Back when I was a YEC a few years ago, I looked at Dr. Jonathan McLatcie’s work and debates. Keep in mind, he has a PhD in Biology PHILOSOPHY not SCIENCE. In my opinion, he is very deceptive in his arguments. He is interested in arriving at only one answer to any question regardless of the evidence.
At this point, I do not consider his material or arguments in any of my research. It is disappointing that someone who considers themselves to be a Christian to be so deceptive. I believe the deception is intentional.
This is the key point. Questions about function are irrelevant in this context because, functional or not, the presence of an ERV or transposon is an indication of a past mutational event.
I haven’t looked in primates, but I just checked one of my plant genome assemblies, and there well over 10,000 retrotransposons in that genome with intact target site duplications.
The TSDs are ~ 5 bp in length. Whether or not they are functional is, again, irrelevant. We understand the biochemical insertion processes that produce them. They are hallmarks of insertion mutation events.
Nobody is saying viruses can’t capture genes from hosts, or arise from combinations of host genes.
But what doesn’t make sense is to claim that independent creation of a functional organism necessitates the independent creation and insertion of hundreds of thousands of copies of entire virus genomes with essentially identical synteny and integration sites, in thousands of different species, such that they end up creating a nested hierarchy. Nothing about that makes any sense.
And it makes even less sense when we look at what the claimed functions of those obviously retroviral insertions even are. Often times they are claimed to be functional by creationists simply because somewhere within the ERV insertion (consisting of tens of thousands of basepairs of DNA, still clearly deriving from what used to be a functional retrovirus, but is now a mutationally decaying remnant of it) a regulatory protein has a mere 8-basepair binding spot, or a histone protein is detected transiently “parking” somewhere on it. Or the space provided by that ERV insertion slows down transcription of some gene. One again has to wonder why you need 30 000 basepairs of DNA that look like a dead retrovirus to park a histone protein on for a few microseconds, or have a regulatory protein bind and enhance transcription of some other downstream gene that has nothing to do with the mutationally decaying LTR-GAG-POL-ENV-LTR sequence it happens to bind to.
It doesn’t make sense. Your ad-hoc rationalization doesn’t make sense of the data. It doesn’t make sense of the integration site (none of the proposed functions actually require identical integration sites), it doesn’t make sense of the nested hierarchy (similar anatomy does not necessitate similar gene sequences), it doesn’t make sense of the biochemical distribution of mutations we see in the ERV sites, it doesn’t make sense of the size of ERV insertions in relation to the functions they are proposed as having(you don’t need tens of thousands of bases encoding nonfunctional reverse trascriptases to park a regulatory protein), it doesn’t make sense of the sheer number of them, and it doesn’t make sense of the actual sequences they have(being obvious retrovirus genes). What does reverse transcriptase (POL) do? It is an RNA-dependent DNA polymerase, it transcribes RNA back into DNA, and has an associated integrase function too. A virus has a use for that, the human genome does not have a use for a million of those. Much less does it need a million of them where most of them have lost the ability to function. What do GAG proteins do? ENV? They form retroviral cores and package the viral genome, and form envelope proteins? Nope, need a million of those too, in the same gene-order observed in actual retroviruses, flanked by LTRs also.
Your rationalization is nonsense. To the point of being idiotic. You’re not really dealing with the data. You’re just inventing various mutually incompatible, ad-hoc excuses to try to explain away obvious evidence for a deep and shared evolutionary history of life. It’s utterly ridiculous. It can’t be entertained by a thinking person.
Err…the retrotransposons I’m referring to are long terminal repeat retrotransposons, which are very similar to ERVs. To the extent that ERVs are often classified as a subset of long terminal repeat retrotransposons.
in addition, what is your logical explanation that ERVs cant survive without the host and vice versa?
lets assume for the sake of the argument that all these ERVs are indeed the result of viral insertions. how many of them we can get at the same spots without common descent? if we cant make a prediction about that, then the argument is meaningless.
Oh, there’s actually way more than 10,000 LTR retrotransposons in the genome assembly I’m working on. Those that I mentioned before are just the copies that are structurally intact.
Sigh. This point has already been addressed at length in this very thread, including citations to the primary literature that is directly related to your question.
And how dishonest Edgar is. The talk.origins article says this: "There are at least seven different known instances of common retrogene insertions between chimps and humans, and this number is sure to grow as both these organism’s genomes are sequenced". It was written before the chimp genome was sequenced, when we simply did not know how many shared ERVs there were.
McLatchie’s article was written after the genomes were published, and he must have known his data was out of date, but chose to use it anyway.
Edgar is citing it a decade later. He knows full well that the number from the t.o. article predates finding out how many shared ERVs there actually are, but is using it anyway.
Some - therefore all hasty generalization again. It a basic fallacy, and doesn’t make sense of the data.
These genes are derived from ancient retroviral insertions, clearly distinguishable from most actual ERV insertions which contain mostly dead and/or inactivated ENV genes. It’s right there in the abstract. Of course, these genes are actually evidence for evolution, and they explain how those genes evolved: from retroviruses.
Finding that there is a class of genes that evolved from ancient retroviral insertions hundreds of millions of years ago doesn’t show that dead ERV insertions aren’t dead ERV insertions.
Did you even read these papers?
In any given species, the vast majority of ERV sequences appear to represent biochemically inert genomic material evolving under no selective constraint. Biochemical repression is imposed by host cellular machineries that appear to be dedicated to silencing the expression and proliferation of both exogenous and endogenous retroelements (2). Failure to muzzle ERV expression leads to rampant deregulation of the genome with likely deleterious consequences (2, 3).
While these observations indicate that ERVs represent a threat to the integrity of genome function, there is also growing evidence that a fraction of this virus-derived genetic material has been adopted during evolution to serve beneficial functions for their host.
It’s a parasite, of course it depends on the survival of the host for it’s own survival. It’s like asking how to explain how humans survive when we need to eat other organisms to live? Well we live by eating them.
If there is an example or an ERV that contains sequences that have somehow become essential to the survival of the organism, then so what? How does that contradict anything I’ve said above?
i think that reference ignore the possibility that the majority of the genome isnt junk. under that notion (say that about 100% of the genome is functional) the probability to get many insertions at the same site is probably high, since there are only few places in the genome that a virus can insert itself without harmful result.
i never said that most of these ERVs are functional. i actually think the opposite. but if some of them are functional then most of them could be functional in the past.
so how it evolved in the first place? you need to assume that this virus could survived by its own somehow. this is why many biologists think that virus origin is from host genome. and they arent creationists.
so what? so how the creature survived before it got that insertion? this is the chicken and the egg problem.
Sure, they were functional(and useful to the viruses they came from) when they were viruses, or when they were still-active transposons.
Ultimately all ERV insertions, whether from viruses or transposons, or transposons that derive from viruses or viruses that derive from transposons, used to be functional at some point in the past, and by that I mean useful to the entity they derive from(either useful to the virus itself, or to the transposon).
But mostly they’re not functional now. And they constitute evidence for evolution in different ways. Some small fraction have subsequently evolved to become useful to the function of the organism they originally infected by mutating and interacting with other normal organismal functions, while others became nonfunctional remnants that have decayed to mutations and no longer are able to perform any functions. Some can still be active, but are suppressed or silenced by host defenses because they interfere with other useful cellular processes.
This has been answered a million times. It became critical to survival. It used to just be beneficial (A helped B perform it’s function, but B could do it by itself), but circumstances changed so it became essential (B lost the ability to function without help by A, so now A, which wasn’t originally critical for function, became essential).
My goodness. It does not appear that you have read the paper at all. Your willingness to speculate seemingly endlessly without regard for the actual evidence is contributing nothing to this conversation.