Evolution News & Science Today has a new article on endogenous retroviruses (ERV’s). It contains the usual conflation of terms such as junk DNA, activity, and function. I haven’t read through the whole thing, but I thought it might be instructive to show how scientists are approaching this topic, and how it contrasts with the depiction in the Discovery Institute’s article.
Not their research though. For an organization that cares so much about this area are they ever gonna do their own research and bench work on it?
When reading the article, keep the following example of fallacious reasoning in mind:
John: Hey Frank, did you know that gun you own was used in a murder?
Frank: What makes you say that, John?
John: I was reading in the paper that forensic investigators found a gun at a crime scene, and they say it was used to murder someone. Therefore, your gun was used in a murder. Obviously, if one gun was used in a murder, then they all were.
First, let’s clear up the following misinformation from the Discovery Institute:
ERV’s really started off as RETROVIRUSES. That’s the whole point. If they are no longer functioning as a retrovirus, but still serving a different function, then it is correct to say they have been co-opted.
Let’s also consider the bulk of the viral genes that are present in many ERV’s. These include capsid proteins, reverse polymerase, and envelope proteins. These genes in many ERV’s are full of substitution and indel mutations that have done away with these proteins. They are pseudogenes by every definition. The one feature of the viral genome that does stick out is the strong promoter sequences that flank the genome. If these promoters are inserted upstream of a region of DNA, it can drive expression of that region.
However, finding viral promoters that have been co-opted for other functions in no way negates their origin. ERV’s are often used by people to evidence common ancestry, and finding functional ERV’s in no way changes that evidence. The reason that ERV’s are evidence for common ancestry is due to the fact that retroviruses insert randomly into host genomes. Therefore, finding multiple ERV’s at the same position in the genomes of two species is evidence for them sharing a common ancestor in which a single insertion occurred. Humans have 200,000+ ERV’s in their genome, and more than 99% of them are found at the same spot in the chimp genome. This isn’t due to separate infections since that wouldn’t produce insertions at the same position. Instead, these are ERV’s inherited from a common ancestor. Notice that nowhere in that argument did I say that ERV’s are evidence for common ancestry because ERV’s lack function.
Exactly. In other words, the word “co-opted” is the opposite of Skell’s “narrative gloss” - it holds tremendous explanatory value. It explains the “big-picture” features of ERVs while claims of functionality only pepper the fringes (single retroviral genes/regulatory elements).
This is positively delusional. They’re talking about scientists describing a result, not about “ID opponents”. Most scientists don’t give a flying, um, fox about intelligent design; if they’re aware of it at all, it’s as some crackpot creationism-lite that was around a few years ago.
not according to everyone. actually many biologists think that retroviruses are the product of ervs and not the opposite. read about the escape hypothesis:
are you sure about that? we know about at least several potential shared ervs without a common descent. and scientists explain it by convergent loss.
I wonder if the DI will ever produce a reference for this claim:
Several? As in how many? There are over 200,000 ERV’s in the human genome, and more than 99% of them are shared with chimps. We would expect a handful of odd results because biology is a messy process with mechanisms like ILS and gene loss, so you need to explain the overwhelming signal instead of putting too much importance on the little bit of noise.
Also, those ERV’s would be shared by common ancestry if the pattern of species distribution was affected by convergent gene loss, so I’m not sure why you would use them as examples of shared insertions that aren’t due to common ancestry.
Your reference does not support that claim if we are talking about mammalian genomes. It is talking about the origin of viruses way, way back in history:
It is NOT saying that ERV’s were the source of retroviruses. Not even close. I am going to assume that you just didn’t understand this article because otherwise this is a serious case of malpractice on your part. I would urge you to read your sources more carefully and ask questions if necessary.
The DI’s central claim is that ERV’s are not junk DNA because they are responsible for the three dimensional structure of chromosomes.
If just one type of ERV is responsible for this function, how can the DI then claim that no ERV’s are junk DNA?
Better yet, how many of this type of endogenous retrovirus have this function? From the paper that the DI references:
So there are just 1,000+ HERV-H insertions total in the study, and of those 1,000 they found <50 which possibly have this function. That’s <50 of the total 200,000+ in the human genome. From this finding, the DI seem to imply that no human ERV’s are junk DNA. I think we can all see how their claims can’t be supported by the studies they are citing.
Edited to add:
They use the same flawed reasoning for transposons:
The DI should know better. 50% of the human genome is not made up of transposoable elements that control CTCF binding locations at TAD boundaries.
I would also like to see DI give a reference for this claim:
Even some simple reasons as to why the theory of evolution would predict every single retroviral insertion would turn into detritus would be welcome. Somehow, I doubt we will see that.
Contrast their statement with the first sentences of the paper’s discussion:
The evolution of multicellular organisms is driven, in large part, by the invention of new gene regulatory circuits responsible for the fitness traits of each species. A long-standing theory holds that retroviruses may play an important role in the evolution of gene regulatory logic50,51.
a simple scenario is that these ervs are integral part of the genome and not the result of common insertions. the evidence for that is the fact that a retroviral parts can be created by taking genes from the host. a second evidence is the fact that a virus cant survive without its host, and in same cases the host cant survive without its ervs. a classic example fo the chicken and egg problem.
indeed. but what is true for the virus origin can also be true for any retrovirus origin.
actually they are saying it in other words: " in which fragments of cellular genomes (either from prokaryotes or eukaryotes) became infectious". if it can happen once it can happen again and again.
We can observe new ERV’s being produced by ongoing retroviral infections. We can watch it happen.
In that study they put retrovirus in with cells, and then mapped the new insertions they produced. Again, this is an observed mechanism.
indeed. and we also observe the opposite situation when a virus can take a part of the host genome and add it to its own genome:
Yes, a retrovirus inserted into the host genome in such a way that it incorporated a gene from the host genome. How does that put the origin of ERV’s in doubt?
It’s hard for me to cope with the continual lies and dishonesty coming from EN, and done so in the name of the ‘Intelligent Designer.’ That is obviously the not so secret alternative hypothesis. And with ERVs any function isn’t even the main argument for common ancestry, it’s the patterns of ERVs found among species.
It is very telling to me that one ID advocate in the thread appears to not really understand why this beyond a shadow of a doubt demonstrates common ancestry. I would even dare say it’s not really his or any other reader’s fault, but it is the authors who are writing such nonsense.
Edit: I used to do the same thing as this article with scientific publications. I would literally grab bits and pieces of scientific articles that fit my YEC worldview, ignore the parts that didn’t and then remarkably claim that it all this research supported my YECism.
it shows that a retrovirus can evolve from genome components. thus we can explain shared ervs by design. another possibility for the similarity between ervs and retroviruses is the fact that ervs parts can protect the cell from viral infections:
isnt it interesting?
How does that explain the nesting hierarchical distribution of ERVs in the genomes of different organisms? How does that explain the nesting hierarchical distribution of mutations in the retroviral insertion sequences? How does that explain the various and progressive stages of retroviral insertion sequence decay?
How parsimonious is your hypothesis here, in light of how frequently ERV sequences in genomes evolve to be come active viruses again, compared to how frequently viruses insert in the germlines of different species?
That straight up makes no logical sense. There is no reason, a priori, why the genes encoding a defense mechanism against viral infections, should exhibit any degree of sequence similarity to the genome of the virus above that of mere chance.
This is an example of how a little knowledge can be a dangerously deceptive thing. You know a bit, but you don’t know enough to know how little you know, and the little you know is such a tiny fragment it is misleading you. To pick just one example, you don’t seem to appreciate how many levels of data that corroborate ERV sequences being bona fide virus insertion remnant having been inherited through common descent. Your rationalizations here simply don’t work. They may sound superficially like they could explain the pattern, but any closer inspection shows that not to be the case.