Hi. 
Thanks for the message.
It’s actually irrelevant if it’s shown to have a function. It’s still evidence for common ancestry. Since the ERV has been inserted it can later evolve a new function. For example, picture a broken mouse trap, it can still be used as a tie clip, or a door wedge. it’s still obviously a mouse trap that being used for a different purpose. So the ERV is clearly an ERV insertion, but it’s taken on a new function. Even then it doesn’t mean they all have functions. 
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Yes and no. The gag-like protein did originate from a retroviral genome, but it was moved about the genome as part of a transposon.
Correct. ERV’s are evidence of common ancestry because of their location in the genomes of various species, the distribution of orthologous ERV’s, and the sequence divergence between and within orthologous ERV’s. Orthologous ERV’s are retroviral insertions found at the same location in two genomes. At no time were ERV’s said to be evidence of common ancestry because they lacked function.
That is a very good analogy.
Since lack of function was never cited as evidence for common ancestry, they are barking up the wrong tree from the very start. But yes, your analogy is still good.
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Correct. Fallacies of composition are a huge part of the IDcreationist rhetorical toolbox, because real-world biology is full of exceptions to rules. They try to convince you that because a few (not even some) ERVs (or stretches of junk DNA) are shown to have function, that those conclusions apply to a vastly larger set.
And right on cue…
There’s someone who’s been bamboozled by such rhetoric, now pretending that we scientists are misinforming people without providing a smidgen of evidence. Note how she implicitly claims to know as much as scientists do!
When faced with ICcreationists claiming that some demonstration for a tiny subset applies to the whole, there are two obvious questions one should ask:
- Did IDcreationists do the experiments that IDcreationists are touting? If not, why not? Don’t they claim to have all sorts of scientific qualifications?
The answer, of course, is that they didn’t do any of it, leading to the question:
- If we scientists truly are so smugly certain (as @thoughtful falsely claimed) in judging all (or even most) ERVs (or junk DNA) to be nonfunctional, why would any of us have done those experiments in the first place?
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So I may sound like I’m repeating myself but just need to clarify if I may. Creation.com article said:
“Earlier … I argued that the origin of RNA viruses can be understood as genetically modified ERVs which acquired virulence genes and thus became disease-causing agents. The ‘VIGE-first hypothesis’ holds that RNA viruses have their origin in ERVs, and that ERVs were created for/with a purpose. ERVs are made of two genes, gag and pol , which are also found in all modern RNA viruses.”
This isn’t entirely true is it? ERVs are made of two genes, gag and pol and ENV. Although I’m
not sure if this is relevant to my point.
“This fact is also the most vital argument for why endogenous retroviruses are always interpreted as remnants of ancient genomic invasions of RNA viruses. The pol gene encodes a large protein with four distinct enzymatic activities: a protease, a reverse transcriptase, an RNase, and an integrase. To produce the individual proteins, the protease, which is synthesized first, proteolytically releases the other three enzymes from the precursor sequence. The transcribed, full-length ERV RNA then functions as a template for reverse transcriptase, the enzyme that catalyzes the synthesis of a double-stranded RNA-DNA hybrid.
Next, the RNase enzyme removes the RNA part, and the remaining single-stranded DNA forms a circular molecule. This circular single-stranded DNA serves as a template for the synthesis of a second DNA strand. The double-stranded DNA copy can now be put back in the genome with the help of the integrase enzyme. The position where this happens is determined by repetitive DNA sequences flanking the ERV element and/or by the sequence specificity of the endonuclease (integrase). Alternatively, the RNA molecule can be packed in a capsule consisting of three proteins, which are specified by the gag gene, and the whole thing looks very much like a virus. Why this packaging is necessary is unclear, but it may prevent the RNA molecule from docking to the wrong places in the cell. On the other hand, the protein-coated viral-like particles may contain biologically active molecules which have to be protected and/or delivered to the right places. In other words, we are dealing with a subcellular transport system.”
Is the author simply giving a description of how ERVs become integrated into the genome? Or is he talking about something else entirely unrelated to ERVS? If he is talking about ERVs then why does he say “the whole thing looks very much like a virus” rather than it is a virus as I thought ERVs were viral insertions. Unless it’s because ERVS aren’t themselves viruses, but are more closely related in their nucleotide sequence to known viruses than to anything else we know of.
“In 2018, two publications addressing this possibility appeared simultaneously in Cell . Neurons use a virus-like construct to pass on messenger RNAs that code for the building blocks of that virus-like construction. These building blocks are known as activity-regulated cytoskeleton-associated protein (ARC). Although the ARC protein was for a long time suspected to be involved in learning and memory processes, nobody knew how or why. ARC is homologous to the gag proteins, which are found in all RNA viruses and ERVs. Although ARC is required for synaptic plasticity and cognition, and mutations in this gene are linked to autism and schizophrenia, its biological function is largely undefined.
The publications in Cell now shed some light on this matter. Jason Shepherd and colleagues from the University of Utah, USA, transferred the ARC gene into bacteria, and observed that ARC proteins self-assemble into capsids which look very much like virus coats. The researchers concluded that that neuronal ARC gene encodes a repurposed retrotransposon gag protein that packages intercellular RNA to mediate intercellular communication in the nervous system. Purified ARC capsids are taken up and transfer ARC mRNA into the cytoplasm of neurons. Apparently, the neurons need ARC in such large amounts that they require a special delivery system. Furthermore, these results show that ARC exhibits molecular properties similar to those of retroviral gag proteins. Of course, the authors spun an evolutionary story around their findings, claiming that ARC is derived from a vertebrate lineage of Ty3/gypsy retrotransposons. In a comment on a Dutch media site, Shepherd admitted: “Other neuroscientists would have laughed at me if I had claimed something like that before.” His response identifies the junk DNA hypothesis of the Darwinian paradigm as a science stopper, and shows that questioning junk DNA still induces scoff and laughter from a scientific community blinded by the erroneous idea that our genome is made of viruses.
In the same issue of Cell , a research group from the University of Massachusetts further disclosed another function of ARC proteins.16 They discovered that the motor neurons of fruit flies control muscles by releasing extracellular vesicles which are packed with ARC capsids. Here too, the ARC protein forms capsid-like structures. They bind dArc1 mRNA in neurons and they are uploaded into extracellular vesicles that are transferred from motor neurons to muscles. The more active the neurons are the more capsids are delivered. These results point to a trans-synaptic mRNA transport mechanism involving retrovirus-like capsids and extracellular vesicles. The paper also reports how cultured genetically modified mouse neurons, which do not express the ARC gene, integrated ARC capsids and started to use the delivered ARC mRNAs. Again, we see a sophisticated delivery system at work, not viruses. The researchers asked whether this form of transport may also play a role in the delivery of additional mRNAs and proteins, and perhaps may promote the spread of Alzheimer’s and other neurological disorders.”
I may be talking utter nonsense now as I’m way out of my depth, but the author says that “ARC proteins self-assemble into capsids which look very much like virus coats.” Does this means that ARC proteins that self-assemble into capsids look like ERVs, and have a gene sequence almost identical to know viruses in the same way that ERVs do?
“Considering these novel facts, we are compelled to also ask whether the ERV system itself is some sort of common delivery mechanism, since ERV-like vesicles readily leave and enter cells of the placenta.”
Is the author trying to extrapolate from the finding that some ERVs have a function to saying that all ERVS have that same function, and were designed to do that function.
“Unfortunately, nobody is really interested in studying this fascinating possibility. Still, it has recently been reported that ERVs can act as DNA regulatory elements as long non-coding RNAs, and as triggers for the innate immune system. ERVs in the human genome are able to bind ‘signal transducer and activator of transcription’ 1 (STAT1), an effector of the interferon (IFN) pathway involved in immune responses. The enrichment of ERVs in IFN-regulated genes suggest that they play an active role as regulators of essential immune system genes.”
This is irrelevant because, as you said previously, lack of function was never cited as evidence for common ancestry, so finding a function is irrelevant. They are barking up the wrong tree from the very start.
That’s not always a correct characterization - if they cite sources that indicate that there may be function in a larger set, it’s not a fallacy of composition. One example: Toppling Another Evolutionary Icon, ENCODE Data Suggests Endogenous Retroviruses Are Functional | Evolution News
Or creationists should at least be clear it is only a hypothesis that most have function.
Should I read this sentence that way?
But to answer your question - I think it’s because other scientists aren’t so certain, they are curious, and they would like to be the first to discover function where it was unknown.
As far as I can tell, from thinking only protein-coding genes were important to continually finding more function throughout the genome when researching specific questions. I tried to find a good article on it.
Or that it could be relevant during embryonic development and silenced otherwise?
If I’m mistaken on that, then please explain.
My own experience here, then reading creationists who mention history of science, then reading popular articles that say the same thing no one here mentioned.
I’d like to hear about some examples of this history of what people used to know or believe about the function of the human genome and how that’s changed over the last few decades, that you think people here won’t readily admit that we don’t know.
And I’m sure you can find popular articles saying things people here disagree with, among other things because as we have established popular articles are often time excessively grandiose and misleading in ways the data they are based on cannot support. But it seems to me that’s a problem with popular articles, not with the people here.
So please elaborate with some examples.
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In this case, it is.
A nonexpert is citing an overinterpretation that has been walked back, not a source. You really should stop doing that and cite evidence instead labeling a hyping of a discredited interpretation as a source.
Do you realize that what you’ve described as filtering the evidence by worldview is, in your case, really ignoring the evidence in favor of hearsay?
That article is very deceptive. The writer is not reliable. He has never done any biology. Why would you cite him instead of citing the evidence?
Why would you rely on someone with a BS in geology from UCSD as an authority?
Why would you NOT rely on someone with a PhD in virology from UCSD plus half of his postdoc in retrovirology at the National Cancer Institute as an authority?
Do you see how you are making my point for me?
It’s perfectly true and properly qualified.
After my PhD, I did a postdoc at the National Cancer Institute in which I studied a recently inserted ERV in detail. Do you and Casey Luskin understand the field better than I do?
And don’t forget that despite my expertise, I am counseling you to get into the actual evidence instead of hearsay. Why are you so reluctant to do so?
I see plenty of uncertainty expressed in Taq’s statement. However, what we are certain about is that IDcreationists frequently use deliberately deceptive rhetoric.
That couldn’t be more ridiculous.
You are invoking a fallacy of composition, the IDcreationist trick of conflating “noncoding” with “junk.” I’m pretty sure that the falsehood of that conflation has been explained to you in detail here. Why do you continue to employ it?
Answering these questions will reveal the fallaciousness of your conflation:
- Are promoters and enhancers protein-coding?
- Do promoters and enhancers have function?
- In what year was the first promoter characterized?
- Are ribosomal and transfer RNA genes protein-coding?
- In which years were they first characterized?
- Are miRNAs and lncRNAs protein-coding?
- What does the “nc” in “lncRNA” stand for?
If you’re going to accuse us of being dishonest, you’ll need to dive into the evidence instead of hearsay. That, of course, involves risking learning that you’ve been fooled. Are you as curious as you claim to be in your handle?
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Based on the first few sentences, you failed. Nobody ever thought that non-coding DNA was synonymous with junk. The first formal definition, by Ohno, wasn’t about coding vs. non-coding. The article encapsulates a common misunderstanding of the history of science.
I recommend a course of Larry Moran, stat:
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No.
If it has any effect at any time, the association will still be detectable by genome-wide association studies.
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By saying only protein coding genes being important I’m going to assume you mean they used to think all non-coding DNA was unimportant in the sense that it had no function and was therefore useless junk.
But this was just never ever the consensus view of the field. It’s pseudo-history to toss out the claim that that was ever the normal thinking of the field. I’m not even sure there was ever really a single person who seriously thought that any sort of DNA that didn’t code for proteins was functionless junk.
In fact, they used to argue against the idea that junk DNA could even exist but for brief moments(on evolutionary timescales) by invoking natural selection. The argument was that carrying around excess nonfunctional DNA would be metabolically costly, and so deletion mutations would be favored leading eventually to no(or very little) junk DNA.
And that popular level article is really crap and doesn’t give a correct history of the field. What’s worse is it seems to be riddled with the authors own characterizations and his own misunderstanding of the difference between junk DNA and non-coding DNA. He seems to casually refer to non-coding DNA as junk, but that was just never the consensus of the field.
No wonder you think what you do when you are so misinformed by that pseudohistorical crap.
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If I understand you correctly, you’re not filtering any actual evidence with your worldview, just filtering hearsay and choosing the hearsay that you wish to be true?
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How weird. You provided an example of exactly what @Mercer was talking about, and talk as if you were disproving what he said. Can you explain why you did that?
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It is and that was me several years back. I am glad I got intellectually liberated.
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I’d be satisfied with a description of HOW she did that. 
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The viral origin of ERV’s is further supported by sequence divergence and species distribution, both of which indicate an insertion of sequence at various times in history. For example, PtERV insertions are only found in gorillas and chimps. Given the known phylogeny, we would expect these insertions to NOT be orthologous, and they aren’t. We would also expect a rough correlation between the sequence divergence between the 3’ and 5’ LTR’s and the number of species that the orthologous ERV is found in. We observe this as well. We would also expect to see a phylogeny based on ERV sequence divergence to mirror the phylogeny based on morphology, and we see that correlation as well. All of these pieces of evidence point to a convergence of sequence to a single insertion event in a common ancestor followed by subsequent divergence due to mutation and speciation.
I already covered this. The virus inserts randomly across the entire genome, not in one spot.
Again, we can observe retroviruses producing new ERV’s in real time in both the lab and in the wild.
the ARC proteins look very much like the proteins that coat viral particles. That’s what the author is saying. Since the gene ultimately came from a virus, this isn’t too surprising.
The author is trying to claim that a creator put them in the original genomes with a function, which is just silly. It’s a bit like saying God created the Earth with what we call fossils which are really just rocks that happen to look like animals and plants. It’s an Omphalos claim.
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Another way of putting it is that the ERV phylogeny can be superimposed on the species phylogeny. This is true for gene phylogenies as well.
Correct. The repeats come from the viral genome, not the host.
Heck, I’ve even made it happen experimentally, by mutagenizing mice to revert a single-base mutation that prevented the gag protein from being made:
https://journals.asm.org/doi/epdf/10.1128/jvi.64.5.2245-2249.1990
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So ERVs don’t resemble ARC proteins? This probably sounds a ridiculous question but as I said before I’m still pretty new to this.
ARC proteins resemble viral proteins found in active retroviruses with the ARC proteins most likely being modification of viral proteins from retroviruses. To use an analogy, does this doorstop resemble a computer or do computers resemble doorstops?
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