Rare example of Darwinism seen in action (Deluded Darwinists alert)

EurekAlert ^ | July 31, 2007

[GodGunsGuts]

RIVERSIDE, Calif. – A research team, including UC Riverside biologists, has found experimental evidence that supports a controversial theory of genetic conflict in the reproduction of those animals that support their developing offspring through a placenta.

The conflict has been likened to a “battle of the sexes” or an “arms race” at the molecular level between mothers and fathers. At stake: the fetus’s growth rate and how much that costs the nutrient-supplying mother.

The new research supports the idea of a genetic “arms race” going on between a live-bearing mother and her offspring, assisted by the growth-promoting genes of the father...

[GodGunsGuts]

==The comparison suffers from small sample size

Is it any smaller than the Vitamin C Synthase/GULO sample size you used to establish a “smoking gun” of ape-human common descent?

==In the sequence comparison ... there are 15 differences between the rat sequence and g-pig sequence, and the human and rat sequence differ at 21 places (rats and g-pigs closer than humans and rats). Over this 90 base pairs Humans and chimps differ at only two locations, humans and g-pigs differ at 14 locations(humans and chimps are closer than humans and g-pigs).

If you use the rat as your starting point, the rat and guinea pig are indeed closer to each other than the rat and the human. But far more interesting is looking at the data in the reverse direction. Namely, the data shows that the guinea pig is more closely related to humans than to the rat. An obvious absurdity if you assume common descent. Thus, if you wish to use the shared mutations in the Vit. C Synthase gene to establish common descent of man and ape, then you also have to accept that guinea pigs are closer to humans than they are to rats/rodents. In short, shared Vit. C Synth. gene mutations between man and ape cannot be used to establish common descent. Indeed, quite the opposite is true. The shared GULO mutations between great apes, guinea pigs and humans suggest a common mechanism (i.e. non-random hotspots) rather than common descent. Most scientists were fooled by the data because of their commitment to NDE (neo-Darwinian evolution/RM + NS/Common Descent.

(1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)16)(17)(18)(19)(20)(21)

Rat<-———————————————>guinea pig<————>Human

[allmendream]

My comment was that ERV genome data was called the “smoking gun” of common descent, not an analysis of a 90 bp segment of the GULO human pseudogene compared to the GULO gene in rats and compared to a different pseudogene in guinea pigs. A comprehensive survey over long analogous sequences is how phylogenetic analysis is done, not a 90 base pair blast.

To say that the data suggests guinea pigs are closer to humans than rats to to suggest that 14 is significantly greater than 15; as well as that 14 and 15 are significantly greater than 21 considering the variability of the sequence (around 17 variability on a range of 90). The only conclusive evidence one could gather is that 2 is significantly less than the others, pairing humans and chimps and placing the others at a distance from the apes and with a distance between each other.

I used those 90 bp’s because it was the sequence under discussion, I pointed out when I did the comparison that it was fairly short and I was not trying to use it to establish anything like human-ape common descent (it is just one of the many thousands of data points) I was using it as a reference to the claims that you referenced in regard to the phylogenetic placement of guinea pigs and the presence of analagous mutations between humans and guinea pigs. Should I do a genome wide survey?

My point with the Vitamin C Synthase pseudogene is that it shows an identical deletion in ape lineages that introduces a STOP codon. Despite this segment of DNA not being under selection it has only two differences between us and chimps out of 90 bases, a few more between us and the other apes but 14 between us and guniea pigs and 21 differences between us and rats. This alone is not enough to establish the phylogenetic tree (especially not a 90 bp comparison) but it fits in with THE PATTERN OF EVIDENCE whereby throughout the genomes of living organisms we see...

1) Conservation of genes and functional elements between related species such that species thought to have a recent common ancestor have DNA similarity unrelated to function, and species thought to have a more distant common ancestor have DNA differences that accumulate that do not functional significance.

2) Divergence in sequences without function or not under selective pressure such that differences accumulate at the neutral mutation rate.

When comparing genomes one can see the clear pattern of common descent. Species in related lineages show similarities in pseudogenes and ERV segments that cannot be explained by function. Neither can the suggestion of mutational “hot spots” explain why changes in sequence would converge in related species and diverge in unrelated species.

[AndyTheBear]

As a scientist, I try to avoid such situations. I try to stick to those fields in which I actually know something.

A good attitude.

And for those of us outside of biology, any acceptance or rejection of common descent is necessarily based on faith. We outsiders must choose who and what to believe, or choose to remain in doubt.

Now obviously the evidence and research are readily available to those who devote themselves to it. For myself, I'm willing to delve into the subject just long enough to get the "big picture" of the case for common descent, but I keep finding what I thought I knew was not as simple as I thought.

[allmendream]

Also your graph is flawed. Using that 90 bp segment to establish your phylogenetic tree isn’t recommended, but if your going to do it you show only 3 points of diff between humans and g-pigs, that is incorrect......

HumanXXXXXXXXXXXXXXG-pigXXXXXXXXXXXXXXRat
HumanXXXXXXXXXXXXXXXXXXXXXRat

Once again I must remind you that ascribing a significant difference between 14 and 15 on a number with a range between 2-21 on a value of 90 is not sound. Besides that isn’t the way it is done. I refer you to any study like the following for a more a scientific and mathematically sound methodology.

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=8587500&ordinalpos=17&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Patterns of divergence during evolution of alpha 1-proteinase inhibitors in mammals.Goodwin RL, Baumann H, Berger FG.
Department of Biological Sciences, University of South Carolina, Columbia 29208, USA.

alpha 1-Proteinase inhibitor (alpha 1-PI), a member of the serine proteinase inhibitor superfamily, has a primary role in controlling neutrophil elastase activity within the mammalian circulation. Several studies have indicated that the reactive center region of alpha 1-PI, the amino acid sequence of which is critical to recognition of and binding to target proteinases, is highly divergent within and among species. This appears to be a consequence of accelerated rates of evolution that may have been driven by positive Darwinian selection. In order to examine this and other features of alpha 1-PI evolution in more detail, we have isolated and sequenced cDNAs representing alpha 1-PI mRNAs of the mouse species Mus saxicola and Mus minutoides and have compared these with a number of other mammalian alpha 1-PI mRNAs. Relative to other mammalian mRNAs, the extent of nonsynonymous substitution is generally high throughout the alpha 1-PI mRNA molecule, indicating greater overall rates of amino acid substitution. Within and among mouse species, the 5’-half of the mRNA, but not the 3’-half, has been homogenized by concerted evolution. Finally, the reactive center is under diversifying or positive Darwinian selection in murid rodents (rats, mice) and guinea pigs yet is under purifying selection in primates and artiodactyls. The significance of these findings to alpha 1-PI function and the possible selective forces driving evolution of serpins in general are discussed.

PMID: 8587500 [PubMed - indexed for MEDLINE]

[allmendream]

15 significantly greater than 14 is what I meant. Sorry if the mistake caused any confusion.

[allmendream]

Even shorter but a phylogenetic analysis base on the 51 base pairs (17 codons) of different species provided in previous posts on this thread.

HumanXChimp
HumanXXXXXOrang
HumanXXXXXXXMacacque
HumanXXXXXXXXG-pig
HumanXXXXXXXXXXXRatus
HumanXXXXXXXXXXMouse
HumanXXXXXXXXXBovine
HumanXXXXXXXXXXPig
RatusXXXXMouse
RatusXXXXXXXG-pig
MouseXXXXXXG-pig
RatusXXXXXXXBovine
RatusXXXXXXXPig
BovineXXXPig
G-pigXXXXXXXXHuman
G-pigXXXXXXXRatus
G-pigXXXXXXMouse

Any surprises?

[allmendream]

http://stanford.edu/~nke/papers/2-treeSVD-slides.pdf

The above type of analysis makes what Borger did look amateurish. Notice also that their assumption as an example started with a thousand base pair analysis. Look in the Journal of Molecular Evolution for many hundreds of papers that used variations of this technique to construct phylogenetic trees.

The following is a phylogenetic tree of guinea pigs constructed from molecular evidence assuming conservation and variance based upon common descent. Notice how they warn about dependence upon too small a data set for construction of phylogenetic trees. It is a scientific “I told you so” about Graur’s 1991 assertion that their model showed guinea pigs outside the rodent clade; a wider analysis showed this to not be the case. In either case guinea pigs are fairly divergent little rodents consistently in comparison of sequences(i.e. they are not THAT close with rats and mice), and as the small data set we have amateurishly played with suggests.

http://mbe.oxfordjournals.org/cgi/reprint/11/4/593.pdf

[AndrewC]

Despite this segment of DNA not being under selection it has only two differences between us and chimps out of 90 bases,

How do you know that?

[allmendream]

By its rate of conservation between species, and the fact that it is incapable of making a full length transcript precluding function as a gene or as a stabilizing transcript producing pseudogene.

[AndrewC]

By its rate of conservation between species, and the fact that it is incapable of making a full length transcript precluding function as a gene or as a stabilizing transcript producing pseudogene.

It has a rate of conservation based upon the assumption that it started from the "same" object(as the others which may be used to gauge difference). The other assumption is that it has no function apart from its classification as a potential/actual protein producer.

[allmendream]

Yes, it is similar in related groups, but wouldn't’ be AS similar as genetic material under selective pressure. Divergence would be at the neutral mutation rate for those sequences not under selection, so that would be the rate of conservation. It has no function because its transcript is terminated, it cannot make a protein.

[AndrewC]

Divergence would be at the neutral mutation rate for those sequences not under selection, so that would be the rate of conservation. It has no function because its transcript is terminated, it cannot make a protein.

Again, assumptions. What sequences are not under selection?(how do you tell things are being selected?) Function and proteins... why do you suppose there was suprise at the "small" of protein coding genes?

"Although the completion of the Human Genome Project was celebrated in April 2003 and sequencing of the human chromosomes is essentially "finished," the exact number of genes encoded by the genome is still unknown. October 2004 findings from The International Human Genome Sequencing Consortium, led in the United States by the National Human Genome Research Institute (NHGRI) and the Department of Energy (DOE), reduce the estimated number of human protein-coding genes from 35,000 to only 20,000-25,000, a surprisingly low number for our species (7). Consortium researchers have confirmed the existence of 19,599 protein-coding genes in the human genome and identified another 2,188 DNA segments that are predicted to be protein-coding genes. "

from --- http://www.ornl.gov/sci/techresources/Human_Genome/faq/genenumber.shtml

[allmendream]

Measurements of divergence at the neutral mutation rate for sequences not under selection confirm the assumptions. You can tell if sequences are not being selected because they do not show conservation and do not have a open reading frame. When comparing genes and pseudogenes between related species the pseudogenes are similar but the genes are even more similar.

The reduction in the estimate of 35,000 genes to 20,000 to 25,000 is very interesting. The predicted protein coded genes are probably predicted based upon genetic conservation and recognizable open reading frames that could code for a protein.

[GodGunsGuts]

Hi Allmendream. I sent some of your posts to Dr. Pitman over at DetectingDesign.com. He was gracious enough to reply. What follows is his point by point response in full:

==My comment was that ERV genome data was called the "smoking gun" of common descent, not an analysis of a 90 bp segment of the GULO human pseudogene compared to the GULO gene in rats and compared to a different pseudogene in guinea pigs. A comprehensive survey over long analogous sequences is how phylogenetic analysis is done, not a 90 base pair blast.

The region under analysis was 165 bp and it was this region that was analyzed by Inai et al in their 2003 paper. Many mutational differences were shared by humans, including the one at position 97 ( i.e., the region of a shared deletion mutation). Inai et al strongly suggested in their own paper that this finding indicates some form of non-random bias to these mutation that was independent of common descent or evolutionary ancestry. The probability of the same substitutions in both humans and guinea pigs occurring at the observed number of positions was calculated, by Inai et al, to be 1.84x10-12 - consistent with mutational hotspots.

==To say that the data suggests guinea pigs are closer to humans than rats to to suggest that 14 is significantly greater than 15; as well as that 14 and 15 are significantly greater than 21 considering the variability of the sequence (around 17 variability on a range of 90). The only conclusive evidence one could gather is that 2 is significantly less than the others, pairing humans and chimps and placing the others at a distance from the apes and with a distance between each other.

The data does not suggest that guinea pigs are more closely related to humans than to rats as far as the number and arrangement of mutations are concerned (my mistake--GGG). What the data does suggest is that the mutations in the regions *shared* among human, chimpanzee, macaque and orangutan and guinea pigs were not simply the result of random mutations and therefore do not support the notion of common ancestry. Rather these "shared errors" support the hypothesis of mutational hotspots.

==I used those 90 bp's because it was the sequence under discussion, I pointed out when I did the comparison that it was fairly short and I was not trying to use it to establish anything like human-ape common descent (it is just one of the many thousands of data points) I was using it as a reference to the claims that you referenced in regard to the phylogenetic placement of guinea pigs and the presence of analagous mutations between humans and guinea pigs. Should I do a genome wide survey?

In your original argument you definitely used this sequence to suggest that identical shared genetic errors between humans and chimps (vs. the rat) strongly indicated common ancestry. The counter argument is that these same identical errors are also shared by the guinea pig, to include position 97 (the area of deletion shared between humans and apes) - strongly indicating a shared mechanism, not common descent. Again, this argument was strongly posed by Inai et al in their 2003 paper.

==My point with the Vitamin C Synthase pseudogene is that it shows an identical deletion in ape lineages that introduces a STOP codon. Despite this segment of DNA not being under selection it has only two differences between us and chimps out of 90 bases, a few more between us and the other apes but 14 between us and guniea pigs and 21 differences between us and rats.

It is not the overall number of mutations that is interesting here. It is the number of shared mutations that is interesting. The shared mutations are clearly not the result of random chance mutations. That's the point here. In short, this indicated a mechanistic process, not common ancestry. Given that some sort of biased mutational mechanism is/was in play, you have to consider the replication/mutation rate for the various organisms in question. Guess which organisms have a more rapid reproductive rate? Humans and apes have a much slower replication rate and are therefore less subject to mutations in the reproductive cell lines than are rats and guinea pigs.

==This alone is not enough to establish the phylogenetic tree (especially not a 90 bp comparison) but it fits in with THE PATTERN OF EVIDENCE whereby throughout the genomes of living organisms we see...

Not true at all. The evidence is enough to establish the hypothesis of biased mechanism, not common ancestry

==1) Conservation of genes and functional elements between related species such that species thought to have a recent common ancestor have DNA similarity unrelated to function, and species thought to have a more distant common ancestor have DNA differences that accumulate that do not functional significance.

Gene conservation is affected by natural selection. When functional elements are in play, all bets are off. It is only when a section of DNA is hypothesized to be truly non-functional that things get a bit more interesting. However, when it is found that the non-functional stretch of DNA is littered with mutational hotspots, all bets are off once more. Such stretches of DNA cannot be used in a meaningful manner to support the hypothesis of common descent.

==2) Divergence in sequences without function or not under selective pressure such that differences accumulate at the neutral mutation rate.

That would be true if the sequences in question really had no function AND if the sequences in question were not subject to mutational hotspots OR different mutation rates. In the case of comparison between rats/guinea pigs and humans/apes, neither of these is true - i.e., there are both mutational hot spots and the mutation rates are quite different over the same period of time.

==When comparing genomes one can see the clear pattern of common descent. Species in related lineages show similarities in pseudogenes and ERV segments that cannot be explained by function. Neither can the suggestion of mutational "hot spots" explain why changes in sequence would converge in related species and diverge in unrelated species.

You are mistaken on both counts. Mutational hot spots explain shared mutations even in non-functional regions of DNA and differences in mutation rates between species over an absolute period of time explains the absolute number of differences.

[GodGunsGuts]

==The following is a phylogenetic tree of guinea pigs constructed from molecular evidence assuming conservation and variance based upon common descent. Notice how they warn about dependence upon too small a data set for construction of phylogenetic trees.

You were the one who said the shared errors in the respective GULO genes of humans and apes proves common descent. We have demonstrated that contrary to proving common descent, those shared errors are better explained by a common mechanism (ie hot spots). So it’s a tad hypocritical for you to now turn around and start complaining about undersized data sets when it was you who tried to use the GULO gene to prove common descent in the first place.

[allmendream]

Proof? I stated no such thing. Science doesn’t deal in “proof”. It is you who thinks that amateurish manipulations of small data sets are sufficient to overturn scientific theories and call into question thousands of peer reviewed journal articles. I merely pointed out that it was one of many million points of data that indicate common descent.

Moreover my use of the data set was precluded by the warning that it was a small sample, but it was the one that your referenced source used. Is it an example of why one shouldn’t argue with idiots, they will drag you down to their level and beat you with experience? If I am taking lumps for engaging in a flawed model in an attempt to address the claims of the model, well you are the one who thinks the guy who made the model analysis deserves a Nobel Prize.

Your post#101: you asked for a “ coherent scientific argument for common descent”

My post#104: Endogenous Retro-viral Insertions.
Why is it that ERV’s that are common in some human populations but not in all humans have reverse transcriptase genes that are nearly perfect?

Why is it that ERV’s that are shared between all humans but not shared by chimpanzee’s are MORE preserved than ones that are common among all apes?

Why is the Vitamin C synthase gene broken in the exact same place in humans and apes? Why would an animal be designed with a broken Vitamin C synthase gene in the first place, and what theory could explain the fact that they are broken in the same place.

All these facts are consistent with common descent.

XXXXXXXXXXXXXXXXXXXXXXXXXXX

Please notice that nowhere did I say that one mutation shared in common between apes (but not guinea pigs or any other animal sequenced) was PROOF of common descent, only that it was consistent with it.

Please reference the Journal of Molecular Biology for how these phylogenetic trees are constructed.

http://mbe.oxfordjournals.org/cgi/reprint/11/4/593.pdf

Here is a good one that deals quite well with your assertion that because the guinea pig is divergent from rats it is somehow closer in relation to humans. They also adress the need for looking at data comprehensively and over as large a sample as reasonable. Notice also the lack of the word “proof”.

As far as mutational ‘hot spots’ you have not yet explained why these hot spots once mutated would tend to converge in related species and diverge in unrelated ones. Once again a detailed survey over 1000 bp’s and between five or more species would be a good place to start. Extraordinary claims need extraordinary evidence.

[GodGunsGuts]

Allmendream: “Despite this segment of DNA not being under selection it has only two differences between us and chimps out of 90 bases”

AndrewC: “How do you know that?”

Allmendream: “By its rate of conservation between species, and the fact that it is incapable of making a full length transcript precluding function as a gene or as a stabilizing transcript producing pseudogene.”

AndrewC: “It has a rate of conservation based upon the assumption that it started from the ‘same’ object(as the others which may be used to gauge difference). The other assumption is that it has no function apart from its classification as a potential/actual protein producer.”

---

I have to agree with Andrew here. As I have pointed out numerous times now, the more pseudogenes are studied the more they prove functional. Moreover, even our ideas of what constitutes function are rapidly changing. For instance, the Darwinists over at Panda’s Thumb assume that if a “pseudogene’s DNA is extensively modified by methylation” it is a “known hallmark of transcriptional inactivity.”

http://www.pandasthumb.org/archives/2006/08/rumors_of_pseud.html

However, the scientists over at Panda’s Thumb are directly contradicted by an international team of scientists who conducted the “first large-scale study of the human genome detailing the sections that are not strictly DNA-sequence based.” In addition to estimating that up to one in six genes might be influenced by external factors, they also concluded that “regions called evolutionary conserved regions (ECRs), lying distant from genes, out in the ‘junk’ DNA, had high concentrations of methylation.” And most importantly, they concluded that said methylation “may indicate that these regions have an undiscovered role to play in gene or chromosome activity.”

http://ec.europa.eu/research/headlines/news/article_06_11_21_en.html

Thus, not only are pseudogenes proving to be increasingly functional, we are also finding that there are numerous functional epigenetic elements that can have a major impact on gene activity/expression. In short, given the rapidly accumulating evidence to the contrary, it is probably best to err on the side of prudence and take pseudogenes out of the “junk” category pending further study of the same.

[allmendream]

ECR’s are Evolutionary Conserved Regions. High methylation is inconsistent with transcription but not function. Centromeres and Telomeres and protein binding regions of DNA all have function and are not transcribed. Once again with ECR’s we see that conservation and divergence is tied to (putative) function.

Not all pseudogenes show conservation of sequence. If you find a function for one that is as divergent as other DNA that hasn’t been shown to have a function and has been shown to change at the neutral mutation rate THEN you break the linkage between function and conservation.

Many elements in DNA are highly divergent and shown to be selectively neutral. Why do you think the group that discovered the first functional pseudogene had a COW when their transgenic mouse showed a phenotype for an insertion within what was thought to be a non-functioning element? They KNEW that this was more interesting than whatever protein/gene they were looking at in the first place. And unlike most pseudogens, this one that had a functional transcript showed conservation, as if it were a gene.

None of the examples you have brought up have broken the linkage between conservation and function. Maybe the Discovery Institute should look into that as a line of research, if they did research.

[GodGunsGuts]

==Proof? I stated no such thing. Science doesn’t deal in “proof”.

If science doesn’t deal in “proof”, then why make statements like “such and such is the smoking gun of common descent”??? If that isn’t a proof statement, I don’t know what is!

==I merely pointed out that it was one of many million points of data that indicate common descent.

And I merely pointed out that comparitive GULO gene studies are indicative of a common mechanism/hot spots (and for that matter, one of many millions of data points that argue against common descent).

==Here is a good one that deals quite well with your assertion that because the guinea pig is divergent from rats it is somehow closer in relation to humans.

Go back and read my sidebar in Dr. Pitman’s response...I already admitted I was in error on this point.

==As far as mutational ‘hot spots’ you have not yet explained why these hot spots once mutated would tend to converge in related species and diverge in unrelated ones.

Sure I did. Back in #202 I answered your question with an obvious question, namely...

If creatures share similar body plans, occupy similar environments, and have similar functional needs, shouldn’t we expect them to have a similar genetic structure for certain types of functional elements like pseudogenes and ERVs?

PS Since you are poking fun at my “amateurish” attempts to answer your challenge re: common descent, I think it’s only fair for you to tell me what your scientific credentials are—GGG

[allmendream]

I said that ERV’s were called the “smoking gun” of common descent, not that a survey of a small section of a pseudogene was proof of something.

ERV’s and pseudogenes are not functional, this explains the observation that the measured neutral mutation rate of that species can be used to predict its time of divergence from related species. Among mammals and a small sample of the GULO (Vitamin C Synthase) gene. MY amateurish map (I didn’t weigh different mutations differently and didn’t apply the mathematical model outlined in...

http://stanford.edu/~nke/papers/2-treeSVD-slides.pdf) was consistent with the proposed evolutionary relationship of the species.

HumanXChimp
HumanXXXXXOrang
HumanXXXXXXXMacacque
HumanXXXXXXXXG-pig
HumanXXXXXXXXXXXRatus
HumanXXXXXXXXXXMouse
HumanXXXXXXXXXBovine
HumanXXXXXXXXXXPig
RatusXXXXMouse
RatusXXXXXXXG-pig
MouseXXXXXXG-pig
RatusXXXXXXXBovine
RatusXXXXXXXPig
BovineXXXPig
G-pigXXXXXXXXHuman
G-pigXXXXXXXRatus
G-pigXXXXXXMouse

This amateurish model I utilized STILL indicates the basics of a chimp-human, rat-mouse, cow-pig (hoofed mammals) relationship.

You seem to be pinning your argument that this observed convergence/divergence is EITHER due to function AND/OR an inherent quality of the sequence itself making it more likely to change at particular positions and into particular base pairs (the magnificent 7 guinea-pig mutations). Why doesn’t it change in all species? Why are the two changes between humans/chimps at different locations than the ones in guinea pigs? They are hot enough for one but not the other? Or is it that ‘circumstance’ makes some mutations happen at some locations and other mutations happen at other locations?