDNA that is truncated at the 5' end.  This truncation, along with a degenerate poly A tail and flanking repeats, are smoking gun evidence of a retrogene or processed pseudogene.  There's just no denying it, Johnson.)  Furthermore, many small RNAs can act as anti-sense oligos, binding complemetary mRNA or DNA for regulation.  These are easy to evolve, because they can be derived straight from the complemetary strand of the gene they regulate.

There is a furhter significance to this example in the fact that sphinx was derived from retrotransposition of an ATP synthase gene.  But sphinx is not a protein coding gene as ATP synthase is, so the functionality of the sequence is not derived from the already adapted sequence of ATP synthase.  Rather, this is more like a random sequence becoming functional, and is thus similar to the example of URF13 that Dembski sweats over in NFL (idea: let's apply Dembski's uniform probability to sphinx like he did with URF13 and see if it beats his universal probability bound.  Better yet, let's multiply the probabilities of both).

On top of all of this, we have a (potential) transposition event too.  So the origin of the gene goes something like this:

Quote
Although the role of retroposition is well defined in the origin of this gene, it should be pointed out that this is an unusual retroposition process. An independent DNA transposon, S element, moved together in the process with the ATP synthase chain F gene. A consequence of this process leaves a partial S fragment attached to the ATP synthase element-derived region in spx. There are several hypothetical scenarios for the origin of this complex structure. The first hypothesis is that the retroposed sequence of ATP synthase gene might have been inserted first into the S element located in the current position of the chromosome. Then the chimeric gene structure evolved by using the sequence of degenerated S element as the recipient site for splicing of the newly created intron between the recruited exon and ATP synthase chain F derived exon. The second hypothesis is that the retrosequence might have landed first in the S element, located in another portion of the genome, before the S element carrying the retrosequence jumped into the current position and degenerated in the S element structure. The third hypothesis is that the portion of the S element, which was located upstream of spx, might have been cotranscribed with the ATP synthase chain F gene and retroposed. The observation that the short repeats flank both S element fragment and the ATP synthase derived portion of spx is consistent with the third hypothesis.


theyeti



Date: 2002/11/26 16:08:25, Link
Author: theyeti
Quote (Mr. Davies @ Nov. 25 2002,20:18)
Hello all,


Thank you for this board for discussion.

I have a question about ID.  In particular, does ID make any assumption in the identity of the designer?  If so who, if not, why not?

Basically no.  The whole premise of the modern ID argument (and that of Paley I suppose) is that one can detect design in the absence of any knowledge of the designer.  

Why not?  I'll try to expand on that later.

theyeti

Date: 2002/11/26 17:20:32, Link
Author: theyeti
Hello all.  What follows is a brief essay (or rant if you prefer) about the claim that ID is an appeal to the best explanation, specifically within the framework of ID's supposed explanatory power.  This is posed as an answer to the question, "what's the logical fallacy here?"  


It's not so much a logical fallacy.  It's just that they're plain wrong as far as explanatory power is concerned.  To actually explain something, you not only need to give an account of why something happened, but why it should have happened and why it didn't happen differently.  In other words, your theory should predict the observed outcome, or at least predict a set of possible outcomes (the smaller the better) that overlap what's observed.  It's pretty safe to say that evolutionary biology predicts a much smaller set of possible outcomes than does ID, which itself predicts an infinite set of outcomes (which is to say that it predicts nothing at all).  So the plain fact of the matter is that ID is not only fails to be the best explanation, but it fails to be any kind of explanation at all.  Evolutionary biology on the other hand, while not only giving us a general explanation for the diversity and unity of living things, also gives us a research paradigm for explaining the exact genesis of specific structures and functions within living things.  Note that this is something that ID doesn't even aspire to.

The hypocritical IDist retort to this is to claim that evolutionary biology predicts an infinite set of outcomes, and is thus not testable itself.  Of course if this were really true, then the IC and SC arguments against evolution would not be logically tenable.  These arguments fail because they don't match up to the facts (and in the case of SC, because it's an excercise in question begging).  But they really can't have it both ways.  They can't claim that IC or SC falsify evolution while simultaneously claiming that evolution isn't falsifiable.

The mere fact that they try to make these arguments shows that evolutionary biology is constrained by what it can predict, and therefore can explain not just why things are as we see them, but why they're not somehow wildy different.  Consider for example if every species on Earth were morphologically and biochemically distinct.  Darwinian evolution could certainly not explain that.  Or what if there were only one species and there had always been only one species?  Again, Darwinian evolution would be untenable.  I often think that people are so used to the facts of nature as they are that they don't stop to think about situations that might make non-evolutionary accounts far superior.  (I also think this is why biologists, who are more aware of the facts of nature than your average joe, have a particularly hard time not accepting evolution.)  But in all of these cases, whether whether nature is like it is now or whether it's completely different, ID accounts for it either way by invoking the same uninformative explanation: The Designer wished it such.

Now it's not impossible to get explanatory power out of this.  But in order to do so you have to ask why the designer wished it such.  This is not an unreasonable demand, as IDists often claim it is.  When we see some sort of putative designed human artifact, the first thing we want to know is what it's for.  And implicit in this demand is knowing how and why a human would have built such a thing, because of course we don't expect humans to be able or willing to build just anything.  In other words, the set of possible outcomes is limited when we assume human construction.  If we can say what object X is for and why humans living in location Y would have built such a thing, then we've gone a long way towards explaining the genesis of object X.  But what's really senseless is that the IDists not only don't want to engage in this sort of discourse, they even claim that it's unscientific!

Naturally, they have their reasons.  Trying to bring the designer and its attributes into the discussion would force a few things.  1) They'd have to admit that it's all speculation.  There's nothing wrong with that per se, because every scientific hypothesis starts out as being speculative, but it would raise the issue of the acutal testing of ID hypotheses, and the lack of data on the Designer would make this difficult.  Furthermore, real world data can eliminate several popular Designer hypotheses if we insist on taking the scientific approach to ID.  2) The Big Tent philosophy, who's purpose is to allow any and every ID hypothesis (except maybe the Raelins) equal access, thus swelling the ranks.  This is just a political strategy.  3) They'd have to start comparing ID to Darwinian evolution.  As it is now, it's advantageous to be completely devoid of any theoretical basis, because it lets them sit back and take pot shots at Darwinian evolution without having to account for the so-called mysteries that they invoke with a model of their own.  And surely there are other reasons, but it's not necessary to figure them all out.  The important point is that they've chosen to uncouple the ID argument from the only thing that would actually give it some explanatory power, which is some actual considerations about what it is that's doing the design, how it's being done, why it's being done, when it was being done, etc., etc., etc...

The uncoupling of the ID argument with any considerations of the desiger is exactly what makes ID devoid of any exaplanatory power.  In the absence of a real design hypothesis, ID cannot ever be a scientific theory.  Instead it's just an argument, and the only point to the argument is to prove a designer, not actually to explain anything.  And it's not even a very good argument.  AFAICT, the ID argument has in remained essentially unchanged since Paley.  It was logically unsound to begin with, as shown by Hume, and then Darwin came along and demonstrated why it's unreliable.  Can anyone tell me what new and interesting explanations for the properties of living things that Paley or his followers were able to come up with?

theyeti



Date: 2002/11/26 17:52:15, Link
Author: theyeti
Okay, now for why ID doesn't identify the designer.  Here is what I posted in a thread in the "collaborations" section

Quote
Naturally, they have their reasons.  Trying to bring the designer and its attributes into the discussion would force a few things.  1) They'd have to admit that it's all speculation.  There's nothing wrong with that per se, because every scientific hypothesis starts out as being speculative, but it would raise the issue of the acutal testing of ID hypotheses, and the lack of data on the Designer would make this difficult.  Furthermore, real world data can eliminate several popular Designer hypotheses if we insist on taking the scientific approach to ID.  2) The Big Tent philosophy, who's purpose is to allow any and every ID hypothesis (except maybe the Raelins) equal access, thus swelling the ranks.  This is just a political strategy.  3) They'd have to start comparing ID to Darwinian evolution.  As it is now, it's advantageous to be completely devoid of any theoretical basis, because it lets them sit back and take pot shots at Darwinian evolution without having to account for the so-called mysteries that they invoke with a model of their own.


I suppose you could divide this into the empirical, the political, and the theoretical respectively.  Keep in mind though that this is at least partially a matter of my opinion, since trying to figure out why they do what they do is a matter of speculation itself.  I think that these reasons are certainly in opperation at least some of the time, but they are not the only ones.  I will try to cull some remarks from IDists from other boards later if I have a chance, and let you see their view.  

One thing that persists among "leading" IDists in their writing is that figuring out the attributes or identity of the designer is a question for philosophy or religion.  But this is clearly wrong, because once we've make detecting design something which can be answered via science, we've also made detecting the designer part of science also.  For example, it would be foolish to say that we've concluded that Stonehenge was designed, but that the scientific method couldn't deduce who designed it or for what reason.  In fact, that's the whole point of sciences that study design, like archeaology or forensics, which the IDists often cite as evidence that their methodology is actually being used.  (This is the crucial difference which shows that their methodology is actually not being used.)  Exactly what the IDists' motivations are for this claim are a matter of speculation, but certainly they'd rather give specific religious interpretations preeminence, which the Wedge Strategy shows is the primary goal of the movement.

theyeti

P.S.  The OP here is kind of in the wrong forum, since it deals with AiG, which is a YEC outfit, and this forum is for ID.  However, we're just now getting this board up and running full steam, so it's not like there are a bunch of threads competing for attention.  Try to be patient; we'll try to generate some steady activity here soon.

Date: 2002/12/07 14:00:23, Link
Author: theyeti
Hi Tom, Welcome to AE.

I disagree that we should just "give in" to the creationists/IDists when it comes to teaching evolution in public schools.  Right now my ideas are kind of scatter-shot and I haven't organized them completely.  But what follows is the basic outline.

1.  First of all, I think there is real value to teaching kids evolutionary theory.  Just like introducing them to any science, it helps them understand why scientists think like they think and do what they do.  I consider it no less valuable than introducing them to basic physics or chemistry.  As for myself, highschool biology was a major turning point, and learning about evolution was one of the more fascinating parts of it.  This is largely why I chose to persue a career in biology.  If we remove or water down evolution, or obscure it by introducing pseudoscience along side, then we may be doing kids and our society a serious disservice.  Furhtermore, any highschool student who goes to college and majors in biology, or even just takes an intro class, is going to have to understand evolutionary theory, and it's best if they get a good taste of it when they're in highschool.  Professors already complain that they have to spend too much class time just catching the students up to where they should have been before taking the class.  We live in a country where most of our scientists have to be imported.  Let's not make things worse.

2.  The fact that evolution is controversial in our culture is not a legitimate reason to quit teaching it or water it down in science class.  It is not controversial for scientists, though of course many subtheories within evolutionary theory are.  The reason evolutionary biology is controversial in our culture is because creationists/IDists spend millions of dollars on an everpresent and highly dishonest propaganda campaign.  By allowing this to affect what we do and don't teach in schools, we're effectively allowing anyone who can stir up a controversy to dictate our science cirricula.  Our science cirricula should be dictated by scientific consensus, not by noisy ideologues.  The cure to their propaganda is better information and teaching.  By removing or watering-down evolution, we will only make the problem worse.  

3.  The goal of the cre/ID crowd is to use to science class for religious and/or ideological indoctrination.  The various "compromises" they suggest are just stepping-stones to their ultimate goal, put forth in lieu of other strategies that have been struck-down by the courts.  If we allow them to teach creationism/ID along side evolution, then we have an equally serious problem on our hands (from a church/state separation viewpoint), which is to prevent them from pushing religious doctrine.  I see alowing pseudoscience into classrooms as making our job tougher, rather than diffusing the situation.  

Anyway, that's my thoughts as disorganized as they are.  The NCSE has a few articles about why we should teach evolution, and maybe I'll post them later time permitting.

theyeti

Date: 2002/12/08 22:26:49, Link
Author: theyeti
A new study finds dozens of retrogenes in Drosophila.

Retroposed New Genes Out of the X in Drosophila

Esther Betrán, Kevin Thornton, and Manyuan Long

Genome Res 2002 Dec;12(12):1854-9

PubMed

Full text  (may need subscription)

Abstract:
Quote
New genes that originated by various molecular mechanisms are an essential component in understanding the evolution of genetic systems. We investigated the pattern of origin of the genes created by retroposition in Drosophila. We surveyed the whole Drosophila melanogaster genome for such new retrogenes and experimentally analyzed their functionality and evolutionary process. These retrogenes, functional as revealed by the analysis of expression, substitution, and population genetics, show a surprisingly asymmetric pattern in their origin. There is a significant excess of retrogenes that originate from the X chromosome and retropose to autosomes; new genes retroposed from autosomes are scarce. Further, we found that most of these X-derived autosomal retrogenes had evolved a testis expression pattern. These observations may be explained by natural selection favoring those new retrogenes that moved to autosomes and avoided the spermatogenesis X inactivation, and suggest the important role of genome position for the origin of new genes.


I'm going to include this little quote from the opening paragraph because it's useful IMO as a summary of sources of new gene evolution, and with references to the earliest papers about them:

Quote
New genes that originated by various molecular mechanisms are an essential component in understanding the evolution of genetic systems (Long 2001). These mechanisms include the classic mechanism of duplication (Ohno 1970), exon shuffling (Gilbert 1978), retroposition (Brosius 1991), and gene fusion through deletions or recruitment of new regions (Nurminsky et al. 1998), or a combination of these mechanisms (Long and Langley 1993; Begun 1997; Nurminsky et al. 1998).


Here are a few other important passages:

Quote
There is increasing evidence, fortunately, that retroposition, which generates new genes in new genomic positions via reverse transcription of mRNA from a parental gene, is important for the origin of new gene functions (Brosius 1999). In mammalian systems, a classic example is the human retrogene Pgk-2 with male specific function (McCarrey and Thomas 1987). Pgk-2 is autosomal (chromosome 19) whereas the parental copy Pgk-1 is X-linked. Pgk-2 evolved late spermatogenesis-specific expression. [theyeti:  I think I posted Pgk-2 before the crash.  I will do it again shortly] This new expression pattern is related to the fact that late spermatogenesis cells are the only ones that do not express Pgk-1 because of male germline X inactivation (McCarrey 1994). Subsequent analyses of retroposed genes in mammalian genomes suggested that retroposition had efficiently sown the seeds of evolution in genomes (Brosius 1991).
...
We have identified, from the annotated genes in the D. melanogaster genome, all pairs of homologs (70% amino acid identity or more) that are located on different chromosomes with hallmarks of retroposition (Table 1). Twenty-four young paralogous pairs fulfilled these criteria: 23 pairs in which the new copy lost the introns (CG12628, one of the 23, is additionally flanked by short repeats), and one pair with no introns in either copy but with the new copy retaining a degenerated poly-A tract (CG 12324/Rp515A). Interestingly, CG12628, which seems to be the youngest of the described retrogenes, is the only one that retains the direct repeats, a hallmark of the recent insertion event. Some other retrogenes also retained a degenerated poly-A tract: CG12628, CG10174, and CG13732. The parental genes have diverse functions, consistent with results from the human genome (Gonçalves et al. 2000).
...
Four possible explanations could account for the observed pattern: (1) nonrandom generation of retrogenes by a disproportionate number of X-linked genes that express in the germline cells; (2) negative selection against insertions in the X chromosome; (3) different recombination rates (or possibly deletion rates) between the autosomes and the X chromosome; and (4) positive Darwinian selection favoring retrogenes generated from the X chromosome to the autosomes.
...
The fourth hypothesis, positive selection, seems more parsimonious to interpret the excess of retroposition from X to autosomes. X inactivation during early spermatogenesis could produce a selective advantage for the retroposed genes with novel functions that escape X linkage and become expressed in testis, as previously suggested (Lifschytz and Lindsley 1972; McCarrey 1994). X inactivation early in spermatogenesis is well documented in Drosophila, mouse, and human (Lifschytz and Lindsley 1972; Richler et al. 1992). Thus, a mutant with a newly retroposed gene on autosomes will have some advantage over an X-linked form, because the mutant can carry out a new function putatively required in male germline cells after the X chromosome becomes inactivated. This hypothesis assumes that retroposition occurs from genes on all chromosomes with the same probability but natural selection favors the ones that avoid X-linkage by moving to an autosome and developing expression in testis.


theyeti

Date: 2002/12/10 21:00:03, Link
Author: theyeti
This one appears to be somewhat speculative (and I don't have the full text) but it's highly relevant nonetheless.

Mol Neurobiol 2002 Oct-Dec;26(2-3):235-50

Structure of the sodium channel gene SCN11A: evidence for intron-to-exon conversion model and implications for gene evolution.

Dib-Hajj SD, Tyrrell L, Waxman SG.

Quote
Exon/intron boundaries in the regions encoding the trans-membrane segments of voltage-gated Na channel genes are conserved, supporting their proposed evolution from a single domain channel, while the exons encoding the cytoplasmic loops are less conserved with their evolutionary heritage being less defined. SCN11A encodes the tetrodotoxin-resistant (TTX-R) sodium channel Nav1.9a/NaN, which is preferentially expressed in nociceptive primary sensory neurons of dorsal root ganglia (DRG) and trigeminal ganglia. SCN11A is localized to human chromosome 3 (3p21-24) close to the other TTX-R sodium channel genes SCN5A and SCN10A. An alternative transcript, Nav1.9b, has been detected in rat DRG and trigeminal ganglion. Nav1.9b is predicted to produce a truncated protein due to a frame-shift, which is introduced by the new sequence of exon 23c (E23c). In human and mouse SCN11A, divergent splicing signals prevent utilization of E23c. Unlike exons 5A/N in genes encoding TTX-sensitive sodium channels, which appear to have resulted from exon duplication, E23c might have evolved from the conversion of an intronic sequence. Although a functional role for Nav1.9b has yet to be established, intron-to-exon conversion may represent a mechanism for ion channels to acquire novel features.


Given that intronic sequences, with the exception of some 5' and 3' conserved bases, are sequence non-specific, this would be the equivalent of a more or less random sequence being converted into a biological function.

theyeti

edited to add this diddy:

Evolution of voltage-gated Na(+) channels.



Date: 2002/12/10 23:26:33, Link
Author: theyeti
Birth of two chimeric genes in the Hominidae lineage.


Courseaux A, Nahon JL.

Science 2001 Feb 16;291(5507):1293-7

PubMed, Full text (May require subscription)

Quote
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.


Here is the proposed model for the evolution of these genes (B):

(Larger Image)
Quote
(B) Proposed model for the emergence of MCH-derived sequence onto chromosome 5p. (a) An AROM mRNA initiating in the CS3-5 region and ending at poly A (b) polyadenylation site was retrotransposed onto the equivalent of chromosome 5p at the time of Catarrhini divergence 25 to 30 Ma. (b) After this first event or concurrent to it, an Alu sequence was inserted in intron A and a fragment corresponding to the 3' end of the retrotransposed mRNA (part of exon II-intron A-Alu) was broken and transposed to the downstream insertion site. This led to the PMCHL gene versions observed in Cercopithecoidea and Hominoidea.


theyeti



Date: 2002/12/12 17:23:25, Link
Author: theyeti
Annu Rev Plant Biol 2002;53:503-21

Complex evolution of photosynthesis.

Xiong J, Bauer CE.

Quote
The origin of photosynthesis is a fundamental biological question that has eluded researchers for decades. The complexity of the origin and evolution of photosynthesis is a result of multiple photosynthetic components having independent evolutionary pathways. Indeed, evolutionary scenarios have been established for only a few photosynthetic components. Phylogenetic analysis of Mg-tetrapyrrole biosynthesis genes indicates that most anoxygenic photosynthetic organisms are ancestral to oxygen-evolving cyanobacteria and that the purple bacterial lineage may contain the most ancestral form of this pigment biosynthesis pathway. The evolutionary path of type I and type II reaction center apoproteins is still unresolved owing to the fact that a unified evolutionary tree cannot be generated for these divergent reaction center subunits. However, evidence for a cytochrome b origin for the type II reaction center apoproteins is emerging. Based on the combined information for both photopigments and reaction centers, a unified theory for the evolution of reaction center holoproteins is provided. Further insight into the evolution of photosynthesis will have to rely on additional broader sampling of photosynthesis genes from divergent photosynthetic bacteria.


theyeti

Date: 2002/12/12 22:52:24, Link
Author: theyeti
Here is a good example of novel gene evolution due to duplication.

Nat Genet 2002 Apr;30(4):411-5

Adaptive evolution of a duplicated pancreatic ribonuclease gene in a leaf-eating monkey.

Zhang J, Zhang YP, Rosenberg HF.

Quote

Abstract:

One of the two ribonuclease genes in a leaf-eating monkey has adapted to a role in the digestion of bacterial RNA. Following duplication of the ancestral ribonuclease gene, adaptation occurred through a series of changes in the amino acid sequence of the protein it encodes. This example is a good illustration of how specialization of protein function after gene duplication can be as source of novel protein functions.


Quote

A subfamily of Old World monkeys, colobines are unique primates that use leaves rather than fruits and insects as their primary food source; these leaves are then fermented by symbiotic bacteria in the foregut13. Similar to ruminants, colobines recover nutrients by breaking and digesting the bacteria with various enzymes, including pancreatic ribonuclease (RNASE1), which is secreted from the pancreas and transported into the small intestine to degrade RNA.
[...]
...we detected one RNASE1 gene in each of the 15 non-colobine primates examined, including 5 hominoids, 5 Old World monkeys, 4 New World monkeys and 1 prosimian. We determined the DNA sequences of these RNASE1 genes; the deduced protein sequences are shown in Fig. 1a. The phylogenetic tree of the RNASE1 sequences (Fig. 2a) is consistent with the known species relationships16 at all nodes, with greater than 55% bootstrap support, suggesting that the RNASE1 genes are orthologous. By contrast, two RNASE1 genes were found in the Asian colobine, douc langur (Pygathrix nemaeus). Phylogenetic analysis (Fig. 2a) suggests that these two genes were generated by recent duplication postdating the separation of colobines from other Old World monkeys (cercopithecines). The branch lengths of the gene tree indicate that the nucleotide sequence of one daughter gene (RNASE1) has not changed since duplication, whereas that of the other gene (RNASE1B) has accumulated many substitutions.
[...]
Taken together, these analyses suggest that the synonymous and noncoding sites at the RNASE1B locus are not subject to selective constraints and that the accelerated evolution of the coding sequence of RNASE1B is due to positive Darwinian selection.
[...]
Earlier studies showed that, for most mammalian genes, the rate of radical substitution is lower than that of conservative substitution, owing to stronger purifying selection on radical substitution22. In RNASE1B, however, the opposite is found. The number of radical substitutions per site since duplication (0.067) is significantly greater than that (0.012) of conservative substitutions per site (P<0.02; Fisher's exact test). There are nine amino-acid substitutions in the mature peptide of RNASE1B, and seven of them involve charge changes. Unexpectedly, all seven charge-altering substitutions increase the negative charge of the protein.
[...]
The charge-altering substitutions reduced the net charge of RNASE1B from 8.8 to 0.8 (at pH 7) and the isoelectric point from 9.1 to 7.3 (Fig. 1a). Because RNA is negatively charged, the net charge of RNase influences its interaction with the substrate and its catalytic performance23. We therefore hypothesized that the charge-altering substitutions may have changed the optimal pH of RNASE1B in catalyzing the digestion of RNA.
[...]
We determined that the optimal pH for human RNASE1 is 7.4, a value that is within the pH range (7.4–8.0) measured in the small intestine of humans24, 25. The same optimal pH was observed for RNASE1 of rhesus monkey and douc langur (Fig. 4a). Probably because of foregut fermentation and related changes in digestive physiology, the pH in the small intestine of colobine monkeys shifts to 6–7 (ref. 13). Notably, the optimal pH for douc langur RNASE1B was found to be 6.3 (Fig. 4a). At pH 6.3, RNASE1B is about six times as active as RNASE1 in digesting RNA, and the difference in their activities is statistically significant (P<0.001, t-test). These results suggest that the rapid amino acid substitutions in RNASE1B were driven by selection for enhanced RNase activity at the relatively low pH environment of the colobine small intestine.


Long story short:  Monkey shifts diet from fruits and insects to leaves.  This causes foregut fermentation which lowers pH in the digestive tract.  A ribonuclease gene duplicates, and one of the duplicates evolves through positive selection for optimal activity at the lower pH.    

Another paper concerning this (shorter for those who don't want to plow through the one above) is here:

Hughes AL.  Adaptive evolution after gene duplication., Trends Genet 2002 Sep;18(9):433-4.

theyeti

Date: 2002/12/12 23:28:37, Link
Author: theyeti
Ah, another example of ribonuclease duplication.

Proc Natl Acad Sci U S A 1998 Mar 31;95(7):3708-13

Positive Darwinian selection after gene duplication in primate ribonuclease genes.

Zhang J, Rosenberg HF, Nei M.

Full Text

Quote

Abstract:

Evolutionary mechanisms of origins of new gene function have been a subject of long-standing debate. Here we report a convincing case in which positive Darwinian selection operated at the molecular level during the evolution of novel function by gene duplication. The genes for eosinophil cationic protein (ECP) and eosinophil-derived neurotoxin (EDN) in primates belong to the ribonuclease gene family, and the ECP gene, whose product has an anti-pathogen function not displayed by EDN, was generated by duplication of the EDN gene about 31 million years ago. Using inferred nucleotide sequences of ancestral organisms, we showed that the rate of nonsynonymous nucleotide substitution was significantly higher than that of synonymous substitution for the ECP gene. This strongly suggests that positive Darwinian selection operated in the early stage of evolution of the ECP gene. It was also found that the number of arginine residues increased substantially in a short period of evolutionary time after gene duplication, and these amino acid changes probably produced the novel anti-pathogen function of ECP.




theyeti

Date: 2002/12/13 11:13:00, Link
Author: theyeti
I normally avoid the ARN peanut gallery threads, but I came across this and just had to post it.

Someone claims, ARN also seems to be getting into censorship mode recently.

And then Jazzraptor replies:

Quote

I really resent this comment. You have political opponents of ID frequenting IDist discussion boards trying to shout down or spam any hint of discussion, and the ID boards are guilty of censorship? Critics typically outnumber IDist here 2 to 1 onthe threads. They often avoid engaging in discussion, but merely link to anti-ID sites! Why aren't you criticizing this bizarre phenomenon?

Here's an example. Some poor guy asks for data supporting ID. If someone doesn't have data supporting ID . . . they should have stayed off of the thread. Right? Is that what happened? No. Look at post 1:

quote:
------------------------------------------------------------------------
You may be out of luck here. There is no valid scientific data because ID does not do that kind of scientific research . . .
------------------------------------------------------------------------

Look at post 2:

quote:
------------------------------------------------------------------------
See www.talkdesign.org and www.talkreason.org for sites which contain a lot of material about the lack of substance to ID.
------------------------------------------------------------------------

Go down and look at XYC's posts on the thread for the very worst examples of this mindless, thoughtless form of anti-ID propaganda. I can't call it anything else. This thread marked a turning point for me, because I recognised that THIS indeed is a form of censorship.  NOT anything that I've done. Give me one example where I've engaged in censorship here at ARN. Pretty much anything goes idea-wise. Please do not confuse me disallowing a form of censorship with censorship itself.


So let's get this straight.  Expressing one's opinion about a controversial subject and providing links to further information is a form of censorship, but deleting people's posts simply because you don't like them isn't?!  And what is this "shut-down or spam any hint of discussion" nonsense?  Since when did the ID critics have a means to "shut down" anything?  Is he calling Ex-YECer's cross-posting of very lengthy posts spam?  (He quickly deletes or bitches about everything Ex-YECer posts, regardless of any potential infraction of the supposed rules.)  This is just too much.  Black is white.  Freedom is slavery.  Blech!

theyeti

Date: 2002/12/13 11:27:00, Link
Author: theyeti
Curr Opin Genet Dev 2002 Dec;12(6):711-8

Conflict begets complexity: the evolution of centromeres.

Malik HS, Henikoff S.

Quote

Abstract:

Centromeres mediate the faithful segregation of eukaryotic chromosomes. Yet they display a remarkable range in size and complexity across eukaryotes, from approximately 125 bp in budding yeast to megabases of repetitive satellites in human chromosomes. Mapping the fine-scale structure of complex centromeres has proven to be daunting, but recent studies have provided a first glimpse into this unexplored bastion of our genomes and the evolutionary pressures that shape it. Evolutionary studies of proteins that bind centromeric DNA suggest genetic conflict as the underlying basis of centromere complexity, drawing interesting parallels with the myriad selfish elements that employ centromeric activity for their own survival.


Quote
...
Despite these difficulties, recent studies have begun to provide `evolutionary snapshots' of the centromere. They suggest that different sequence variants jockey for evolutionary dominance, even as homogeneous arrays of satellite repeats are destroyed by the insertion of a variety of mobile elements. Parallel studies of centromere-binding proteins also suggest that competition may drive the sequence complexity at centromeres, and may be responsible for rapidly changing karyotypes throughout evolution.
...

Female meiotic success as a major evolutionary force

Another means to turn the tables on `centromere-drive' would be to alter the meiotic tetrad at female meiosis, in effect switching the preferred position in the tetrad to an unpreferred position. One case where centromeres exploit female meiosis is evident in the relative ability of Robertsonian fusions –– when acrocentrics (chromosomes in which the centromere is towards one end) fuse at their centromeres to form a metacentric (chromosomes in which the centromere is in the middle) –– to survive female meiosis relative to its two acrocentric ancestors. In humans and chicken, Robertsonian fusions do better than acrocentrics in female meiosis, whereas the reverse is true in mice [37 and 38]; there is no difference in male meiotic transmission. A survey of karyotype evolution in mammals reveals that genomes have a high proportion of all acrocentric (e.g. mouse) or all metacentric (e.g. human) karyotypes with a distinct paucity of `mixed' karyotypes. This suggests that the switch in female meiotic `preference' has occurred frequently in mammalian evolution and can quickly reshape karyotypes once it happens ( Fig. 4). No other selective force would be expected to make such a rapid impact on karyotype evolution [38].
...

Conclusions

In yeast that have symmetric meioses, centromere competition is not expected to occur at all; removal of this genetic conflict may have allowed the optimal co-evolution of centromeric histones and centromeres, along with the gradual simplification of the centromeric sequences themselves. Under this model, S. cerevisiae centromeres, which are believed to consist of one nucleosome each, represent the ultimate stage of centromere optimization, whereas other genomes, including our own, constantly struggle with the consequences of unfair advantages in female meiosis.

Update

In humans, the bias in favor of transmitting Robertsonian fusions in female meiosis has been documented [37 and 38], but Daniel et al. [48 and 49] also reiterate another dramatic effect of Robertsonians –– reduced male fertility. Among families with Robertsonian arrangements coming to prenatal diagnosis, there are 2.4 fold fewer male parent carriers compared to female parents. This is despite the fact that in their progeny there is an ~1:1 ratio of male:female transmission of Robertsonian rearrangements. This points to a significant decline in fertility in male carriers of Robertsonian fusions, compared to female carriers. This duality (i.e. increased chromosomal transmission in female meiosis offset by lowered male fertility) provides strong support for the centromere-drive model.



theyeti

Date: 2002/12/13 12:12:26, Link
Author: theyeti
Curr Issues Mol Biol 2002 Jul;4(3):65-76

Transposable elements and the evolution of eukaryotic complexity.

Bowen NJ, Jordan IK.

Quote
Eukaryotic transposable elements are ubiquitous and widespread mobile genetic entities. These elements often make up a substantial fraction of the host genomes in which they reside. For example, approximately 1/2 of the human genome was recently shown to consist of transposable element sequences. There is a growing body of evidence that demonstrates that transposable elements have been major players in genome evolution. A sample of this evidence is reviewed here with an emphasis on the role that transposable elements may have played in driving the evolution of eukaryotic complexity. A number of specific scenarios are presented that implicate transposable elements in the evolution of the complex molecular and cellular machinery that are characteristic of the eukaryotic domain of life.


Will want to get the full text and see some of these "specifc scenarios" for the evolution of "complex molecular and cellular machinery"...  

Let me know if you can get your hands on it Nic (or anyone).

theyeti

Date: 2002/12/18 17:03:28, Link
Author: theyeti
Quote
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.


I believe the technical term for this is "lie".  The vaugely worded sentence does not compel students to learn anything, especially no unspecified "evidence against evolution".  For them to try to spin this as requiring or even encouraging the teaching of ID is exceptionally mendacious.

The major tactic that West uses here is to speak in generalities while avoiding specifics whenever possible.  So we have statements like, "the underlying research is now questioned by many biologists."  How many is many?  Five?  There's precious little to debunk science-wise because West avoids making any positive statements that can be debunked.  This mysterious "evidence against evolution" is never brought out at all, except for a reference to the Cambrian Explosion, but even here he offers no details, and instead simply claims that it was "seemingly" too fast while omitting the actual time frame (several million years).  Peppered Moths and Haeckel's embryos cannot under any stretch of the imagination be construed as "evidence against evolution".  At most they should simply be omitted as evidence for evolution.  So we're not left with any indication as to what this "evidence against evolution" is at all.  (When this question was put to ARNies, there were no answers that could withstand simple criticism IIRC; given that IDists agree on precious little, including common descent, one is left wondering just what this vauge reference means.  Added in edit: here is the thread.)  What we are left with is spin, spin, spin.  For example this:

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


This guy must not get out much.  The efforts in Ohio and Georgia are simply two examples of anti-evolutionist activity that's been going on for decades now.  They are not "gaining ground", they're doing what they've always done.  Having been shot down by the courts simply means that they're changing tactics.

Quote
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.


DeHart was teaching creationism, plain and simple.  It wasn't until much later, with the goading of the Discovery Institute, that he brought in materials about the peppered moth etc.  The whole affair dragged on for several years, and eventually local parents had enough.  But the DI sent in Jonathan Wells and its other minions to support DeHart, who steadfastly refused to cater to any of the school board's wishes.  So locals get upset and the DI sends in its troops from out of town, and they bandy about accusations of "thought police".  What nerve.

Quote
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.


Ludicrous?  The stated goal of the C®SC is religious apologetics, and they actively court biblical literalists.  Talk about doublethink!  

Quote
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."


The statement that these people signed onto was carefully worded such that it's not controversial at all.  Nevertheless, most of the signatories were not biologists, and 150 is an insignificant number anyway.  There are tens of thousands of scientists who accept Darwinian evolution.  Nor is there any indication that their number is growing in any major way; all of these people were most likely evolution-doubters prior to the DI's propaganda efforts.  Same is true with the Ohio list.

There's really nothing new here.  Same old canards, same old arguments from authority, same old carefull avoidance of any straitforward scientific claims, same old demonization and hypocritical cries of persecution.

theyeti



Date: 2002/12/18 19:36:32, Link
Author: theyeti
Quote (niiicholas @ Dec. 18 2002,18:24)
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.

After having gone 'round and 'round with Mike about this issue several times, he finally let loose the notion that he's using "suspect" in a completely different way than I was.  As he was using it, he seemed to mean "suspect as a possibility" whereas I figured he meant, "suspect as being reasonably likely".  Given the first meaning, it's a somewhat trivial question.  I would simply say that I would suspect design as a possibility for the same reason that Paley did.  Living things and their parts are complex, and do serve functions (i.e. have teleos) like our designs.  So I accept ID as a possiblity, if a remote one.  Yet it's another story entirely whether or not ID is testable, and whether or not the available evidence supports it. What I do soundly reject is Paley's logic in concluding that this is a sufficient hallmark of design.  And then there's this guy named Darwin who showed that the Palian argument generates false positives.  

Suspecting that ID is true, on the other hand, carries with it a much higher burden of evidence, and it depends entirely on what theory of ID you're talking about, which itself will depend on some assumptions about the designer.  But mainstream IDists reject this entirely, instead claiming that "design" can be detected in the absence of any theory about who, how, when, where, etc., that would actually lead to specific predictions.  They claim that design can be detected because of the supposed impossibility of natural mechanisms.  But when someone answers Mike by saying that this would need to be demonstrated, he complains about it being an unfair demand!  Having been shown this point, Mike still advances the notion that no one's interested or capable of answering his question, even though he knows it's not true.  He simply maintains it as a rhetorical device.

theyeti (aka Grape Ape)

Date: 2002/12/18 20:41:39, Link
Author: theyeti
Here is a good timeline of the whole DeHart affair:

http://www.scienceormyth.org/discoveryinstitute.html

It's amazingly long and complex.  DeHart apparently taught creationism for many years before being asked to stop, and before being used as a pawn of the DI.

theyeti

Date: 2002/12/20 01:15:32, Link
Author: theyeti
I decided to start this thread to collect references about protein evolution specifically as it relates to folding.  First I'll repost an essay that I posted to the ISCID forum, skipping the irrelevant parts:

[...]

Now for some more general stuff about protein folding and evolution.  Josh gives us a very educational post about some of the complexities of protein folding and what it means to biology.  I'm going to skip most of the stuff about the dynamics of protein folding, because I think, at least as it relates to the suboptimality argument, I've addressed that above, and also because I don't have the necessary background in physics to know that much about it.  I think Josh can appreciate that, because he notes that there's tons of stuff that we don't know.  The literature on the dynamics of protein folding is very large, but it's also difficult to read (for me anyway).  But I have reviewed some of the literature at it pertains to the evolution of protein folds, and I'll present some of that.

First of all, it’s a misconception even among many biochemists that all proteins need to fold to be functional.  In fact, the importance of disordered proteins and those with long disordered regions is now becoming more clear.  Try searching the lit for “intrinsically disordered proteins” and you’ll come up with a number of hits.  These proteins (or certain domains) are unfolded and yet are perfectly functional, and in many cases are just as highly conserved as folded protein domains, though often of lower sequence complexity [1] (and hence, easier to evolve via random generation).  In fact, there is evidence that disordered proteins outnumber ordered proteins, but that the ordered ones represent more resolved structures in the PDB simply because (big shock) they’re easier to crystallize.  So one possible way for folded proteins to come about is by evolving from functional yet disordered proteins, and in this case there would never be a period of time when there was not a selectable function.  And of course it’s not like there are only two kinds of proteins, folded and unfolded.  There is also the intermediate molten globule state.  

However, most protein folds are thought to evolve from other folds.  This can be seen with the arrangement of protein folds into scale free networks.  Two recent papers on this are relevant.  The first one is Proc Natl Acad Sci U S A 2002 Oct 29;99(22):14132-6, Expanding protein universe and its origin from the biological Big Bang.  I posted a number of excerpts from this paper here, so I won’t bother reproducing them.  The point however is that the scale-free network in which protein folds fit is highly indicative of a duplication / divergence process from one or a few initial folds.  The second paper, which came out about the same time, is Nature 2002 Nov 14;420(6912):218-23, The structure of the protein universe and genome evolution.  Here’s the abstract:

Quote
Despite the practically unlimited number of possible protein sequences, the number of basic shapes in which proteins fold seems not only to be finite, but also to be relatively small, with probably no more than 10,000 folds in existence. Moreover, the distribution of proteins among these folds is highly non-homogeneous -- some folds and superfamilies are extremely abundant, but most are rare. Protein folds and families encoded in diverse genomes show similar size distributions with notable mathematical properties, which also extend to the number of connections between domains in multidomain proteins. All these distributions follow asymptotic power laws, such as have been identified in a wide variety of biological and physical systems, and which are typically associated with scale-free networks. These findings suggest that genome evolution is driven by extremely general mechanisms based on the preferential attachment principle.


So both of these papers support the idea that an evolutionary process not only can account for the emergence of protein folds, but that the distribution of folds is a predicted consequence of evolution.

Now finally, if you want a “beginning to end” account for protein evolution, there is this recent review article (and there are others out there):

FEBS Lett 2002 Sep 11;527(1-3):1-4, Molecular evolution from abiotic scratch.

I’ll see if I can reproduce what they’ve got listed as the five stages of protein evolution, though I’ll have to skip the discussion:

1. Homopeptides of Ala and Gly encoded by (GCC)-(GGC) duplexes.
2. Mixed peptides of two alphabet types.
3. Chains of optimal length close the ends by interactions between two amino acid residues.
4. The loops are joined in linear arrays and form folds (domains)
5. Modern, multidomain proteins are formed.

I don’t know if this model will last, or even if it can stand up to serious scrutiny right now, but it’s the kind of thing that needs to be explored in detail before we can really say anything about the likelihood of protein evolution de novo.  Keep in mind that this particular model is trying to account for the evolution of proteins from the origin of life, which is necessarily tricky because it’s difficult to learn about this just from looking at modern life.  However, once you have a functioning cell, I don’t see any problem with the ability of current theory to account for protein evolution.  

[This last reference is at the end here for no real good reason]

1. Proteins 2001 Jan 1;42(1):38-48, Sequence complexity of disordered protein.
Quote
Intrinsic disorder refers to segments or to whole proteins that fail to self-fold into fixed 3D structure, with such disorder sometimes existing in the native state. Here we report data on the relationships among intrinsic disorder, sequence complexity as measured by Shannon's entropy, and amino acid composition. Intrinsic disorder identified in protein crystal structures, and by nuclear magnetic resonance, circular dichroism, and prediction from amino acid sequence, all exhibit similar complexity distributions that are shifted to lower values compared to, but significantly overlapping with, the distribution for ordered proteins.

Date: 2002/12/21 20:24:42, Link
Author: theyeti
My suspicion is that a few IDists complained to the ARN management, however one does that, and they finally decided to take charge.  There had been at least a few IDists who objected to Langan's insulting behavior only to have his venom turned on them.  How ironic is it for an ISCID fellow to get banned from an ID board?  I guess the only question now is if ARN will return to a semi-interesting board.  Although I'd get a real kick out of hearing some details about the banning if anyone hears about them. ;)

theyeti

Date: 2002/12/30 14:51:11, Link
Author: theyeti
I thought we had a thread for the evolution of the genetic code, and some of the IDists claims about it.  I guess it got lost in the server crash.  Anyway, I thought I'd start this one up anew, and post a recent paper that's relevant to the origins of the genetic code.

Philos Trans R Soc Lond B Biol Sci 2002 Nov 29;357(1427):1625-42

No accident: genetic codes freeze in error-correcting patterns of the standard genetic code.

Ardell DH, Sella G.


Quote
The standard genetic code poses a challenge in understanding the evolution of information processing at a fundamental level of biological organization. Genetic codes are generally coadapted with, or 'frozen' by, the protein-coding genes that they translate, and so cannot easily change by natural selection. Yet the standard code has a significantly non-random pattern that corrects common errors in the transmission of information in protein-coding genes. Because of the freezing effect and for other reasons, this pattern has been proposed not to be due to selection but rather to be incidental to other evolutionary forces or even entirely accidental. We present results from a deterministic population genetic model of code-message coevolution. We explicitly represent the freezing effect of genes on genetic codes and the perturbative effect of changes in genetic codes on genes. We incorporate characteristic patterns of mutation and translational error, namely, transition bias and positional asymmetry, respectively. Repeated selection over small successive changes produces genetic codes that are substantially, but not optimally, error correcting. In particular, our model reproduces the error-correcting patterns of the standard genetic code. Aspects of our model and results may be applicable to the general problem of adaptation to error in other natural information-processing systems.


theyeti

Date: 2002/12/30 15:04:26, Link
Author: theyeti
Earlier paper by the same authors  (unfortunately, I don't have full text access to either of these):

J Mol Evol 2002 May;54(5):638-51

The impact of message mutation on the fitness of a genetic code.

Sella G, Ardell DH.


Quote

The Standard Genetic Code is organized such that similar codons encode similar amino acids. One explanation suggested that the Standard Code is the result of natural selection to reduce the fitness "load" that derives from the mutation and mistranslation of protein-coding genes. We review the arguments against the mutational load-minimizing hypothesis and argue that they need to be reassessed. We review recent analyses of the organization of the Standard Code and conclude that under cautious interpretation they support the mutational load-minimizing hypothesis. We then present a deterministic asexual model with which we study the mode of selection for load minimization. In this model, individual fitness is determined by a protein phenotype resulting from the translation of a mutable set of protein-coding genes. We show that an equilibrium fitness may be associated with a population with the same genetic code and that genetic codes that assign similar codons to similar amino acids have a higher fitness. We also show that the number of mutant codons in each individual at equilibrium, which determines the strength of selection for load minimization, reflects a long-term evolutionary balance between mutations in messages and selection on proteins, rather than the number of mutations that occur in a single generation, as has been assumed by previous authors. We thereby establish that selection for mutational load minimization acts at the level of an individual in a single generation. We conclude with comments on the shortcomings and advantages of load minimization over other hypotheses for the origin of the Standard Code.

Date: 2002/12/31 12:52:03, Link
Author: theyeti
Thanks!

Date: 2002/12/31 15:25:52, Link
Author: theyeti
Just came across this recent article.  I haven't read the full-text, but according to the abstract it gives an account of the evolution of vertebrate coagulation factors from those of the invertebrates.

Blood Cells Mol Dis 2002 Jul-Aug;29(1):57-68

 Comprehensive Analysis of Blood Coagulation Pathways in Teleostei: Evolution of Coagulation Factor Genes and Identification of Zebrafish Factor VIIi.

Hanumanthaiah R, Day K, Jagadeeswaran P.


Quote
It is not clear how the complex mammalian coagulation pathways evolved from an entirely dissimilar invertebrate coagulation cascade. Comprehensive analysis of pro-coagulant factors and their regulators is lacking in early vertebrates to discern the mechanism of evolution of these genes from the invertebrates. To elucidate the coagulation pathways found in early vertebrates, zebrafish cDNAs/gene orthologues for major coagulant, anticoagulant, and fibrinolytic proteins were identified and characterized by homology to mammalian sequences. We found that zebrafish carry all hemostatic genes present in mammals, providing evidence that the coagulation system of teleosts is nearly identical to mammals. Zebrafish factor VII and X genes were identified and analyzed to reveal a novel factor VII-like gene flanked by the factor VII and factor X genes. This gene encodes a protein homologous to factor VII, but lacks critical residues for factor VII activity. Expression of the factor VII-like protein (named factor VIIi) demonstrated that it functions as an inhibitor of blood coagulation in biochemical assays using zebrafish or human plasmas. Analysis of intergenic DNA between the zebrafish VII/VIIi/X gene cluster and a Drosophila trypsin gene cluster revealed significant homology, and based upon these data, we propose a model for a rapid evolution of coagulation factors from the invertebrates.


theyeti

Date: 2003/01/05 13:53:07, Link
Author: theyeti
John Calvert compares Darwinists to Nazis and Communists.

ID Net letter to Kansas BOE

Quote
What if our newspaper reporters were directed by their editors to write accounts of past events using the philosophical assumption that all democratic viewpoints are not valid? We have seen the results of this kind of censorship on open and objective reporting in all dictatorial regimes, such as the Third Reich in Germany and communist Russia under Stalin. I can remember when we had Radio Free Europe radio stations beaming all the news to Russians because their government censored any views that were inconsistent with the communist manifesto.

The precise same thing is happening in our country with regard to the issue of what causes life and its diversity. That is essentially a historical question. If the history is driven by a Naturalistic agenda that censors one of the two competing hypotheses we will be engaging in the same sort of propaganda that characterized Nazi Germany and Communist Russia.


theyeti

Date: 2003/01/07 11:16:25, Link
Author: theyeti
Dembski compares "Darwinism" to former Soviet Block:

Quote
With the Intelligent Design movement this dissent has now become focused, promising to overturn the cultural dominance of Darwinism much as the freedom movements in eastern Europe overturned the political dominance of Marxism at the end of the 1980s.


From The Intelligent Design Movement at ARN.

theyeti

Date: 2003/01/09 09:32:10, Link
Author: theyeti
Quote (JxD @ Jan. 06 2003,21:43)
Quote
What members of the DI post at ARN?
 I am positive Paul Nelson has been there from the start.  You can probably guess his pseudonym, though lately his contributions have also tapered off.  With less certainty, I believe Jay Richards and Michael Behe may also have posted.

As for ISCID fellows, I have seen posts from Walter Remine, Langans, and Ronald Hirsch.

Just out of curiosity, do you know this for a fact (Behe, Richards, and Nelson specifically) or is this at least partially a matter of speculation on your part?  If you do know for a fact, do you mind sharing how you came about this knowledge?  (I'm aware that Dembski, ReMine, Langan, and Hirsch have all used their real names there.)

theyeti

Date: 2003/01/17 13:56:38, Link
Author: theyeti
Trends Genet 2002 Sep;18(9):472-9

Genome trees and the tree of life.

Wolf YI, Rogozin IB, Grishin NV, Koonin EV.

Quote
Genome comparisons indicate that horizontal gene transfer and differential gene loss are major evolutionary phenomena that, at least in prokaryotes, involve a large fraction, if not the majority, of genes. The extent of these events casts doubt on the feasibility of constructing a 'Tree of Life', because the trees for different genes often tell different stories. However, alternative approaches to tree construction that attempt to determine tree topology on the basis of comparisons of complete gene sets seem to reveal a phylogenetic signal that supports the three-domain evolutionary scenario and suggests the possibility of delineation of previously undetected major clades of prokaryotes. If the validity of these whole-genome approaches to tree building is confirmed by analyses of numerous new genomes, which are currently being sequenced at an increasing rate, it would seem that the concept of a universal 'species' tree is still appropriate. However, this tree should be reinterpreted as a prevailing trend in the evolution of genome-scale gene sets rather than as a complete picture of evolution.


theyeti

Date: 2003/01/21 00:48:24, Link
Author: theyeti
Hi John!  Welcome to AE.  Do you have a link for the Touchtone Article by any chance?  It would be very informative and useful.  (Pearcy's statement about ID's "scientific research program" being well accepted is so hilarious that I have to see it in context. :D)

theyeti

P.S.  great website!

Date: 2003/01/21 20:04:28, Link
Author: theyeti
Quote
The second reason design is a winner is that it is a full-fledged scientific research program, not a narrowly conceived ideological position.


Ha Ha Ha!

This statement is preceded by several paragraphs in which Pearcy justifys the ID movement on nothing more than narrow ideological grounds.  Then she offers us this gem.  I sure would love to see ID's scientific research program, but even if there were such a thing, I doubt anyone could find it buried under the mountains of ideological polemics.

theyeti

Date: 2003/01/21 20:11:50, Link
Author: theyeti
Oh yeah, this has got to rank in the top 10 dumbest arguments ever put forth by an IDist:

Quote
A few years ago, Carl Sagan enchanted a huge television audience by presenting naturalism as an alternative religion in his PBS program Cosmos. The mere fact that he capitalized the word "Cosmos" (as religious believers capitalize"God") was a dead giveaway that he was gripped by a religious intensity.


Is she seriously suggesting that a televison show should have its name written in lower case?  

I guess the fact that "Friends" is capitalized should make us warry of its anti-God message?  Man, the whole line-up is one huge conspiracy against God!  Good grief, what is world comming to...

theyeti

Date: 2003/01/22 20:05:37, Link
Author: theyeti
No, there is no conceivable basis for this claim.  Wells has not done any research that is relevant to evolutionary biology, and in fact he's done hardly any research of any kind at all.  In ten years of post-graduate study, he managed to get all of two papers published, neither of which he was first author on.  This claim is therefore a falsehood, but whether it's purpertrated by him or others is hard to tell.  The fact that it appears on his Icons website is pretty damning, but then again the members of the ID movement have a habit of puffing each other up.

You can read a discussion of this particular issue and the related issue of Wells' honesty on this ARN thread.

theyeti

Date: 2003/02/04 00:30:37, Link
Author: theyeti
Quote (msparacio @ Feb. 03 2003,20:06)

Quote
The current role of peer-review in the sciences is a relatively recent phenomena  (post 1930s).


Yeah, and just look how non-productive post 1930's science has been.  ;)

Quote
One could argue the current role of peer-review is an outgrowth of the "scientist myth" where even hypotheses making is a calm, collected, methodological process void of any creativity or speculation.


One could make that claim, but it would fly in the face of the innumerable creative hypotheses (continental drift, transposable elements, and endosymbiosis, to name a few) that have been proposed and ultimately accepted via peer-reviewed literature.  

One could also ignore the bevy of pseudoscience that the 20th century's fascination with science fiction has engendered, and which the peer-review process, despite its imperfections, is particularly good at weeding out.  

I'm not saying that ID is necessarily pseudoscience (well to be honest, I think it is), but even stauch IDists will admit that for every good speculative hypothesis that should be looked at seriously, there are tons of bad ones that don't deserve the time of day.  That's the real point of peer-review, though you may disagree with how it's applied.  

theyeti

Date: 2003/02/05 15:35:00, Link
Author: theyeti
Reading a back issue of Science during lunch today, I read an interesting letter about the creation of functional protein modules via selfish DNA.  Here's the original paper to which the letter refers:

Science 2000 Oct 13;290(5490):347-50

Selfish DNA in protein-coding genes of Rickettsia.

Ogata H, Audic S, Barbe V, Artiguenave F, Fournier PE, Raoult D, Claverie JM.


abstract:
Quote
Rickettsia conorii, the aetiological agent of Mediterranean spotted fever, is an intracellular bacterium transmitted by ticks. Preliminary analyses of the nearly complete genome sequence of R. conorii have revealed 44 occurrences of a previously undescribed palindromic repeat (150 base pairs long) throughout the genome. Unexpectedly, this repeat was found inserted in-frame within 19 different R. conorii open reading frames likely to encode functional proteins. We found the same repeat in proteins of other Rickettsia species. The finding of a mobile element inserted in many unrelated genes suggests the potential role of selfish DNA in the creation of new protein sequences.
 

Here is the PubMed link to the letter by Donard S. Dwyer that was written in response:

Selfish DNA and the origin of genes.

Here are some excerpts from that letter:

Quote
The authors suggest that the amino acid segments in the DNA conform to a general motif -- an alpha helix flanked by turns or loops.  Finally, Ogata et al. propose that these Rickettsia palindromic elements (RPEs) represent an example of selfish DNA (DNA that has no apparent cellular function) participating directly in the creation of new protein sequences.
...
[skip a bunch of stuff where Dwyer says that his previous work corroborates that of Ogata et al.]
...

I also found that the duplication unit was encoded by a short inverted repeat segment of DNA that resembled transposable genetic elements (see the figure).  I termed these segments "trexons," for transposable exons.  The RPE's described by Ogata et al. appear to be very similar to trexons.  I proposed that the trexons arose from the initial building blocks of RNA and suggested that these segments represented "selfish DNA" acting at the level of the exon rather than the intron.
[...]


The reference for Dwyer's earlier work is   J Theor Biol 1998 Sep 7;194(1):11-27.

Ogata et al. reply to Dwyer's letter:

Quote
Structural and functional modularity of proteins is well established.  Occurrences of homologous domains in otherwise different proteins suggest the recurrent use orf modular units in evolution.  The combinatorial advantage of modular units to design diverse proteins is obvious, but the precise relation between evolutionarily successful modules and mobile sequence units is not yet clear.  The "trexon" hypothesis proposed by Dwyer and the palindromic element (RPE) that we discovered in several Rickettsia species provide an interesting alternative to the "exon shuffling theory," in which the mobile element precisely coincides with the limitsof existing coding exons, thus restricting the evolutionary game to some sort of "card shuffling."  The finding of the RPE's suggests a greater flexibility in the evolution of genes.

First, the insertions of RPEs realize a flow of genetic material across the boundary between noncoding and protein-coding sequences. [...]


theyeti

edited to add this recent paper by Ogata which addresses the same issue:

Trends Biochem Sci 2003 Feb;28(2):75-80.

The insertion of palindromic repeats in the evolution of proteins.

Claverie JM, Ogata H.

Quote
The current theory of protein evolution is that all contemporary proteins are derived from an ancestral subset. However, each new sequenced genome exhibits many genes with no detectable homologues in other species, leading to the paradoxical picture of a universal ancestor with more genes than any of its progeny. Standard explanations indicate that fast evolving genes might disappear into the 'twilight zone' of sequence similarity. Regardless of the size of the original ancestral subset, its origin and the potential mechanisms of its subsequent enlargement are rarely addressed. Sequencing of Rickettsia conorii genome recently led to the discovery of three families of repeat-mobile elements frequently inserted into the middle of protein coding genes. Although not yet identified in other species of bacteria, this discovery has provided the first clear evidence for the de novo creation of long protein segments (up to 50 amino acid residues) by repeat insertion. Based on previous results and theories on the coding potential of palindromic elements, we speculate that their insertion and mobility might have played a significant role in the early stages of protein evolution.




Date: 2003/02/18 16:37:17, Link
Author: theyeti
This is way cool:

J Mol Evol 2003 Feb;56(2):162-8

Can an arbitrary sequence evolve towards acquiring a biological function?

Hayashi Y, Sakata H, Makino Y, Urabe I, Yomo T.

Quote
To explore the possibility that an arbitrary sequence can evolve towards acquiring functional role when fused with other pre-existing protein modules, we replaced the D2 domain of the fd-tet phage genome with the soluble random polypeptide RP3-42. The replacement yielded an fd-RP defective phage that is six-order magnitude lower infectivity than the wild-type fd-tet phage. The evolvability of RP3-42 was investigated through iterative mutation and selection. Each generation consists of a maximum of ten arbitrarily chosen clones, whereby the clone with highest infectivity was selected to be the parent clone of the generation that followed. The experimental evolution attested that, from an initial single random sequence, there will be selectable variation in a property of interest and that the property in question was able to improve over several generations. fd-7, the clone with highest infectivity at the end of the experimental evolution, showed a 240-fold increase in infectivity as compared to its origin, fd-RP. Analysis by phage ELISA using anti-M13 antibody and anti-T7 antibody revealed that about 37-fold increase in the infectivity of fd-7 was attributed to the changes in the molecular property of the single polypeptide that replaced the D2 domain of the g3p protein. This study therefore exemplifies the process of a random polypeptide generating a functional role in rejuvenating the infectivity of a defective bacteriophage when fused to some preexisting protein modules, indicating that an arbitrary sequence can evolve toward acquiring a functional role. Overall, this study could herald the conception of new perspective regarding primordial polypeptides in the field of molecular evolution.


theyeti

Date: 2003/02/18 16:46:14, Link
Author: theyeti
And also from the lab of Dr. Yomo:

Protein Eng 2002 Jul;15(7):619-26.

Evolvability of random polypeptides through functional selection within a small library.

Yamauchi A, Nakashima T, Tokuriki N, Hosokawa M, Nogami H, Arioka S, Urabe I, Yomo T.

Quote
A directed evolution with phage-displayed random polypeptides of about 140 amino acid residues was followed until the sixth generation under a selection based on affinity to a transition state analog for an esterase reaction. The experimental design deliberately limits the observation to only 10 clones per generation. The first generation consists of three soluble random polypeptides and seven arbitrarily chosen clones from a previously constructed library. The clone showing the highest affinity in a generation was selected and subjected to random mutagenesis to generate variants for the next generation. Even within only 10 arbitrarily chosen polypeptides in each of the generations, there are enough variants in accord to capacity of binding affinity. In addition, the binding capacity of the selected polypeptides showed a gradual continuous increase over the generation. Furthermore, the purified selected random polypeptides exhibited a gradual but significant increase in esterase activity. The ease of the functional development within a small sequence variety implies that enzyme evolution is prompted even within a small population of random polypeptides.


Those wily Japanese.  Such willing partners in the Grand Evolutionist Conspiracy.  ;)

theyeti

Date: 2003/02/18 16:56:17, Link
Author: theyeti
Plant Physiol 2003 Feb;131(2):610-20.

Recently Duplicated Maize R2R3 Myb Genes Provide Evidence for Distinct Mechanisms of Evolutionary Divergence after Duplication.

Dias AP, Braun EL, McMullen MD, Grotewold E.

Quote
R2R3 Myb genes are widely distributed in the higher plants and comprise one of the largest known families of regulatory proteins. Here, we provide an evolutionary framework that helps explain the origin of the plant-specific R2R3 Myb genes from widely distributed R1R2R3 Myb genes, through a series of well-established steps. To understand the routes of sequence divergence that followed Myb gene duplication, we supplemented the information available on recently duplicated maize (Zea mays) R2R3 Myb genes (C1/Pl1 and P1/P2) by cloning and characterizing ZmMyb-IF35 and ZmMyb-IF25. These two genes correspond to the recently expanded P-to-A group of maize R2R3 Myb genes. Although the origins of C1/Pl1 and ZmMyb-IF35/ZmMyb-IF25 are associated with the segmental allotetraploid origin of the maize genome, other gene duplication events also shaped the P-to-A clade. Our analyses indicate that some recently duplicated Myb gene pairs display substantial differences in the numbers of synonymous substitutions that have accumulated in the conserved MYB domain and the divergent C-terminal regions. Thus, differences in the accumulation of substitutions during evolution can explain in part the rapid divergence of C-terminal regions for these proteins in some cases. Contrary to previous studies, we show that the divergent C termini of these R2R3 MYB proteins are subject to purifying selection. Our results provide an in-depth analysis of the sequence divergence for some recently duplicated R2R3 Myb genes, yielding important information on general patterns of evolution for this large family of plant regulatory genes.


theyeti

Date: 2003/03/16 12:57:10, Link
Author: theyeti
Proc Natl Acad Sci U S A 2003 Mar 4;100(5):2507-11

The Tre2 (USP6) oncogene is a hominoid-specific gene.

Paulding CA, Ruvolo M, Haber DA.


Quote
Gene duplication and domain accretion are thought to be the major mechanisms for the emergence of novel genes during evolution. Such events are thought to have occurred at early stages in the vertebrate lineage, but genomic sequencing has recently revealed extensive amplification events during the evolution of higher primates. We report here that the Tre2 (USP6) oncogene is derived from the chimeric fusion of two genes, USP32 (NY-REN-60), and TBC1D3. USP32 is an ancient, highly conserved gene, whereas TBC1D3 is derived from a recent segmental duplication, which is absent in most other mammals and shows rapid amplification and dispersal through the primate lineage. Remarkably, the chimeric gene Tre2 exists only in the hominoid lineage of primates. This hominoid-specific oncogene arose as recently as 21-33 million years ago, after proliferation of the TBC1D3 segmental duplication in the primate lineage. In contrast to the broad expression pattern of USP32 and TBC1D3, expression of Tre2 is testis-specific, a pattern proposed for novel genes implicated in the emergence of reproductive barriers. The sudden emergence of chimeric proteins, such as that encoded by Tre2, may have contributed to hominoid speciation.


Thumbs up to "MyKell" on IIDB for pointing this one out.

theyeti

Date: 2003/03/16 13:08:11, Link
Author: theyeti
This one just came out.  Sure to be useful for blood-clotters.

Thromb Haemost 2003 Mar;89(3):420-8

Molecular evolution of the vertebrate blood coagulation network.

Davidson CJ, Hirt RP, Lal K, Snell P, Elgar G, Tuddenham EG, McVey JH.


Quote
In mammalian blood coagulation 5 proteases, factor VII (FVII), factor IX (FIX), factor X (FX), protein C (PC) and prothrombin act with two cofactors factor V and factor VIII to control the generation of fibrin. Biochemical evidence and molecular cloning data have previously indicated that blood coagulation involving tissue factor, prothrombin and fibrinogen is present in all vertebrates. Using degenerate RT-PCR we have isolated and characterized novel cDNAs with sequence identity to the blood coagulation serine proteases and cofactors from chicken and the puffer fish (Fugu rubripes). Sequence alignments, phylogenetic and comparative sequence analysis all support the existence of the Gla-EGF1-EGF2-SP domain serine proteases FVII, FIX, FX, PC and the A1-A2-B-A3-C1-C2 domain protein cofactors FV and FVIII in these species. These results strongly suggest that the blood coagulation network is present in all jawed vertebrates and evolved before the divergence of tetrapods and teleosts over 430 million years ago; and that vertebrate blood coagulation may have benefited from two rounds of gene or whole genome duplication. Sequences identified in Fugu coding for additional FVII-like, FIX-like and PC-like sequences support the possibility of further tandem and large-scale duplications in teleosts. Comparative sequence analyses of amino acid residues in the active site region suggest these additional sequences have evolved new and as yet unknown functions.


theyeti

Date: 2003/04/01 15:36:02, Link
Author: theyeti
I ran accross this interesting one the other day:

Proc Natl Acad Sci U S A 2003 Mar 18;100(6):3328-32

Relaxed selective pressure on an essential component of pheromone transduction in primate evolution.

Liman ER, Innan H.

Quote
The vomeronasal organ (VNO) detects pheromones in many vertebrate species but is likely to be vestigial in humans. TRPC2(TRP2), a gene that is essential for VNO function in the mouse, is a pseudogene in humans. Because TRPC2 is expressed only in the VNO, the loss of selective pressure on this gene can serve as a molecular marker for the time at which the VNO became vestigial. By analyzing sequence data from the TRPC2 gene of 15 extant primate species, we provide evidence that the VNO was most likely functional in the common ancestor of New World monkeys and Old World monkeys and apes, but then became vestigial in the common ancestor of Old World monkeys and apes. We propose that, at this point in evolution, other modalities, notably the development of color vision, may have largely replaced signaling by pheromones.


So we have an organ, the VNO, which appears to require a gene that has been rendered a pseudogene.

theyeti

Date: 2003/04/09 08:39:38, Link
Author: theyeti
Quote
I have spent quite a few words trying to show that the ID movement is both larger than its well-publicized and strongly criticized attempts to question Darwinism and also that it is justified in publicly and strongly criticizing Darwinism. I believe that this analysis allows us to see the merit of the work done so far by ID proponents Michael Behe and William Dembski.


Greater and greater numbers of scientists are joining the ID movement, which is why we keep referring to the same three (or two) year after year.

It appears that the ID movement is little more than a mutual admiration society.

theyeti

Date: 2003/04/10 13:07:15, Link
Author: theyeti
This is interesting.

Genomics 2003 Apr;81(4):391-9

BAGE genes generated by juxtacentromeric reshuffling in the hominidae lineage are under selective pressure.

Ruault M, Ventura M, Galtier N, Brun ME, Archidiacono N, Roizes G G, De Sario A.

Quote
In this paper, we show that the BAGE (B melanoma antigen) gene family was generated by chromosome rearrangements that occurred during the evolution of hominoids. An 84-kb DNA fragment derived from the phylogenetic 7q36 region was duplicated in the juxtacentromeric region of either chromosome 13 or chromosome 21. The duplicated region contained a fragment of the MLL3 gene, which, after juxtacentromeric reshuffling, generated the ancestral BAGE gene. Then, this ancestral gene gave rise to several independent genes through successive rounds of inter- and intrachromosome duplications. Comparison of synonymous and nonsynonymous mutations in putative coding regions shows that BAGE genes, but not the BAGE gene fragments, are under selective pressure. Our data strongly suggest that BAGE proteins have a function and that juxtacentromeric regions, whose plasticity is now largely proved, are not a simple junkyard of gene fragments, but may be the birth site of novel genes.


theyeti

Date: 2003/06/05 10:47:33, Link
Author: theyeti
Here's a recent article about Chl binding proteins.

FEMS Microbiol Lett 2003 May 16;222(1):59-68

Origin and evolution of transmembrane Chl-binding proteins: hydrophobic cluster analysis suggests a common one-helix ancestor for prokaryotic (Pcb) and eukaryotic (LHC) antenna protein superfamilies.

Garczarek L, Poupon A, Partensky F.

Quote
All chlorophyll (Chl)-binding proteins constituting the photosynthetic apparatus of both prokaryotes and eukaryotes possess hydrophobic domains, corresponding to membrane-spanning alpha-helices (MSHs). Hydrophobic cluster analysis of representative members of the different Chl protein superfamilies revealed that all Chl proteins except the five-helix reaction center II proteins and the small subunits of photosystem I possess related domains. As a major conclusion, we found that the eukaryotic antennae likely share a common precursor with the prokaryotic Chl a/b antennae from Chl-b-containing oxyphotobacteria. From these data, we propose a global scheme for the evolution of these proteins from a one-MSH ancestor.


This is interesting because I remember an IDist (math professor at University of South Carolina, can't remember his name) mentioning these antennae as something whose evolution was "implausible".

theyeti

Date: 2003/06/11 14:50:48, Link
Author: theyeti
Quote (niiicholas @ June 11 2003,03:31)
...particularly the response from Nilsson himself, and then see how many of his/Berlinski's claims are left standing.

Sorry, I don't have anything useful to add, but I didn't realize that Nilsson had replied to Berlinski.  This is priceless:

Quote
Contrary to Berlinski's claim, we calculate the spatial resolution (visual acuity) for all parts of our eye evolution sequence. The functions in Figure 1 display the results. These plots are computer generated, using small increments. Values and units are given on the axes of the plots, and procedures are explained in the legend. The underlying theory is explained in the main text, including the important Equation 1 and a reference to Warrant and McIntyre (1993) where this theory is derived. Yet, Berlinski insists that "Nilsson and Pelger do not calculate the visual acuity of any structure". It would be much simpler for Berlinski if he went just a tiny step further and denied the existence of our paper altogether.


theyeti

Date: 2003/06/17 14:41:36, Link
Author: theyeti
Retrotransposable, non-coding Alu elements being turned into protein coding exons.  Pretty cool.  

Science. 2003 May 23;300(5623):1288-91.

The birth of an alternatively spliced exon: 3' splice-site selection in Alu exons.

Lev-Maor G, Sorek R, Shomron N, Ast G.

Quote
Alu repetitive elements can be inserted into mature messenger RNAs via a splicing-mediated process termed exonization. To understand the molecular basis and the regulation of the process of turning intronic Alus into new exons, we compiled and analyzed a data set of human exonized Alus. We revealed a mechanism that governs 3' splice-site selection in these exons during alternative splicing. On the basis of these findings, we identified mutations that activated the exonization of a silent intronic Alu.


About 5% of alternatively spliced internal exons lead with an Alu sequence, which makes this a fairly common method of creating new "information".  

Here's a excerpt from the commentary that appears in the issue:

Quote
It appears that in addition to the distance between two AG dinucleotides, a nucleotide immediatesly upstream of proximal AG is also important.  Hence, a proximal GAG sequence serves as a signal weak enough to create an alternatively spliced Alu exon.  Any mutation of a proximal GAG in the first position results in a constitutive Alu exon.  This is an important observation, because most of the more than 1 million Alu elements in the human genome contain such a potential 3' splice site.  Of these, 238,000 are located within introns of protein-coding genes, and each one can become an exon.  Unfortunately, most mutations will lead to abnormal proteins and are likely to result in disease.  Yet a a small number may create an evolutionary novelty, and nature's "alternative splicing approach" guarantees that such a novelty may be tested while the original protein stays intact.

Another way to exploit an evolutionary novelty without disturbing the function of the original protein is gene duplication (see the figure.)  Gene duplication is one of the major ways in which organisms can generate new genes.  After a gene duplicates, one copy maintains its original function while the other is free to evolve and can be used for "nature's experiments."  Usually, this is accomplished through point mutations and the whole process is very slow.  However, recycling some modules that already exist in a genome (for example, in transposons) can speed up the natural mutagenesis process tremendously.  Several years ago, Iwashita and colleagues discovered a bovine gene containing a piece of a transposable element (called a TE-cassette) in the middle of its open reading-frame.  This cassette contributes a whole new domain to the bovine BCNT protein, namely an endonuclease domain native to the ruminant retrotransposable element-1 (RTE-1).

[Skip stuff about how BCNT is the result of a gene duplication.]

The reports by Lev-Maor et al. and Iwashita and collegues describe different ways in which genes can be rapidly rearranged and acquire evolutionary novelty through the use of so-called junk DNA. These discoveries wouldn't be so exciting if they didn't show how genomes achieve this wihtout disturbing an original protein.  To quote an old Polish proverb: "A wolf is sated and a lamb survived."


The Iwashita paper is still in press, to be published in Molecular Biology and Evolution.  Will be posted here when it's available on PubMed.  :D  

theyeti



Date: 2003/06/18 09:43:04, Link
Author: theyeti
Russel Doolittle has a new article out in PNAS.  Unfortunately, it's not available online yet.  But it's on PubMed.

Proc Natl Acad Sci U S A. 2003 Jun 13 [Epub ahead of print].

The evolution of vertebrate blood coagulation as viewed from a comparison of puffer fish and sea squirt genomes.

Jiang Y, Doolittle RF.

Quote
The blood coagulation scheme for the puffer fish, Fugu rubripes, has been reconstructed on the basis of orthologs of genes for mammalian blood clotting factors being present in its genome. As expected, clotting follows the same fundamental pattern as has been observed in other vertebrates, even though genes for some clotting factors found in mammals are absent and some others are present in more than one gene copy. All told, 26 different proteins involved in clotting or fibrinolysis were searched against the puffer fish genome. Of these, orthologs were found for 21. Genes for the "contact system" factors (factor XI, factor XII, and prekallikrein) could not be identified. On the other hand, two genes were found for factor IX and four for factor VII. It was evident that not all four factor VII genes are functional, essential active-site residues having been replaced in two of them. A search of the genome of a urochordate, the sea squirt, Ciona intestinalis, did not turn up any genuine orthologs for these 26 factors, although paralogs and/or constituent domains were evident for virtually all of them.


theyeti

Date: 2003/07/24 19:28:43, Link
Author: theyeti
Quote (niiicholas @ May 30 2002,00:02)
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:

A new paper is out about Sdic, giving more detail about its origins and some insight about the evolution of novel genes in general:

Genetica. 2003 Jul;118(2-3):233-44.

Origin and evolution of a new gene expressed in the Drosophila sperm axoneme.

Ranz JM, Ponce AR, Hartl DL, Nurminsky D.

Quote
Sdic is a new gene that evolved recently in the lineage of Drosophila melanogaster. It was formed from a duplication and fusion of the gene AnnX, which encodes annexin X, and Cdic, which encodes the intermediate polypeptide chain of the cytoplasmic dynein. The fusion joins AnnX exon 4 with Cdic intron 3, which brings together three putative promoter elements for testes-specific expression of Sdic: the distal conserved element (DCE) and testes-specific element (TSE) are derived from AnnX, and the proximal conserved element (PCE) from Cdic intron 3. Sdic transcription initiates within the PCE, and translation is initiated within the sequence derived from Cdic intron 3, continuing through a 10 base pair insertion that creates a new splice donor site that enables the new coding sequence derived from intron 3 to be joined with the coding sequence of Cdic exon 4. A novel protein is created lacking 100 residues at the amino end that contain sequence motifs essential for the function of cytoplasmic dynein intermediate chains. Instead, the amino end is a hydrophobic region of 16 residues that resembles the amino end of axonemal dynein intermediate chains from other organisms. The downstream portion of Sdic features large deletions eliminating Cdic exons v2 and v3, as well as multiple frameshift deletions or insertions. The new protein becomes incorporated into the tail of the mature sperm and may function as an axonemal dynein intermediate chain. The new Sdic gene is present in about 10 tandem repeats between the wildtype Cdic and AnnX genes located near the base of the X chromosome. The implications of these findings are discussed relative to the origin of new gene functions and the process of speciation.


theyeti

Date: 2003/07/27 15:34:29, Link
Author: theyeti
In the same issue of Genetica as the above article, there are two more articles relevant here:

Genetica. 2003 Jul;118(2-3):171-82.

Origin of new genes: evidence from experimental and computational analyses.

Long M, Deutsch M, Wang W, Betran E, Brunet FG, Zhang J.
Department of Ecology and Evolution, The University of Chicago,

Quote

Exon shuffling is an essential molecular mechanism for the formation of new genes. Many cases of exon shuffling have been reported in vertebrate genes. These discoveries revealed the importance of exon shuffling in the origin of new genes. However, only a few cases of exon shuffling were reported from plants and invertebrates, which gave rise to the assertion that the intron-mediated recombination mechanism originated very recently. We focused on the origin of new genes by exon shuffling and retroposition. We will first summarize our experimental work, which revealed four new genes in Drosophila, plants, and humans. These genes are 10(6) to 10(8) million years old. The recency of these genes allows us to directly examine the origin and evolution of genes in detail. These observations show firstly the importance of exon shuffling and retroposition in the rapid creation of new gene structures. They also show that the resultant chimerical structures appearing as mosaic proteins or as retroposed coding structures with novel regulatory systems, often confer novel functions. Furthermore, these newly created genes appear to have been governed by positive Darwinian selection throughout their history, with rapid changes of amino acid sequence and gene structure in very short periods of evolution. We further analyzed the distribution of intron phases in three non-vertebrate species, Drosophila melanogaster, Caenorhabditis elegans, and Arabidosis thaliana, as inferred from their genome sequences. As in the case of vertebrate genes, we found that intron phases in these species are unevenly distributed with an excess of phase zero introns and a significant excess of symmetric exons. Both findings are consistent with the requirements for the molecular process of exon shuffling. Thus, these non-vertebrate genomes may have also been strongly impacted by exon shuffling in general.


And..

Genetica. 2003 Jul;118(2-3):193-208.

Birth of 'human-specific' genes during primate evolution.
Nahon JL.


Quote
Humans and other Anthropoids share very similar chromosome structure and genomic sequence as seen in the 98.5% homology at the DNA level between us and Great Apes. However, anatomical and behavioral traits distinguish Homo sapiens from his closest relatives. I review here several recent studies that address the issue by using different approaches: large-scale sequence comparison (first release) between human and chimpanzee, characterization of recent segmental duplications in the human genome and analysis of exemplary gene families. As a major breakthrough in the field, the heretical concept of 'human-specific' genes has recently received some supporting data. In addition, specific chromosomal regions have been mapped that display all the features of 'gene nurseries' and could have played a major role in gene innovation and speciation during primate evolution. A model is proposed that integrates all known molecular mechanisms that can create new genes in the human lineage.


That would be a good issue to get ahold of.

theyeti

Date: 2003/08/01 18:14:30, Link
Author: theyeti
Nucleic Acids Res. 2003 Aug 1;31(15):4401-9.

Structural diversification and neo-functionalization during floral MADS-box gene evolution by C-terminal frameshift mutations.

Vandenbussche M, Theissen G, Van de Peer Y, Gerats T.

Quote
Frameshift mutations generally result in loss-of-function changes since they drastically alter the protein sequence downstream of the frameshift site, besides creating premature stop codons. Here we present data suggesting that frameshift mutations in the C-terminal domain of specific ancestral MADS-box genes may have contributed to the structural and functional divergence of the MADS-box gene family. We have identified putative frameshift mutations in the conserved C-terminal motifs of the B-function DEF/AP3 subfamily, the A-function SQUA/AP1 subfamily and the E-function AGL2 subfamily, which are all involved in the specification of organ identity during flower development. The newly evolved C-terminal motifs are highly conserved, suggesting a de novo generation of functionality. Interestingly, since the new C-terminal motifs in the A- and B-function subfamilies are only found in higher eudicotyledonous flowering plants, the emergence of these two C-terminal changes coincides with the origin of a highly standardized floral structure. We speculate that the frameshift mutations described here are examples of co-evolution of the different components of a single transcription factor complex. 3' terminal frameshift mutations might provide an important but so far unrecognized mechanism to generate novel functional C-terminal motifs instrumental to the functional diversification of transcription factor families.


From the discussion:

Quote
Based on these observations and the results presented here, we propose a model for the functional diversification of duplicated members of transcription factor families (Fig. 5). After duplication of an ancestral gene X, one of the copies (Y) may accumulate mutations in the C-terminus, while retaining features such as DNA binding, essential for its function as a transcription factor, in the upstream coding regions. Apart from in frame insertions/deletions and single nucleotide substitutions, mutations in the coding sequence at the 3' end will also induce frameshifts, as such masking the ancestral origin of the motif at the protein level. While most frameshift mutations will be deleterious for the existing function, in specific cases they may yield novel functional C-terminal motifs. The three cases we have described are perfect examples of such a neo-functionalization process. This widens the emerging view that plant transcription factors evolve mainly by changes in cis-regulatory elements that affect their expression pattern (37,38), and that after gene duplication, mainly degeneration and selection of complementary functioning, i.e. sub-functionalization occurs (39,40). At first sight, it may seem extraordinary that in all three cases, frameshift mutations of highly conserved motifs yielded novel highly conserved motifs. However, this specific situation is the only type of motif generation that can still be recognized after millions of years of independent evolution of both copies. If the new motif had been recruited from a sequence in a non-conserved (Y3 and Y4, Fig. 5) or less conserved region of the C-terminus (e.g. Y2), it would be impossible to trace back the ancestral motif. Equally important, either the new or the ancestral motif must contain amino acid residues that are not too highly degenerate in order to be able to recognize the related motif after frameshifting. Thus, the only cases of frameshift mutations that we still can recognize are those in highly conserved motifs that yield novel highly conserved motifs. Finally, novel motifs may be acquired in an additive way downstream of existing motifs as an extra feature, with retention of the ancestral motif that in such a case becomes internal (e.g. Y3); or with subsequent loss of the ancestral motif (all other cases).


'Da model:


Quote
Figure 5. Model for the generation of novel C-terminal motifs within the MADS-box gene family. After duplication of an ancestral gene X, the Y copy accumulates mutations in the C-terminal domain, while retaining the essential MIK domain. Insertions or deletions will cause a frameshift in the coding sequence. Rarely, these frameshift mutations may yield novel functional motifs that consequently will be conserved. In cases where the novel motif is recruited from poorly conserved regions (e.g. Y 2–4) in the ancestral sequence, the sequence relation with the ancestral gene X will become unclear after a period of independent evolution. In the Y copy, new motifs may be added downstream of the ancestral motif as an extra feature, with retention of the ancestral motif which in this case becomes internal (e.g. Y3); or with subsequent loss of the ancestral motif (all other cases).


...other good stuff in the paper too long to reproduce here.

theyeti

Date: 2003/08/26 18:18:46, Link
Author: theyeti
Evidence of more retrogenes in the human genome.    

Nucleic Acids Res. 2003 Aug 1;31(15):4385-90.

The human genome contains many types of chimeric retrogenes generated through in vivo RNA recombination.

Buzdin A, Gogvadze E, Kovalskaya E, Volchkov P, Ustyugova S, Illarionova A, Fushan A, Vinogradova T, Sverdlov E.

Quote
L1 retrotransposons play an important role in mammalian genome shaping. In particular, they can transduce their 3'-flanking regions to new genomic loci or produce pseudogenes or retrotranscripts through reverse transcription of different kinds of cellular RNAs. Recently, we found in the human genome an unusual family of chimeric retrotranscripts composed of full-sized copies of U6 small nuclear RNAs fused at their 3' termini with 5'-truncated, 3'-poly(A)-tailed L1s. The chimeras were flanked by 11-21 bp long direct repeats, and contained near their 5' ends T2A4 hexanucleotide motifs, preferably recognized by L1 nicking endonuclease. These features suggest that the chimeras were formed using the L1 integration machinery. Here we report the identification of 81 chimeras consisting of fused DNA copies of different RNAs, including mRNAs of known human genes. Based on their structural features, the chimeras were subdivided into nine distinct families. 5' Parts of the chimeras usually originated from different nuclear RNAs, whereas their 3' parts represented cytoplasmic RNAs: mRNAs, including L1 mRNA and Alu RNA. Some of these chimeric retrotranscripts are expressed in a variety of human tissues. These findings suggest that RNA-RNA recombination during L1 reverse transcription followed by the integration of the recombinants into the host genome is a general event in genome evolution.


To remind everyone, retrogenes are created as follows:

1.  mRNA from existing gene --> reverse transcription into cDNA.

This is carried out by an endogenous reverse transcriptase, which may come from endogenous retroviruses, Alu elements, etc.

2.  cDNA is integrated into genome.

This is also carried out by endogenous integration proteins.  Again, these can also come from endogenous retroviruses, etc.

The result is a gene duplicate that usually has the following attributes:

A.  No introns.
B.  Trucated at the 5' end.
C.  The remnants of a poly-A tail at the 3' end.
D.  Flanking repeats.

These attributes make identifying retrogenes relatively easy, and they provide extremely strong evidence that these genes did indeed arise through retrotransposition.  Given that they contain a truncation, and are integrated without regulatory sequences, the most common fate for a retroelement of this kind is to be non-functional.  However, examples of functional retrogenes exist.  

The chimeras observed in the present study are formed when an RNA-RNA hybrid, consisting of two unrelated RNA transcripts, is acted upon by a reverse transcriptase.  Here is the proposed mechanism:

Quote
Figure 4. A probable mechanism for the chimeras’ formation. (Step 1) An L1 pre-integration complex binds L1, Alu or the host mRNA in the cytoplasm. (Step 2) The ribonucleoprotein formed is transferred to the nucleus. (Step 3) Reverse transcription of the bound mRNA primed by a genomic DNA single-stranded break within the TTTTAA sequence. (Step 4) Another (nuclear) RNA binds to the L1 reverse transcription/integration complex. (Step 5) Switch of templates for the reverse transcription. (Step 6) The DNA reparation mediated formation of a new chimeric retrogene insertion flanked by short direct repeats and carrying a poly(A) sequence at the 3' terminus.


The authors found that at least 6 of the chimeric retrogenes that they found (out of 81) are being expressed in human tissues, indicating that they likely have a function.  Whether or not the rest have a function isn't known, but the authors only directly tested (via RT-PCR analysis) 6 of the sequences and found that 4 were unexpressed.  So these identified retroelements probably contain a mixture of functional and non-functional sequences.

Moreover, the presence of these chimeric retrogenes also provides evidence for common descent, since they have integrated at various times during primate evolution, and yet they follow the standard phylogeny:

Quote
Figure 3. Results of the 12 chimeric retrogenes insertional polymorphism study. The chimeras’ integration times were estimated according to the presence/ absence of the inserts in genomic DNAs of different primate species.


One of the retrogenes is polymorphic within the human population, indicating that it arose since the last common ancestor of all humans.

This is very strong evidence for common descent, along the lines of shared errors in pseudogenes.  

theyeti



Date: 2003/09/01 15:36:55, Link
Author: theyeti
Quote (theyeti @ June 17 2003,14:41)
The Iwashita paper is still in press, to be published in Molecular Biology and Evolution.  Will be posted here when it's available on PubMed.  :D  

Well, it's available:

Mol Biol Evol. 2003 Sep;20(9):1556-63.

A Transposable Element-Mediated Gene Divergence that Directly Produces a Novel Type Bovine Bcnt Protein Including the Endonuclease Domain of RTE-1.

Iwashita S, Osada N, Itoh T, Sezaki M, Oshima K, Hashimoto E, Kitagawa-Arita Y, Takahashi I, Masui T, Hashimoto K, Makalowski W.

Quote
Ruminant Bcnt protein with a molecular mass of 97 kDa (designated p97Bcnt) includes a region derived from the endonuclease domain of a retrotransposable element RTE-1. Human and mouse Bcnt proteins lack the corresponding region but have a highly conserved 82-amino acid region at the C-terminus that is not present in p97Bcnt. By screening a bovine BAC library, we found two more bcnt-related genes: human-type bcnt (h-type bcnt) and its processed pseudogene. Whereas the pseudogene is localized on chromosome 26, both bcntp97 and the h-type bcnt genes are found on bovine chromosome 18, a synteny region of human chromosome 16 on which human BCNT is localized. Complete nucleotide sequencing of the BAC clone reveals that the bcntp97 and h-type bcnt genes are located just 6 kb apart in a tandem manner. The two h-type bcnt and bcntp97genes are active at both the transcriptional level and the protein level. H-type bovine Bcnt is more like human BCNT than p97Bcnt, when compared at their N-terminal regions. However, phylogenetic analysis using the N-terminal region of the bcnt gene family revealed that the duplication of bovine genes occurred within the bovine lineage with significantly accelerated substitution in bcntp97. This acceleration was not ascribed definitely to positive selection. After duplication, one of the bovine bcnt genes recruited the endonuclease domain of an intronic RTE-1 repeat accompanied by the accelerated substitution at the 5'-ORF, resulting in creation of a novel type of Bcnt protein in bovine.


theyeti

edit:  Here's an earlier paper on this protein:

Gene. 2001 May 2;268(1-2):59-66.

Gene organization of bovine BCNT that contains a portion corresponding to an endonuclease domain derived from an RTE-1 (Bov-B LINE), non-LTR retrotransposable element: duplication of an intramolecular repeat unit downstream of the truncated RTE-1.



Date: 2003/09/04 14:10:50, Link
Author: theyeti
I don't think this one's been posted yet.  

Gene. 2002 May 1;289(1-2):1-6.

SCAN domain-containing 2 gene (SCAND2) is a novel nuclear protein derived from the zinc finger family by exon shuffling.

Dupuy D, Duperat VG, Arveiler B.

Quote
The SCAN domain is a recently recognized protein domain that characterizes a subfamily of the Kruppel-like zinc finger proteins. We have previously described a novel SCAN domain-containing 2 gene (SCAND2) that does not belong to the zinc finger family. We report structural and sequence analyzes of all known members of the SCAN family and use these data to illustrate a model of gene family evolution. Most of the SCAN containing genes share common gene organization features that support the proposed origin for SCAND2 by disruption of an ancestral SCAN-zinc finger gene by a retroposition event and subsequent exon shuffling.


Here's their model:

[oops, can't post it]

Quote
Fig. 2. Proposed model for SCAND2 gene origin. (A) Insertion of a C1orf12 cDNA in the first intron of a SCAN-containing ancestor gene located in 15q25 allowed a shadow exon from C1orf12 to be spliced downstream of a SCAN encoding exon, thus producing a new protein product. White boxes: exons from C1orf12; Hatched boxes: exons from the ancestral SCAN gene; dotted box: shadow exon from C1orf12. (B) Alignment between C1orf12 and SCAND2 cDNAs. The inserted retroposon contains a consensus acceptor splice site located upstream of the C1orf12 original translation start site. Asterisks indicate differences between the nucleotide sequences.


theyeti

Date: 2003/09/29 15:16:17, Link
Author: theyeti
Interesting recent article:

Proc Natl Acad Sci U S A. 2003 Sep 17

A noncognate aminoacyl-tRNA synthetase that may resolve a missing link in protein evolution.

Skouloubris S, Ribas De Pouplana L, De Reuse H, Hendrickson TL.

Quote
Efforts to delineate the advent of many enzymes essential to protein translation are often limited by the fact that the modern genetic code evolved before divergence of the tree of life. Glutaminyl-tRNA synthetase (GlnRS) is one noteworthy exception to the universality of the translation apparatus. In eukaryotes and some bacteria, this enzyme is essential for the biosynthesis of Gln-tRNA(Gln), an obligate intermediate in translation. GlnRS is absent, however, in archaea, and most bacteria, organelles, and chloroplasts. Phylogenetic analyses predict that GlnRS arose from glutamyl-tRNA synthetase (GluRS), via gene duplication with subsequent evolution of specificity. A pertinent question to ask is whether, in the advent of GlnRS, a transient GluRS-like intermediate could have been retained in an extant organism. Here, we report the discovery of an essential GluRS-like enzyme (GluRS2), which coexists with another GluRS (GluRS1) in Helicobacter pylori. We show that GluRS2's primary role is to generate Glu-tRNA(Gln), not Glu-tRNA(Glu). Thus, GluRS2 appears to be a transient GluRS-like ancestor of GlnRS and can be defined as a GluGlnRS.


theyeti

Date: 2003/10/01 18:20:33, Link
Author: theyeti
Dembski compares treatment of ID to trial and death of Socrates

ID Will Win in the End

Quote
When the Athenian court convicted Socrates for subverting the youth of Athens, he was given the option of proposing an appropriate punishment for his misdeeds.

Since Socrates was convinced, not merely of his innocence, but also of his good worth, he proposed that Athens “punish” him by honoring him as a city benefactor.

This proposed punishment did not set well with the Athenian court. Had Socrates proposed exile, he probably would have lived. As it was, his proposal earned him a hemlock milkshake.

Just as Socrates was a benefactor for Athens, so intelligent design is a benefactor for science. Just as the Athenian court thought otherwise, so does the scientific community.


theyeti

Date: 2004/01/05 01:47:15, Link
Author: theyeti
Here's a new article of obvious relevance:

Mol Immunol. 2004 Feb;40(12):897-902.

Evolution of the complement system.

Nonaka M, Yoshizaki F.

Quote
The human complement system is composed of more than 30 serum and cell surface components, and most of these components show a characteristic domain structure, enabling us to trace the evolution of the genes based on their structures. Ongoing genome projects in both vertebrates and invertebrates revealed that most domains used by mammalian complement components are found in both protostomes and deuterostomes. However, the unique combinations of them as found in mammalian complement components are present only in deuterostomes, indicating that the complement system was established in the deuterostome lineage. Unexpectedly, the complement system of an invertebrate deuterostome, ascidian, shows a similar level of complexity as that of mammals. However, phylogenetic analysis suggested that expansion of complement genes by gene duplications occurred independently both in the ascidian and vertebrate lineages. Although most characteristic domain structures of the mammalian complement components are found in ascidians, detailed evolutionary analysis casts doubt on their mutual reactivity. Thus, the vertebrate complement system seems to be established by integrating some independent parts into one reaction system.

Date: 2004/01/28 11:36:50, Link
Author: theyeti
Mol Biol Evol. 2004 Jan 22

Leptin Receptor Isoform 219.1: An Example of Protein Evolution by LINE-1 Mediated Human Specific Retrotransposition of a Coding SVA Element.

Damert A, Lower J, Lower R.

Quote

Phylogenetically new insertions of repetitive sequences may contribute to genome evolution by altering the function of pre-existing proteins. One example is the SVA sequence which forms the C-terminal coding exon of the human leptin receptor isoform 219.1. Here, we report that the SVA insertion into the LEPR locus has occurred after divergence of humans and chimpanzees. The SVA element was inserted into a Hal-1/LINE element present in all monkeys and apes tested. Structural features point towards an integration event that was mediated by the L1 protein machinery acting in trans. Thus our findings add evidence to the hypothesis that retrotransposition events are a driving force in genomic evolution and that the presence or absence of specific retroelements are one distinguishing feature that separates humans from chimpanzees.


theyeti

Date: 2004/02/14 17:21:03, Link
Author: theyeti
Here's a good one.  A recently aquired endogenous retrovirus has had its Env gene coopted to serve a function in placental physiology.  The Env gene normally codes for envelope proteins in retroviruses.

Proc Natl Acad Sci U S A. 2004 Feb 10;101(6):1731-6.

The endogenous retroviral locus ERVWE1 is a bona fide gene involved in hominoid placental physiology.

Mallet F, Bouton O, Prudhomme S, Cheynet V, Oriol G, Bonnaud B, Lucotte G, Duret L, Mandrand B.

Quote
The definitive demonstration of a role for a recently acquired gene is a difficult task, requiring exhaustive genetic investigations and functional analysis. The situation is indeed much more complicated when facing multicopy gene families, because most or portions of the gene are conserved among the hundred copies of the family. This is the case for the ERVWE1 locus of the human endogenous retrovirus W family (HERV-W), which encodes an envelope glycoprotein (syncytin) likely involved in trophoblast differentiation. Here we describe, in 155 individuals, the positional conservation of this locus and the preservation of the envelope ORF. Sequencing of the critical elements of the ERVWE1 provirus showed a striking conservation among the 48 alleles of 24 individuals, including the LTR elements involved in the transcriptional machinery, the splice sites involved in the maturation of subgenomic Env mRNA, and the Env ORF. The functionality and tissue specificity of the 5' LTR were demonstrated, as well as the fusogenic activity of the envelope polymorphic variants. Such functions were also shown to be preserved in the orthologous loci isolated from chimpanzee, gorilla, orangutan, and gibbon. This functional preservation among humans and during evolution strongly argued for the involvement of this recently acquired retroviral envelope glycoprotein in hominoid placental physiology.


theyeti

Date: 2004/02/14 17:38:05, Link
Author: theyeti
Nat Genet. 2004 Feb 1 Epub 2004 Feb 01.

Evolutionary innovation of the excretory system in Caenorhabditis elegans.

Wang X, Chamberlin HM.

Quote
The evolution of complexity relies on changes that result in new gene functions. Here we show that the unique morphological and functional features of the excretory duct cell in C. elegans result from the gain of expression of a single gene. Our results show that innovation can be achieved by altered expression of a transcription factor without coevolution of all target genes.


theyeti

Date: 2004/03/03 12:29:48, Link
Author: theyeti
Interesting paper:

Protein Eng Des Sel. 2004 Jan;17(1):13-20.

A native-like artificial protein from antisense DNA.

Fischer N, Riechmann L, Winter G.

Quote

We describe the creation of folded chimaeric proteins by combining a designed polypeptide segment (bait) derived from a beta-sheet of a human antibody variable domain with random polypeptide segments encoded by human cDNA fragments. The repertoire of polypeptides was displayed on the surface of filamentous bacteriophage and folded polypeptides were selected by proteolysis. One of these, 2a6, was readily expressed in the Escherichia coli cytoplasm as a soluble and protease-resistant protein and could be purified after heating the bacterial lysate to 90 degrees C. Soluble 2a6 is dimeric and its CD spectrum is consistent with components of both alpha and beta structure. 2a6 cooperatively and reversibly unfolds by heat or urea with a folding energy of 11.4 kcal mol(-1) for the transition between folded dimer and unfolded monomer and its refolding steps proceed without the formation of detectable aggregates. Its stability and folding properties are therefore typical of native proteins. Sequence analysis revealed that the cDNA segment in 2a6 was recruited from the antisense strand of a human gene, suggesting that antisense sequences can provide a reservoir for the evolution of soluble and stable proteins.


theyeti

Date: 2004/03/11 17:31:59, Link
Author: theyeti
Cockroaches making milk.  How adorable.

Evol Dev. 2004 Mar-Apr;6(2):67-77.

Evolution of a novel function: nutritive milk in the viviparous cockroach, Diploptera punctata.

Williford A, Stay B, Bhattacharya D.

Quote
Cockroach species show different degrees of maternal contribution to the developing offspring. In this study, we identify a multigene family that encodes water-soluble proteins that are a major component of nutritive "Milk" in the cockroach, Diploptera punctata. This gene family is associated with the evolution of a new trait, viviparity, in which the offspring receive nutrition during the gestation period. Twenty-five distinct Milk complementary DNAs were cloned and partially characterized. These complementary DNAs encode 22 distinct Milk peptides, each of length 171 amino acids, including a 16-amino acid signal peptide sequence. Southern blot analysis confirms the presence of multiple copies of Milk genes in D. punctata. Northern analysis indicates tissue- and stage-specific Milk gene expression. Examination of the deduced amino acid sequences identifies the presence of structurally conserved regions diagnostic of the lipocalin protein family. The shared exon/intron structure of one of the Milk loci with lipocalin genes further supports a close evolutionary relationship between these sequences.


theyeti

Date: 2004/03/23 10:59:39, Link
Author: theyeti
Nat Struct Mol Biol. 2004 Mar 14

A novel ADP- and zinc-binding fold from function-directed in vitro evolution.

Surdo PL, Walsh MA, Sollazzo M.

Quote
A great challenge to biologists is to create proteins with novel folds and tailored functions. As an alternative to de novo protein design, we investigated the structure of a randomly generated protein targeted to bind ATP. The crystal structure reveals a novel alpha/beta fold bound to its ligand, representing both the first protein structure derived from in vitro evolution and the first nucleotide-binding protein stabilized by a zinc ion.


theyeti

Date: 2004/03/30 11:18:54, Link
Author: theyeti
In an amazing display of orginality, Johnson compares "naturalism" to the Soviet Union.  

http://www.worldmag.com/world/issue/04-03-04/cover_2.asp  (This is one of a series of articles in which ID advocates fantasize about what their inevitable victory is going to look like.)

Quote
New historical scholarship reflected in a stunning PBS television documentary exposed the Inherit the Wind portrayal of the Scopes trial as a hoax, kicking off an era of historical revisionism in which book after scholarly book exposed how propaganda techniques had been employed to create a mythology of inevitable progress toward naturalism, similar to the governing mythology of the Soviet Union, which had proclaimed the inevitable replacement of capitalism by communism.

The collapse of the Soviet Union put an end to the Soviet myth, just as the scientific collapse of Darwinism, preceded as it was by the discrediting of Marxism and Freudianism, prepared the way for the culture to turn aside from the mythology of naturalism to rediscover the buried treasure that the mythology had been concealing.


theyeti



Date: 2004/05/04 13:49:17, Link
Author: theyeti
FEBS Lett. 2004 Apr 30;564(3):274-80.

Evolution of photosystem I - from symmetry through pseudosymmetry to asymmetry.

Ben-Shem A, Frolow F, Nelson N.

Quote
The evolution of photosystem (PS) I was probably initiated by the formation of a homodimeric reaction center similar to the one currently present in green bacteria. Gene duplication has generated a heterodimeric reaction center that subsequently evolved to the PSI present in cyanobacteria, algae and plant chloroplasts. During the evolution of PSI several attempts to maximize the efficiency of light harvesting took place in the various organisms. In the Chlorobiaceae, chlorosomes and FMO were added to the homodimeric reaction center. In cyanobacteria phycobilisomes and CP43' evolved to cope with the light limitations and stress conditions. The plant PSI utilizes a modular arrangement of membrane light-harvesting proteins (LHCI). We obtained structural information from the two ends of the evolutionary spectrum. Novel features in the structure of Chlorobium tepidum FMO are reported in this communication. Our structure of plant PSI reveals that the addition of subunit G provided the template for LHCI binding, and the addition of subunit H prevented the possibility of trimer formation and provided a binding site for LHCII and the onset of energy spillover from PSII to PSI.


theyeti

Date: 2004/05/26 10:04:02, Link
Author: theyeti
This is a good review article about the origin of alternative splicing, and provides evidence of non-coding intronic sequences being transcribed as part of the protein.  In other words, more or less random non-coding DNA being adapted to be part of a functional protein.

Trends Genet. 2003 Mar;19(3):115-9.

Evolution of alternative splicing: deletions, insertions and origin of functional parts of proteins from intron sequences.

Kondrashov FA, Koonin EV.

Abstract:

Quote
Alternative splicing is thought to be a major source of functional diversity in animal proteins. We analyzed the evolutionary conservation of proteins encoded by alternatively spliced genes and predicted the ancestral state for 73 cases of alternative splicing (25 insertions and 48 deletions). The amino acid sequences of most of the inserts in proteins produced by alternative splicing are as conserved as the surrounding sequences. Thus, alternative splicing often creates novel isoforms by the insertion of new, functional protein sequences that probably originated from noncoding sequences of introns.


Some relevant text:

Quote
From the evolutionary standpoint, inserted alternative sequences could be expected to be short if they evolved from noncoding sequences because in-frame stop codons are likely to occur in long noncoding sequences. None of the inserted alternative sequences showed significant similarity to any protein sequences except for their counterparts in orthologs from other species. Furthermore, inserted alternative sequences never included more than one exon (Fig. 2). These observations are compatible with the origin of inserts in LDAS [length difference alternative splicing] from noncoding sequences, most likely from a part of the intron separating the adjacent constitutive exons. On four occasions, this was supported by more direct observations whereby the inserted alternative sequence comprised either an entire intron or a portion of intron joining the adjacent exon.

....

Thus, in addition to straightforward exon skipping, a major route for origin of LDAS is insertion of new exons, which encode new, functionally important protein sequences, thus creating functionally distinct isoforms of the respective proteins. Such new exons might in some cases have evolved by tandem duplication of adjacent exons, but more often, they appear to have evolved de novo from noncoding intron sequences. Most of these intron sequences apparently have been recruited to become new coding sequences relatively recently; for example, only in mammals (supplementary material at http://archive.bmn.com/supp/tig/march_Kondrashov_supply.pdf). These observations suggest that evolution of new coding sequences from noncoding ones is an active, ongoing process in eukaryotes. It seems probable that we uncovered only the tip of the proverbial iceberg.  Indeed, we detected insertion of new exons that probably originate from intron sequences only for LDAS and only for those cases where yeast and/or prokaryotic orthologs were readily detectable. The actual contribution of intron sequences to the emergence of new protein sequences in eukaryotes is probably substantially greater.


theyeti

Date: 2004/06/19 12:16:07, Link
Author: theyeti
Immunol Rev. 2004 Apr;198:36-58.

Evolution of the innate immune system: the worm perspective.

Schulenburg H, Kurz CL, Ewbank JJ.

Quote
Simple model organisms that are amenable to comprehensive experimental analysis can be used to elucidate the molecular genetic architecture of complex traits. They can thereby enhance our understanding of these traits in other organisms, including humans. Here, we describe the use of the nematode Caenorhabditis elegans as a tractable model system to study innate immunity. We detail our current understanding of the worm's immune system, which seems to be characterized by four main signaling cascades: a p38 mitogen-activated protein kinase, a transforming growth factor-beta-like, a programed cell death, and an insulin-like receptor pathway. Many details, especially regarding pathogen recognition and immune effectors, are only poorly characterized and clearly warrant further investigation. We additionally speculate on the evolution of the C. elegans immune system, taking into special consideration the relationship between immunity, stress responses and digestion, the diversification of the different parts of the immune system in response to multiple and/or coevolving pathogens, and the trade-off between immunity and host life history traits. Using C. elegans to address these different facets of host-pathogen interactions provides a fresh perspective on our understanding of the structure and complexity of innate immune systems in animals and plants.


theyeti

Date: 2004/09/21 17:25:35, Link
Author: theyeti
Nat Genet. 2004 Sep 19

Birth and adaptive evolution of a hominoid gene that supports high neurotransmitter flux.

Burki F, Kaessmann H.

Quote
The enzyme glutamate dehydrogenase (GDH) is important for recycling the chief excitatory neurotransmitter, glutamate, during neurotransmission. Human GDH exists in housekeeping and brain-specific isotypes encoded by the genes GLUD1 and GLUD2, respectively. Here we show that GLUD2 originated by retroposition from GLUD1 in the hominoid ancestor less than 23 million years ago. The amino acid changes responsible for the unique brain-specific properties of the enzyme derived from GLUD2 occurred during a period of positive selection after the duplication event.

Date: 2004/10/15 21:56:44, Link
Author: theyeti
FEBS Lett. 2004 Oct 8;576(1-2):1-4.

The evolution of A-, F-, and V-type ATP synthases and ATPases: reversals in function and changes in the H(+)/ATP coupling ratio.

Cross RL, Muller V.

Department of Biochemistry and Molecular Biology, SUNY Upstate Medical University, Syracuse, NY 13210, USA.


Quote
Members of the F(o)F(1), A(o)A(1) and V(o)V(1) family of ATP synthases and ATPases have undergone at least two reversals in primary function. The first was from a progenitor proton-pumping ATPase to a proton-driven ATP synthase. The second involved transforming the synthase back into a proton-pumping ATPase. As proposed earlier [FEBS Lett. 259 (1990) 227], these reversals required changes in the H(+)/ATP coupling ratio from an optimal value of about 2 for an ATPase function to about 4 for an ATP synthase function. The doubling of the ratio that occurred at the ATPase-to-Synthase transition was accomplished by duplicating the gene that encodes the nucleotide-binding catalytic subunits followed by loss of function in one of the genes. The halving of the ratio that occurred at the Synthase-to-ATPase transition was achieved by a duplication/fusion of the gene that encodes the proton-binding transporter subunits, followed by a loss of function in one half of the double-sized protein. These events allowed conservation of quaternary structure, while maintaining a sufficient driving force to sustain an adequate phosphorylation potential or electrochemical gradient. Here, we describe intermediate evolutionary steps and a fine-tuning of the H(+)/ATP coupling ratio to optimize synthase function in response to different environments. In addition, we propose a third reversal of function, from an ATPase back to an ATP synthase. In contrast to the first two reversals which required a partial loss in function, the change in coupling ratio required for the third reversal is explained by a gain in function.

Date: 2005/01/10 11:59:34, Link
Author: theyeti
Rep. Cynthia Davis of Missouri compares ID opponents to Al-Qaeda hijackers.

As quoted in the New York Times:

Quote
State Representative Cynthia Davis of Missouri prefiled two bills for the next session of the Legislature that she said "reflect what people want." One would remove the state's requirement that all forms of contraception and their potential health effects be taught in schools, leaving the focus on abstinence. Another would require publishers that sell biology textbooks to Missouri to include at least one chapter with alternative theories to evolution.

"These are common-sense, grass-roots ideas from the people I represent, and I'd be very surprised if a majority of legislators didn't feel they were the right solutions to these problems," Ms. Davis said.

"It's like when the hijackers took over those four planes on Sept. 11 and took people to a place where they didn't want to go," she added. "I think a lot of people feel that liberals have taken our country somewhere we don't want to go. I think a lot more people realize this is our country and we're going to take it back."


Lovely.

theyeti

Date: 2005/01/26 13:06:57, Link
Author: theyeti
Curr Biol. 2005 Jan 26;15(2):87-93.

Origin and neofunctionalization of a Drosophila paternal effect gene essential for zygote viability.

Loppin B, Lepetit D, Dorus S, Couble P, Karr TL.

Quote
Background: Although evolutionary novelty by gene duplication is well established, the origin and maintenance of essential genes that provide entirely new functions (neofunctionalization) is still largely unknown. Drosophila is a good model for the search of genes that are young enough to allow deciphering the molecular details of their evolutionary history. Recent years have seen increased interest in genes specifically required for male fertility because they often evolve rapidly. A special class of genes affecting male fertility, the paternal effect genes, have also become a focus of study to geneticists and reproductive biologists interested in fertilization and sperm-egg interactions. Results: Using molecular genetics and the annotated Drosophila melanogaster genome, we identified CG14251 as the Drosophila paternal effect gene, ms(3)K81 (K81). This assignment was subsequently confirmed by P-element rescue of K81. A search for orthologous K81 sequences revealed that the distribution of K81 is surprisingly restricted to the 9 species comprising the melanogaster subgroup. Phylogenetic analyses indicate that K81 arose through duplication, most likely retroposition, of a ubiquitously expressed gene before the radiation of the melanogaster subgroup, followed by a period of rapid divergence and acquisition of a critical male germline-specific function. Interestingly, K81 has adopted the expression profile of a flanking gene suggesting that transcriptional coregulation may have been important in the neofunctionalization of K81. Conclusion: We present a detailed case history of the origin and evolution of a new essential gene and, in so doing, provide the first molecular identification of a Drosophila paternal effect gene, ms(3)K81 (K81).

Date: 2006/03/11 20:33:05, Link
Author: theyeti
Hi.  Steve Reuland here.  Given that my bouncing messages here has caused some amount of consernation, I figured I'd explain myself.

1. The person known as "Andy H" and various other pseudonyms has effectively been banned.  He apparently uses multiple IP addresses which makes it very hard to ban him outright.  Reed and Wesley, who run the technical aspects of the blog (all props to them) are doing what they can, but they work their tails off to make this blog what it is, and problems like this just come with the territory.  I am NOT trying to give anyone a hard time while ignoring the root of the problem.  The root of the problem is being dealt with, but it ain't an easy problem to deal with (and out of my hands anyway).  

2.  When I moved "Andy H's" comment and all of those that responded to him, I purposely did not try to differentiate those that were legit from those that weren't.  The obvious reason for that is that I don't want to pass judgment on those responses that were okay vs. those that were not.  That puts me in a position that I don't want to be in.  All of them were off-topic, and I figured it would be best if I treated them all the same way.  If I let some of them stand and others not stand, then I'd be yelled at for selective moderation.  (Of course got yelled at anyway, but like I say, it comes with the territory...  ;) )

3.  I screwed up when I used the "junk" function to try to move comments here.  I thought that would move comments to the BW, but instead it put them into another category of "unpublished" comments.  They are not deleted.  But I also don't know how to get them back or put them here.  This is my fault, and not what I intended.  If it really matters to anyone, I'll try to do what I can to get them here.  (Unfortunately, that means leaning on Wesley to fix the problem, since I don't know how to do it.)

4.  I really don't take kindly to the suggestion that moderation equals censorship.  That is nonsense.  We have a fairly liberal policy concerning comments, and have banned very few people, but that never means that one can post whatever one pleases.  I consider comments to be a valuable tool for generating feedback, critique, and to add additional information.  If I didn't see things this way, I wouldn't even open them in the first place (every poster can just keep them closed if he or she pleases).  That being said, it really defeats the purpose of having comments when a lot of people use them to lob insults at each other, regardless of who started it.

5.  And my final comment is not really related to my current bouncing of messages, but I'd like to make a plea to those of us who are pro-evolution and anti-ID not to make comments that have no other purpose other than to insult IDists (please don't call them IDiots), so-called "fundies", or worst of all, religion in general.  I honestly don't see the point in any of that.  Our goal is to explain to the population at large what's wrong with ID/creationist claims and arguments.  If you don't like religion, I hate to break it to you, but several of our contributors (including Wesley) are religious.  And yet we all manage to get along because we find common ground in science and reason.  If you want to make jabs at people who have conservative, fundamentalist beliefs, well guess what?  You're preaching to the choir.  You are saying nothing profound or original by pointing out that there is something wrong with the way some of these people think.  Who, precisely, do you think such attacks manage to influence?  Not me -- I'm already on board.  Not them, they just use such attacks to reinforce their inaccurate view that all of us are a bunch of as pinko atheist humanistic anti-religious whatever the #### it is we're suppsed to be.  How about those people sitting on the fence?  You'll influence them, one hopes, with lucid explanations about what's wrong with creationism, not with crude attacks on religion or political points of view with which they may have sympathy.  Just saying is all.

Date: 2006/03/11 20:48:57, Link
Author: theyeti
Quote
But, Arden, make it a game. See what you can get away with!
...
So if you want to get back at him, tease him, don't go away mad. Try to stay nominally on topic but look through the historical postings. If you took OT posts out many threads would have no posts at all. It is a broad topic and peevish behavior is to be expected from anyone from time to time.


Um, no, this is exactly what you should not be doing.  Trying to test me is not cool.  It is what is called trolling, and if you keep it up, it will get you banned.  Not because I don't love you (I do! ) but because it is against the rules.  And it is very much counter-productive to what we are trying to do.  

theyeti

 

 

 

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