I am a layman who is agnostic about religion, but has something like 90%+ credence in common ancestry.
One of the more powerful arguments I’ve seen in favor of common ancestry is the existence of similar retroviral DNA in related species (e.g. humans and chimpanzees). As I understand it, the standard explanation for this is that a virus (1) entered the DNA of one or more members of the parent species, (2) spread throughout the population of the parent species primarily due to selective pressure, and then (3) was passed down into the DNA of the daughter species.
My question is a devil’s advocate question. Specifically, if in (2), the retroviral DNA could only spread throughout the population of the parent species due to the presence of selective pressure, why couldn’t an (old earth) creationist claim the following alternative explanation for retroviral DNA: the virus (I) entered the DNA of members of similar, but distinct species A and B, (II) spread throughout the populations of both species primarily due to selective pressure (and it could do so because the two species have similar DNA), and then (III) was passed down into the DNA of current members of each species.
For example, the retroviral DNA we find in humans and chimpanzees today is pretty widespread in both species, which suggests it provided an evolutionary advantage in the past. So is it possible that it simply infected both humans and chimpanzees (separately) in the past, and then spread throughout both of the two distinct populations because it provided both of them with an evolutionary advantage?
I suspect there are good answers to this question. I’m just looking to learn what they are.
NOTE TO THE MODERATORS: I did search for an answer to this question in the forum. I found several discussions about retroviral DNA, but it looks like they did not address this specific question (unless I missed it).
I think this paragraph reveals some confusion and incomplete knowledge. First of all, it is not merely the “existence” of similar retroviral sequences in humans and other apes that constitutes evidence best explained by common ancestry. It is the nearly complete conservation of the exact locations (in the genome) of these elements. Second, “primarily due to selective pressure” is almost entirely the opposite of the “standard explanation.” Individual retroviral insertions (by the millions) were almost certainly ignored by selection in the vast majority of cases. The exceptions (e.g. retroelements that were co-opted and “domesticated”) are extremely interesting but rare.
So, unfortunately, in order for the “alternative explanation” to have any credibility, it would have to overcome the fact that retroelements unique to apes exist in the millions (look up Alu elements), are distributed in almost completely identical patterns/locations in humans and chimps (for example), and are not known to depend on the “presence of selective pressure” for their presence in genomes and at those precise identical locations. Those facts are the facts explained by common ancestry; again, it is not the mere presence of retroelements that are “similar” that makes common ancestry shine through.
To be clear, I don’t mean to suggest that Alu elements are all invisible to selection in all cases; we know of interesting examples of retroelements that affect gene expression and that we can assume exert influence on selection. My guess is that this applies to less than 1% of retroelements, but that’s just a guess. And I’m focusing on Alu elements because they are so young, and so interesting, in human phylogeny. I hope you see what the alternative hypothesis would need to accomplish.
My suggestion is to read about the elements themselves, and to revisit your assumption about “selective pressure.” Maybe the “alternative explanation” can be tweaked to make some sense. I doubt it, but it’s worth having a fun conversation about.
Thanks, Stephen. That’s extremely helpful. I hadn’t fully appreciated the point about the retroelements appearing in the same locations previously. One follow-up question: If the retroelements we observe today in both humans and chimps are not fixed primarily as a result of selective pressure, why are they fixed? Is it simply because, out of the extremely large number of historical retroviral insertions, some small subset will by pure chance become widespread?
To emphasize part of @sfmatheson comment: That is not the standard explanation.
The explanation is more like this:
A population of organisms is subject to retroviral infections.
A proportion of these infectious agents undergo mutations such that they are inactivated, and remain as “fossils” of viruses in an organism’s genome.
These “fossils” (aka ERV’s) remain dormant in the genome and spread thru the population primarily thru genetic drift, since they perform no function.
The fact that identical ERV’s are found in identical genomic loci in different species, then, indicate that these species shared a common ancestor, since that is the only plausible explanation for why these pieces of junk DNA would be shared in common. It is precisely because they they are not subject to selection that they provide such strong evidence for common ancestry.
In other words, the vast majority of retroviral insertions quickly disappear from the gene pool, and what we see are the tiny fraction that happen to drift to fixation. The small number that were subject to selection were most likely to have been deleterious, because they broke a gene in half, for example, and so mostly disappeared even faster than the ones subject to drift.
Hi Joshua! Welcome to the forum. The reason why this scenario isn’t the case is because ERVs appear in the same locations in the genomes of both humans and other apes.
For more, see this thread, and especially this series of posts from that thread (also this). Simply put: the chance of this occurring randomly, on terms most favorable to creationists, is less than 1 in 10^1,000,000. No that’s not a typo.
How do you know they perform no function?
For example, on the Eiffel Tower, 2.5 million rivets assemble 12,000 metal parts. Do you think that because it would be possible to remove a few rivets here and there with no observable effect on the building, it would be legitimate to conclude that these rivets serve no purpose?
All the usual evidence for ERV insertions being mostly junk DNA. In the case of ERVs they’re also often specifically actively silenced to prevent them from having any latent activity that might disturb cellular processes.
For example most members of the HERV-K family of ERV insertions are actively kept silenced (this is true for basically all ERV families; a few are functional, the rest are actively kept in a repressed state), and when they nevertheless occasionally become active (when the silencing mechanisms are disturbed or stressed) they can contribute to some cancers.
Some of them certainly have a function, such as the long terminal repeats at the ends of ERVs functioning as promoters and enhancers of nearby genes. There’s also ERV involvement with syncytin proteins of placental development which has benefits for the mammalian placentas. [By the way, The Mammalian Placentas was the name of my post-grunge rock band in the late 1990s.] There are certainly others but I am not qualified to try to put a number on the percentage of ERVs with functions described in the peer-reviewed literature.
That said, as a former anti-evolution Young Earth Creationist—a very long time ago—I understand the popularity of irrelevant analogies to the community. (I admit to emitting a quiet groan upon reading the Eiffel Tower missing rivet analogy for the thousandth time.) And as much as I have grown weary of such PRATTs, I think there is much benefit to seeing several of our regulars here at PS step up for some batting practice and hitting that ball into the center field stands. (Yes, I’m lazy and I enjoy watching the pros do it so well.)
We know exactly what the function of rivets are. Further, we know what a margin of safety is, and so removing rivets does affect the tower.
We also know that ERV’s are genetic material from viruses, where they to served the interest of the virus; thus known function. Generally, a host has not been waiting around to get infected in order to remedy some genetic deficit, so neutral viral insertions are just tag alongs, not fulfilling any function for virus nor human.
We see this happening right now in a big way with the koala retrovirus. Do you suggest that there is some unknown but essential function being supplied to koala’s by this viral invasion? Or to come to the ID implication, do you contend that the epidemic is necessary to koala design?
Let’s adjust your metaphor a bit. Suppose that instead of connecting two parts, those rivets were randomly scattered over the structure, generally just making holes in a single part or lying on a surface. Suppose you saw a tourist throwing handfuls of rivets onto the tower. What would you conclude then?
Of course the best Eiffel Tower analogy comes from Mark Twain. Let’s see it again:
“Man has been here 32,000 years. That it took a hundred million years to prepare the world for him is proof that that is what it was done for. I suppose it is. I dunno. If the Eiffel tower were now representing the world’s age, the skin of paint on the pinnacle-knob at its summit would represent man’s share of that age; & anybody would perceive that that skin was what the tower was built for. I reckon they would. I dunno.”
I am a bit disappointed to learn that I am not the first one to have used this analogy for Alu elements . I should have reminded to myself ECCLESIASTES 1:9!
No, I am pretty sure that you could remove rivets without being able to see a change of the tower phenotype.
Velcro is another analogy that may help. Velcro consists of two complementary components: one with tiny hooks and the other with soft loops. Do you think that by removing one hook or one soft loop in a Velcro would impair the system? Yet, that doesn’t mean that these elements have no function, does it?
Are you saying that the Alu elements are randomly scattered over the genome? If yes, how do you know? For example, abundant content of CpG dinucleotides are found in Alu elements, contributing to up to 30% of the methylation sites in the human genome. So wouldn’t be possible that these elements play an important role in regulated chromatin organization and dynamics?
For one thing, we know how they get inserted. They weren’t put in there at the creation, you know.
You can make up any story you like, but Alu elements are just a recently active family of retroposons that are inserted in various different locations in various primate species. Why, the insertion locations even form a nested hierarchy. If this is design, it’s an odd sort that perfectly mimics common descent. But of course you’re a YEC, and you have to ignore that sort of hypothesis.
The vast majority were fixed in a common ancestor because they were there and didn’t do enough harm to be seen by negative selection. This is what biologists call “genetic drift.” Especially in slowly-reproducing animals that exist in relatively small populations (humans are both), drift is a strong influence on evolution. If you want to learn about this phenomenon and ongoing theory work on its influences, read a little on the drift-barrier hypothesis. (Here is a recent interesting technical paper on related subjects.)
But the basic answer to your question is: when a driblet of DNA gets fixed, this means simply that it exists in a piece of a genome that became so widespread in the population that it was the new normal. That driblet could have exerted zero selective influence, or it could have exerted some positive influence, or it could have exerted negative influence that was counteracted by neighboring driblets with positive influence, or it could have exerted negative influence that wasn’t enough to make a difference in a smallish population at a particular time in history. John Harshman added the very important point that many of these rogue elements landed in a gene and generated a strong negative selection pressure/event that was “visible” to selection but not to us, due to a highly complex technical process called “death.” (Or “failure to reproduce” if we want to split the hairs our species lost along the way.)
In short, when a DNA driblet (or larger genomic section) gets fixed, the story can range from high drama (a selective sweep! ) to utter tedium (just another piece of retroviral debris picked up on the road to Canterbury ).
I can’t help but mention that in the case of The Canterbury Tales there were scribes long ago who introduced changes in Chaucer’s text. Those insertions—via what I will call “literary genetic drift”—became “standard” over time and simply got automatically carried along with the text, even when copyists suspected they were not part of the original Chaucer text. (They didn’t want to tamper with it.)
Of course, I suppose it is possible [wink wink] that Chaucer himself put those odd snippets into his text in such a way that they appeared to be later insertions, even making some of them stylistically odd in order to confuse modern scholars. Yeah, I bet that is what happened.
. I should have reminded to myself ECCLESIASTES 1:9!
) to utter tedium (just another piece of retroviral debris picked up on the road to Canterbury 
).