Asyncritus, endogenous retroviruses and plagiarism (Discussion about how Christadelphians love to hate each other in the comments at the end!)

By Ken Gilmore
Ken is not an Ex-Christadelphian (We live in hope)
Source: Click Here




Poor arguments against evolutionary biology not only make special creationists look ignorant and intellectually dishonest, but make the scientifically informed person who is potentially interested in the Christian faith less inclined to investigate our message.

Appeal to authority and quote mining are two of the most commonly found logical fallacies in special creationist attacks on evolution. When you add plagiarism to the mix, it is easy to see why many non-theists regard special creationists with contempt.

 

 

One of the most powerful demonstrations of common descent is the presence of identical shared retroviral elements at identical locations in the genomes of species. As retroviruses insert randomly into the genome, the odds of the same retrovirus inserting into the same location in the genome purely by chance is billions to to one against. As the respected virologists John Coffin and Welkin Johnson point out:

Therefore, an ERV locus shared by two or more species is descended from a single integration event and is proof that the species share a common ancestor into whose germ line the original integration took place. Furthermore, integrated proviruses are extremely stable: there is no mechanism for removing proviruses precisely from the genome, without leaving behind a solo LTR or deleting chromosomal DNA. The distribution of an ERV among related species also reflects the age of the provirus: older loci are found among widely divergent species, whereas younger proviruses are limited to more closely related species. [1]

 

This does not mean that the genome cannot later co-opt retroviral elements for another function. There is strong evidence that the development of the mammalian placenta was contingent on syncytin, a retroviral envelope protein that had inserted itself into the mammalian line millions of years ago. [2] There is no doubt that this is a viral gene, not a vertebrate gene. Furthermore, syncytin is in the same place in the genomes of humans, apes and monkeys. [3] Science writer Carl Zimmer comments:

Viruses have insinuated themselves into the genome of our ancestors for hundreds of millions of years. They typically have gotten there by infecting eggs or sperm, inserting their own DNA into ours. There are 100,000 known fragments of viruses in the human genome,  making up over 8% of our DNA. Most of this virus DNA has been hit by so many mutations that it’s nothing but baggage our species carries along from one generation to the next. Yet there are some viral genes that still make proteins in our bodies. Syncytin appeared to be a hugely important one to our own biology. Originally, syncytin allowed viruses to fuse host cells together so they could spread from one cell to another. Now the protein allowed babies to fuse to their mothers. [4]

The fact that it is functional is not the issue - it is performing a completely different function to what it used to to when it was a viral gene. Rather, we have an identical gene completely alien to the mammalian genome in the same place in primate genomes, which is proof that primates - including humans - have a common ancestor which had been originally infected by the retrovirus which carried the syncytin gene.

Special creationist attempts to rebut this unarguable evidence for common descent invariably miss the point, and fixate on the co-option of elements of the endogenous retrovirus by the host genome, and ignore the fact that it is the presence of identical retroviral elements (many of which have not been co-opted by the host genome) at the same place in the genomes of related species which provides the evidence for common descent.

 

One example comes from the creationist Asyncritus, who has provided us with an ironic example of 'independent error' versus 'plagiarism'. The irony is that Asyncritus was attempting to argue that shared ERV elements don't prove common descent. Asyncritus argues that:

In his "29+ Evidences for Macroevolution" on TalkOrigins, Douglas Theobald claims that "Endogenous retroviruses provide yet another example of molecular sequence evidence for universal common descent." The presumption behind his argument is that endogenous retroviruses (ERVs) are functionless stretches of "junk" DNA that persist because they are "selfish"—but they have no function for the organism. If we find the same ERVs in the same genetic loci in different species of primates, Theobald concludes they document common ancestry.  

That's Theobald, and now you. Here are the facts:

A recent 2008 paper, "Retroviral promoters in the human genome," in the journal Bioinformatics (Vol. 24(14):1563–1567 (2008)) discusses the fact that "Endogenous retrovirus (ERV) elements have been shown to contribute promoter sequences that can initiate transcription of adjacent human genes. However, the extent to which retroviral sequences initiate transcription within the human genome is currently unknown." The article thus "analyzed genome sequence and high-throughput expression data to systematically evaluate the presence of retroviral promoters in the human genome."

The results were striking:

We report the existence of 51,197 ERV-derived promoter sequences that initiate transcription within the human genome, including 1743 cases where transcription is initiated from ERV sequences that are located in gene proximal promoter or 5' untranslated regions (UTRs).

[…]

Our analysis revealed that retroviral sequences in the human genome encode tens-of-thousands of active promoters; transcribed ERV sequences correspond to 1.16% of the human genome sequence and PET tags that capture transcripts initiated from ERVs cover 22.4% of the genome. These data suggest that ERVs may regulate human transcription on a large scale.

(Andrew B. Conley, Jittima Piriyapongsa and I. King Jordan, "Retroviral promoters in the human genome," Bioinformatics, Vol. 24(14):1563–1567 (2008).)

     

I have some familiarity with the evidence for common descent from ERVs, the literature and the special creationist abuse, and both the paper and the commentary sound - familiar. Well, guess what. Casey Luskin, a lawyer and former geology student who works  for the Discovery Institute, an intelligent design advocacy group said something strikingly similar:

In his "29+ Evidences for Macroevolution" on TalkOrigins, Douglas Theobald claims that "Endogenous retroviruses provide yet another example of molecular sequence evidence for universal common descent." The presumption behind his argument is that endogenous retroviruses (ERVs) are functionless stretches of "junk" DNA that persist because they are "selfish"--but they have no function for the organism. If we find the same ERVs in the same genetic loci in different species of primates, Theobald concludes they document common ancestry. But what if ERVs do perform important genetic functions? Even theistic evolutionist Francis Collins acknowledges that genetic similarity "alone does not, of course, prove a common ancestor" because a designer could have "used successful design principles over and over again." (The Language of God, pg. 134.) The force of Theobald's argument thus depends upon the premise that ERVs are selfish genetic "junk" that do not necessarily perform any useful function for their host.

In contrast, ID proponents would predict function for ERVs. This isn't because ID has an inherent quarrel with common descent--it doesn't. Rather, ID predicts function because the basis for ID's predictions is observations of how intelligent agents design things, and intelligent agents tend to design objects that perform some kind of function. As William Dembski wrote in 1998, "If, on the other hand, organisms are designed, we expect DNA, as much as possible, to exhibit function." It seems that the expectations of ID are turning out to be right.

A recent 2008 paper, "Retroviral promoters in the human genome," in the journal Bioinformatics (Vol. 24(14):1563--1567 (2008)) discusses the fact that "Endogenous retrovirus (ERV) elements have been shown to contribute promoter sequences that can initiate transcription of adjacent human genes. However, the extent to which retroviral sequences initiate transcription within the human genome is currently unknown." The article thus "analyzed genome sequence and high-throughput expression data to systematically evaluate the presence of retroviral promoters in the human genome."

The results were striking:

We report the existence of 51,197 ERV-derived promoter sequences that initiate transcription within the human genome, including 1743 cases where transcription is initiated from ERV sequences that are located in gene proximal promoter or 5' untranslated regions (UTRs).

[...]

Our analysis revealed that retroviral sequences in the human genome encode tens-of-thousands of active promoters; transcribed ERV sequences correspond to 1.16% of the human genome sequence and PET tags that capture transcripts initiated from ERVs cover 22.4% of the genome. These data suggest that ERVs may regulate human transcription on a large scale.

(Andrew B. Conley, Jittima Piriyapongsa and I. King Jordan, "Retroviral promoters in the human genome," Bioinformatics, Vol. 24(14):1563--1567 (2008).)

Darwinists who labeled ERVs as a form of "selfish" and "junk" DNA have been chasing explanations down a blind alley. It should be stated that the authors do not deviate from the neo-Darwinian paradigm, putting the obligatory evolutionary spin on the data. They claim that it's a possibility that some of the transcribed ERVs are "not functionally significantl," exposing that even in the face of this compelling contrary data, it is difficult for many Darwinists to let go of their seductive but science-stopping "junk-DNA" paradigm.

 

I've highlighted the similarities in bold. It is possible that both Luskin and Asyncritus independently chanced upon the same paper, abused it in exactly the same way, and wrote up their misunderstandings using the same prose. They may have even included the same  [...] ellipse in the same location between the same paragraphs quoted from the Conley et al paper. Possible, but extremely unlikely. What we see here is Asyncritus plagiarising something from a disreputable organisation, demonstrating in the process:

• Intellectual and moral dishonesty
• Complete ignorance of the reason why ERVs are evidence for common descent
• That - once again - he doesn't know the first thing about evolutionary biology

Once again, ERVs are evidence for common descent as: 

• They integrate randomly into the host genome
• Once integrated, there is no easy way they can be excised
• Therefore, the presence of ERV loci at identical points in the genomes of two species is evidence that both species had a common ancestor in which ERV integration took place, and has been subsequently inherited.

Luskin (they're not Alleyne's words, so I'll show why Luskin is poorly regarded by mainstream science) uses an  inept bait-and-switch here:

Theobald concludes they document common ancestry. But what if ERVs do perform important genetic functions? Even theistic evolutionist Francis Collins acknowledges that genetic similarity "alone does not, of course, prove a common ancestor" because a designer could have "used successful design principles over and over again." (The Language of God, pg. 134.)

Similarity alone does not prove common descent, but ERVs are not 'indigenous' to the species. They are clearly viral in origin, and evidence of prior retroviral infection. Luskin fails to mention this point because as mentioned earlier, the presence of identical viral material at the same loci is consistent with infection in a common ancestor.
The question of function is irrelevant - the human genome has co-opted retrotransposons and ERV promoters to perform function over time. However, this was never their intended function in the first place - retrotransposons are mobile genomic elements whose presence is evidence of an earlier copying and insertion event and primarily exist solely to copy themselves, while ERVs are as mentioned evidence of ancient retroviral infection.

The force of Theobald's argument thus depends upon the premise that ERVs are selfish genetic "junk" that do not necessarily perform any useful function for their host. In contrast, ID proponents would predict function for ERVs. This isn't because ID has an inherent quarrel with common descent--it doesn't.

The force of Theobald's argument has been shamelessly misrepresented by Luskin. This is what Theobald said:

Endogenous retroviruses provide yet another example of molecular sequence evidence for universal common descent. Endogenous retroviruses are molecular remnants of a past parasitic viral infection. Occasionally, copies of a retrovirus genome are found in its host's genome, and these retroviral gene copies are called endogenous retroviral sequences. Retroviruses (like the AIDS virus or HTLV1, which causes a form of leukemia) make a DNA copy of their own viral genome and insert it into their host's genome. If this happens to a germ line cell (i.e. the sperm or egg cells) the retroviral DNA will be inherited by descendants of the host. Again, this process is rare and fairly random, so finding retrogenes in identical chromosomal positions of two different species indicates common ancestry. (Emphasis mine)

Theobald's argument is not primarily based on 'junk' DNA, but the simple fact that shared identical ERV genomic material in two species is evidence of common descent. Luskin got it wrong, and Asyncritus blindly parroted him, ironically providing in the process a demonstration of why plagiarised errors provide evidence for common descent.

 

What makes Asyncritus' position even worse is that apart from yet another plagiarism, he's demonstrated that he does not understand the subject well enough to see the flaws in Luskins' argument, let alone be taken seriously as an informed critic of evolution.

This article has been adapted from here with the permission of the author.

References

1. Johnson WE Coffin JM "Constructing primate phylogenies from ancient retrovirus sequences" Proc Natl Acad Sci USA (1999) 96:10254-10260

2. McCoy J.M. et al "Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis" Nature (200) 403:785-789

3. Mallet F et al "The endogenous retroviral locus ERVWE1 is a bona fide gene involved in hominoid placental physiology" Proc Natl Acad Sci USA (2004) 191:1731-1736

4. Zimmer C "Mammals Made by Viruses" The Loom Feb 14th 2012