I Get A Kick Out Of Endogenous Retroviruses

I've mentioned it before. That dreaded 29+ Evidences for Macroevolution by Dr. Douglas Theobald. I took the time to examine what has been pontificated as the "smoking-gun evidence for evolution" and the "irrefutable evidence." What many Darwinians believe is the most irrefutable argument for their views is the evidence from endogenous retrovirus insertion sites. I am petrified of this evidence. In fact, I am biting my nails. After gathering a few facts, I sent the following email to Dr. Douglas Theobald, concerning this astounding piece of evidence:

 Dear Dr. Douglas Theobald,

In your 2004 article “29+ Evidences for Macroevolution” you write (Part 4: The Molecular Sequence Evidence, Prediction 4.5: Molecular evidence - Endogenous retroviruses):

   “Endogenous retroviruses provide yet another example of molecular sequence evidence for universal common descent.”

You then go on to propose how this molecular sequence evidence for universal common descent could be potentially falsified:

      “It would make no sense, macroevolutionarily, if certain other mammals (e.g. dogs, cows, platypi, etc.), had these same retrogenes in the exact same chromosomal locations. For instance, it would be incredibly unlikely for dogs to also carry the three HERV-K insertions that are unique to humans, as shown in the upper right of Figure 4.4.1, since none of the other primates have these retroviral sequences.”

       Consider this molecular sequence evidence for universal common descent falsified. Essentially, in order to falsify this evidence, we must find an outgroup species that shares with a species of a certain clade the same retrogene or retrogenes insertions, but these insertion sites are not shared by the other species of that clade. This is what it boils down to.

    Interestingly enough, Barbulescu et al. (2001) have identified “a human endogenous retrovirus K (HERV-K) provirus that is present at the orthologous position in the gorilla and chimpanzee genomes, but not in the human genome.”

What we have here is an outgroup species (gorilla) that shares a retrogene insertion site with a species (chimpanzee) of a certain clade (human-chimpanzee clade), but this insertion site is not shared by the other species of that clade. This alone, by your own criteria, falsifies the retrogene evidence for universal common descent you advance in your article.

    

      Similarly, Bonner et al. (1982) report that the endogenous retrovirus colobus type C virus CPC-1 is shared by the chimpanzee and the gorilla but it is absent from the human genome.

Also note that certain classes of type C retroviruses are found in wooly monkeys and the gibbon ape, but it is not found in African great apes [Lieber et al. 1975].

     Humans and Asian apes lack PTERV1 retroviruses, but they are present in African great apes and Old World monkeys [Yohn et al. 2005].

  To quote Yohn et al. 2005:

“For example, only one interval is shared by gorilla and chimpanzee; however, two intervals are shared by gorilla and baboon; while three intervals are apparently shared by macaque and chimpanzee.…If these sites were truly orthologous and, thus, ancestral in the human/ape ancestor, it would require that at least six of these sites were deleted in the human lineage. Moreover, the same exact six sites would also have had to have been deleted in the orangutan lineage if the generally accepted phylogeny is correct. Such a series of independent deletion events at the same precise locations in the genome is unlikely.”

In summary, the very criteria that you stated would falsify this evidence for universal common descent has been met, and hence this evidence is effectively falsified. I am writing you so that you might add a correction to your article and realize that this evidence has been falsified.

Respectfully,

Livingstone Morford

References:

Barbulescu M, Turner G, Su M, Kim R, Jensen-Seaman MI, Deinard AS, Kidd KK, Lenz J. A HERV-K provirus in chimpanzees, bonobos and gorillas, but not humans. Curr. Biol. 11(10):779-83 (2001).

Bonner TI, Birkenmeier EH, Gonda MA, Mark GE, Searfoss GH, et al. Molecular cloning of a family of retroviral sequences found in chimpanzee but not human DNA. J. Virol. 43: 914–924 (1982).

Lieber MM, Sherr CJ, Todaro GJ, Benveniste RE, Callahan R, et al. Isolation from the Asian mouse Mus caroli of an endogenous type C virus related to infectious primate type C viruses. Proc. Natl. Acad. Sci., 72: 2315–2319 (1975).

Yohn CT, et al. Lineage-specific expansions of retroviral insertions within the genomes of African great apes but not humans and orangutans. PLoS Biol, 3:110 (2005).

There. Now I've gotten this load off my chest. That's some absolutely amazing piece of evidence.

The Tangled Web: Darwinian Evolution and Morality

Of late, my friend Chris has been blogging about the moral argument for the existence of God. Atheists typically respond to the moral argument by saying that morals evolved. While some very good refutations of that view are available, I wish to add my own comments regarding the atheist position. I'll tackle that position from the angle of genetics and not philosophy et al.

First off, is it morally acceptable for a member of the species homo sapiens to kill another homo sapiens without cause? Not at all, and most people, including atheists, will agree with me. So, here's another question: is it morally acceptable for humans to kill chimpanzees, for no reason other than, say for the chimpanzee's fur? If the answer is "no," then is it morally acceptable to kill (without cause other than profit) a gorilla? A lemur? To get to the meat of my argument, at what percent of DNA similarity to our DNA does it become morally acceptable to kill an animal for no real cause? Are we allowed to kill an animal whose DNA is say, 99.99% similar to our own DNA? Is it okay to kill an animal whose DNA is 98% similar to our own? 97%? You see, if morals evolved without any guiding intelligence, at what percentage of DNA similarity are we supposed to draw the line that separates those creatures that we may kill and those we may not kill? Something to ponder over. After all, we share 97.5% similarity to mice [Mural et al. 2002], and yet, intriguingly, tonight I am setting up some mice traps to catch those nasty pests. So, I would love to hear an atheist response to this. 

References:

R. J. Mural et al. A Comparison of Whole-Genome Shotgun-Derived Mouse. Science 296: 1661 (2002). 

My Response To Dryden et al.

The science journals appear to have come up with a clever strategy to keep papers critical of Darwinian evolution out of the peer-reviewed literature: simply reject the papers or letters to the editor on the grounds that "your response would not be of interest to our readers.” This is evidenced by the refusal to publish Michael Behe's responses to various papers. In short: if you're critical of a paper that attempts to explain a problem for Darwinian evolution, then your paper is not interesting, and hence it won't be published. It's a neat trick, and one that I suspect I fell for.

         First off, I submitted a manuscript to the Journal of the Royal Society Interface. My paper was a critique of a paper by Dryden et al. 2008, "How much of protein sequence space has been explored by life on Earth?" In this paper, Dryden et al. argue that by reducing the functional amino acid repertoire, to, among others, a binary amino acid alphabet consisting of hydrophobic and hydrophilic amino acids, then evolutionary processes can easily navigate the whole of functional protein sequence space. Consider that for a protein only 100 amino acids in length, there are 20^100 potential amino acid combinations. By reducing the functional amino acid alphabet to one consisting of only hydrophobic and hydrophilic amino acids, then protein sequence space has a potential of only 2^100 functional sequences. Essentially, they argue that the only thing that matters for a protein to function is that the protein has the right sequence arrangement of hydrophobic and hydrophilic residues. They try to reduce the amino acid repertoire through other means, but the point is this: the paper is nonsense. There are many glaring errors in that paper, some of which I point out in the response I submitted to the Journal of the Royal Society Interface (I submitted the manuscript on August 28, 2010).

Well, gee, but ten days later I received the journal's decision regarding my paper. It shouldn't be hard to guess why they rejected my paper.

Here's a hint: it's not because the reviewers sent a rebuttal to my paper, and it's not because my paper made some error in biology.

So, anyway, here's why they rejected my paper:

"Thank you for submitting your manuscript entitled "On the Reduction of the Amino Acid Repertoire in Functional Protein Structures" to J. R. Soc. Interface.

...Many more good manuscripts are submitted to us than we have space to publish, and we give preference to those that present significant advances of broad interest. Unfortunately, your manuscript has been rejected at this stage, as it was not considered to have sufficient appeal for the general readership of J. R. Soc. Interface."  [emphasis added]

Okay, I'll admit that my paper did not represent any real experimental research. But interestingly enough, Dryden et al.'s paper wasn't an experimental paper either, but purely theoretical. However, since I guess it had sufficient appeal for the general readership of the journal, it got published. No problem.

Oh, and I forgot to include this last line the journal sent me:

"Thank you for your paper and I hope that it will be published elsewhere." That makes me feel better.

   Now for those of you interested in my critique of Dryden et al.'s paper, I will link to my response at the end of this post (too bad, but my paper didn't refer to some fairly recent work that further supports my paper).

Here's the abstract:

Abstract

It has been postulated by Dryden et al. [Dryden David T.F, Thomson Andrew R, White John H. How much of protein sequence space has been explored by life on Earth? J. R. Soc. Interface, 5,25:953-956 (2008)] that the amino acid repertoire of functional protein structures may be reduced to a binary one consisting of hydrophobic and hydrophilic residues without affecting protein function. Moreover, they point to proteins with a low degree of functional complexity and posit that such structures demonstrate that the actual identity of most of the amino acids in a protein is irrelevant. They conclude that, as a result of such reduction there is no role for molecular contingency, and furthermore that potential functional protein sequence space is completely explorable.

        Here, based on presented data and through a protein sequence alignment, it is shown that the stated postulate does not hold. For this reason, I conclude that there is a role for molecular contingency and not all of functional protein sequence space has been explored by life on earth.

Here's the full paper:

On The Reduction of The Amino Acid Repertoire In Functional Protein Structures.

And finally, here are all the beta-tubulin sequences I aligned from 30 different organisms (that took quite a toll on my hands):

Beta-tubulin sequences.

Now I have to go and revise a paper that I'm having a little better luck with. And I have to go eat a sandwich because I actually am not a robot behind a computer screen, contrary to popular opinion.

The finishing touch to this will be two quotes from two different Darwinians:

"...at the molecular level, there is no role for contingency."
-Dryden et al. 2008, "How much of protein sequence space has been explored by life on Earth?"

"... historical contingency is especially important when it facilitates the evolution of key innovations that are not easily evolved by gradual, cumulative selection."

-Blount ZD, Borland CZ, Lenski RE (2008) Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli. Proc Natl Acad Sci U S A 105(23):7899-7906.


Addendum:

In my paper, one of the conserved residues in beta-tubulin is cys-12. Since this residue is conserved in all thirty organisms, one would predict that this residue is critical to beta-tubulin function. This prediction is confirmed by site-directed mutagenesis of this residue by Gupta et al. 2001:
"The results suggest that the C12 and C354 residues play important roles in the structure and function of tubulin."

Gupta ML, et al. Mutagenesis of beta-tubulin cysteine residues in Saccharomyces cerevisiae: mutation of cysteine 354 results in cold-stable microtubules. Cell Motil. Cytoskeleton, 49(2):67-77 (2001).

Giving Both Barrels: A Two-Part Response To Professor Larry Moran, Part 1

    I had the guts to make several comments on Professor Larry Moran’s blog, Sandwalk; he has responded to one of these comments with two blog posts (here and here). And now, I have the chutzpah to respond to Professor Larry Moran (to get the gist of what’s going on see my comments on Sandwalk) on BioTalk.

The comment to which Prof. Moran responded to was pretty straightforward. Namely, I argued that “intelligent design proponents need only demonstrate that the odds of a particular biochemical system evolving are 10^-40 or less in order for intelligent design to be a more adequate explanation for the origin of such a biochemical system. This is because there have been no more than 10^39 bacterial cells in the history of life on earth.”

       

    Prof. Moran contends that the above argument cannot possibly hold much water, and he attempts to substantiate that assertion by bringing up the following argument:

That the odds of a specified sperm uniting with an egg is deplorably low, and as a result, through various calculations he does, he concludes that the probability of his four great-grandparents being born is lower than 10^-64 – a probability significantly lower than my stated 10^-40.

     

        Unfortunately by arguing thusly our dear professor is opening a can of worms for the entire common descent framework in that he is tacitly “refuting” the evidence for common descent. One of the oft-cited evidences for common descent are the shared insertion sites of endogenous retroviruses between humans and chimpanzees. However, if we are to accept Prof. Moran’s dictum that something having a probability of occurring of 10^-64 is in fact perfectly plausible, then we must accept that it is perfectly plausible that the shared ERV insertion sites between humans and chimpanzees may be the result of mere coincidence. Prof. Moran is trying to have it both ways but that is a of course a  blatant contradiction.

       

   Moreover, I would like to ask Prof. Moran to please explain to me in terms of probability, why precisely polyvalent antimalarial treatments are more effective than standard treatments? It seems as if Prof. Moran is wishing to go against the peer-reviewed literature, where we see that White (2004) says,

"If two drugs are used with different modes of action, and therefore different resistance mechanisms, then the per-parasite probability of developing resistance to both drugs is the product of their individual per-parasite probabilities. This is particularly powerful in malaria, because there are only about 10¹⁷ malaria parasites in the entire world. For example, if the per-parasite probabilities of developing resistance to drug A and drug B are both 1 in 10¹², then a simultaneously resistant mutant will arise spontaneously every 1 in 10²⁴ parasites. As there is a cumulative total of less than 10²⁰ malaria parasites in existence in one year, such a simultaneously resistant parasite would arise spontaneously roughly once every 10,000 years — provided the drugs always confronted the parasites in combination. Thus the lower the de novo per-parasite probability of developing resistance, the greater the delay in the emergence of resistance.”

Now, to support my assertion that it is implausible to expect Darwinian processes to produce a biochemical system having a probability of origin less than 10^40, we must merely use a little logic.

If the per-E.coli probability of evolving biochemical system A is 10^40, then a mutant E. coli with this biochemical system will arise every 1 in 10^40 cells. As there is a cumulative total of about 10^30 bacterial cells in existence in one year [Whitman et al. 1998], such a mutant E. coli would arise roughly once every 3.55 billion years.

      Sound familiar? I’m using the exact same math that White 2004 is using, yet amusingly I don’t see Prof. Moran talking about how the referee(s) of White’s paper messed up in their review of his paper; nor for that matter do I see him criticizing N.J. White’s work; nor for that matter have I seen a letter from Prof. Moran to the Journal of Clinical Investigation correcting White’s work. I wonder why that could be? Oh right, I forgot, I’m advocating intelligent design so only I can be wrong when I use the same reasoning a peer-reviewed paper uses. Neat, isn’t it?

References:

1. White, Nicholas J. Antimalarial drug resistance. J. Clin. Invest, 113(8):1084–1092 (2004). 

2. Whitman W.B, Coleman D.C, Wiebe W.J. Prokaryotes: the unseen majority Proc. Natl Acad. Sci. 95(12): 6578-6583 (1998). 


Addendum: I said that,
"If the per-E.coli probability of evolving biochemical system A is 10^40, then a mutant E. coli with this biochemical system will arise every 1 in 10^40 cells. As there is a cumulative total of about 10^30 bacterial cells in existence in one year [Whitman et al. 1998], such a mutant E. coli would arise roughly once every 3.55 billion years." 

I might add that " thus the lower the  per-E.coli probability of developing biochemical system A the greater the delay in the emergence of biochemical system A", a statement consistent with White's paper.

How To Build A Strawman And Knock It Down

This morning I got up and turned my computer on. I began randomly browsing the web, glass of water in hand. I almost choked to death. Carumbas Blog got my attention. According to that blog, intelligent design can never be science because intelligent design isn't falsifiable.

To quote the author of the blog:

"ID cannot be science because it can never be falsified – a requirement of a scientific hypothesis. ID never can be falsified – and therefore cannot be science - as long as one possibility for the designer is an omnipotent and omniscient God. Such a God, by definition, can do anything and do so for reasons that we mere humans might not be able to understand. As long as such a God is a possible designer – even if not the only possibility – any natural phenomenon is possible. Because of that, until the possibility of an omnipotent and omniscient God is specifically excluded as a possible designer, ID cannot possibly be science."

Right off the bat Randy Crum (the author of the blog) gets it wrong. What we essentially have here is Mr. Crum constructing a man made out of straw and then proceeding to destroy it. Let's deconstruct his straw-man.

   To do this, we need to define intelligent design. In a word, intelligent design holds that certain features of the biological world are more adequately explained by an intelligence rather than a mindless process like Darwinian evolution.

 So can intelligent design be falsified? You bet. If for example one observed the evolution of a biochemical system that required several dozen specifically arranged amino acid residues, then intelligent design proponents would stay up till 4 o'clock in the morning pondering over how they could have messed up so badly. Mr. Crum of course, by his argument, would argue that this wouldn't really falsify intelligent design because if an omnipotent God was the designer, then the designer could "do anything and do so for reasons that we mere humans might not be able to understand." However this is fallacious because it is irrelevant whether or not the designer did things we could understand; what is the real issue here is whether intelligent design is a more adequate explanation for something in the biological world than a mindless process. Even if God decided to allow such a described biochemical system to evolve in real-time, intelligent design would still have been falsified because to us humans intelligent design would cease to be a more adequate explanation for the origin of said biochemical system. 

And I thought Darwinians didn't use straw-men arguments.