No one doubts that retroviral insertions can incorporate features from the host genome on rare occasions. This also doesn’t change the fact that ERV’s come from viral insertions.
That doesn’t follow. In the scenario you are describing the ERV’s are still coming from viral insertions.
Yes, and it still doesn’t cast doubt on the viral origin of ERV’s. Can you tell us why expression of ERV genes casts doubts on their viral origin? Afterall, expression of viral genes in the host genome is part of the life cycle of retroviruses. It’s doing exactly what viral genes are supposed to do.
Bingo. We can add red herrings to the list of things in the DI arsenal.
It has always been interesting to see quote mines circulated within the YEC community. The Darwin quote mine about the evolution of the eye is still making rounds. Dawkins should do a study on memes in the YEC community.
ok. first i want to be in focus here. so lets deal with two points and we will go on to the other points of you want. as for the nesting hierarchical distribution of ERVs smong other species. we actually have several potential evidence that contradict that suppose hieirarchy, as you can see in fig s3 in this paper:
“While it is clear that this particular class of endogenous retroviruses shares a common origin, the retroviral phylogeny is inconsistent with the generally accepted primate species tree based on molecular data”
and: “First, we examined the distribution of shared sites between species. We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates”
but even if there was such hiearchy we can expain it by common descent for these apes (except for human under the non-common descent scenario), or by common design (say chimp and human share more ervs with each other because they are more similar to each other genetically).
so how you explain the fact that some specific ervs protect from the same kind of retrovirus?
no. what i suggest is that these viruses were created from the host parts. very similar to the mechanism of transposons.
i never said it is. i just pointed out that some ervs are similar to the retroviruses they protect from.
They didn’t find a single ERV that violated the expected species distribution in that paper at a resolution of one base. That paper is strong evidence for our side of the argument. Can you tell us why they couldn’t find one PtERV insertion that was at the same base in both the gorilla and chimp genomes, just as we would expect from the predictions made by the theory of evolution?
These are quote mines. Read the paragraph just before it:
What are the limits of the BAC based method? The resolution is in the 100,000+ base pair range, not the single base pair range. They break the genome up into big chunks and put them in plasmids which are propagated in bacteria. What they are saying is that the ERV is found somewhere in that big chunk of DNA, but they don’t know exactly where. That is not one base resolution, the resolution needed to determine if they are truly orthologous.
Of they potential violations at the BAC based level, all of the ERV’s they were able to resolve down to one base resolution were not at the same base. They were not orthologous. The placement of the others is not known, but the authors expect them to be non-orthologous.
The parts you quoted are examples of the authors acting as Devil’s advocate. It is dishonest to pretend as if the authors hold a position they do not hold. Again, it would serve you well to better understand the references you are using because you have once again offered up information that is very misleading.
Why? You don’t offer your reasoning here. Where are humans using these viral proteins in other functions? What use do humans have for viral envelope proteins, or reverse transcriptase?
That’s because THE ERV’S CAME FROM RETROVIRUSES!!!
They came from retroviruses. The restriction endonucleases are part of the insertion mechanism employed by retroviruses. They need to open up double stranded DNA in the host to insert their genome sequence. The genome sequence they inserts encodes the enzymes that cut open the DNA.
I like how that statement is simultaneously a straw man fallacy and exhibits good old dichotomous thinking.
The sentiment seems to be that for the synteny-based argument for common descent to work, it must be the case that synteny is completely unimportant and gene-order could be anything imaginable, but if gene-order is not then we should think it is absolutely one hundred percent constrained for functional reasons and any other order would completely break gene-function so it can’t be evidence for common descent.
Some therefore all. They do the same thing with ERVs, introns, synonymous codons etc. Nuance is completely absent in the creationist world.
are you saying that evolution predict that we will not find even a single “out of place”? because we actually do ( A HERV-K provirus in chimpanzees, bonobos and gorillas, but not humans. [Barbulescu et al. (2001)]
and yet scientists have no problem to expain it. so there is no real prediction here as you can see
and yet they are in very similar place on the genome. up to a tiny spot of 1/30,000 of the genome (100,000 bases out of 3 billion).
we actually do have evidence that these proteins (or variation of them) have functions in the cell:
so we have all the evidence we need to conclude that these retroviruses were created from the host genes. this is at least possible scenario that explain other things like the chicken and the egg problem (some species cant survive without ervs and retrovirus cant survive without host). its also expain why we dont find homologous for some ervs.
but how is that relevant to the type of virus that they protected from? i mean that if we have an erv of type A, that erv give a protection from a retrovirus of type A too. why it doesnt give a protection from other kinds of virus too but just from type A?
You are correct. However, scientists still think that both the 1-dimensional and 3-dimensional structure of DNA is important. It’s very strange that the DI would claim otherwise. The whole point of the paper they were referencing is the importance of large structural changes in DNA that could be important in evolution.
ILS and gene loss can produce anomalies, but as I stated earlier the noise should we swamped by the
This doesn’t change the fact that they were unable to find a single unambiguous orthologous PtERV insertion shared by chimps and gorillas in the study you were citing. You clearly quote mined that paper.
Similar is not a synonym for same. Orthologous ERV’s are found at the same locus, not in the same general area.
Or variations of them? Sounds like co-option to me.
We can directly observe retroviruses producing new ERV’s. You are forgetting about that.
I’m quite aware of that, thanks. My point is that synteny was neither discovered nor defined in a 3-dimensional context, only in the one, linear dimension.
And we can use extant ERVs in different species to reconstruct the ancestral sequences of ERVs, and lo and behold they look just like a retroviral sequence!
Exactly what would be predicted if they were retroviral genomes first, ERVs second.
Exactly. In the scenario we are describing, there is a functional retrovirus that produces the initial ERV and then mutations accumulate in that ERV over time. This moves the ERV away from the sequence needed for producing an infectious retrovirus. If you line up different ERV’s and get the consensus sequence you can remove those host derived mutations from the sequence, and what you get is a functional retrovirus.
This doesn’t fit with the scenario where the retroviruses are ERV’s first.
However, one could hope to find gene loss because the flanking sequences would not be expected to be perfectly restored to the condition prior to the insertion. Of course you need to sequence the area including flanking sequences in order to see that. (And there are a handful of cases in which it does look as if there’s been a perfect excision.)
so where is the limit? for instance: how many “out of place” ervs we need to find to falsify the common descent prediction?
to me its sound more like the erv first scenario. and we also have other evidence such as the lack of some viral homologous to the host ervs, and the chicken and egg problem (virus cant survive without host and vice versa in some cases). combine it with the fact that a tipical retrovirus contain only about 3-4 genes and its not hard to see where retroviruses come from.
as i said- we also see the opposite:
“Giant viruses have frequently taken up genes from their hosts by horizontal gene transfer”
why not? if that erv was functional in the past it will be just evidence for degeneration.
That’s not how it works. We see a strong tree like signal. We need an alternate model to explain this other than common descent. Failing to find one, no amount of exceptions to the rule will cause is to reject a model that explains so much of the fine grain detail of the data.
Remember we already know of actually mechanisms that allow horizontal transfer of genes so we expect some violations. We don’t expect a perfect tree. We do, however, demand an alternate mathematical model that works at least as well as common descent to move away from common descent.
