Hey I like how SCD is counting changes on a tree by using a ruler. Gotta admit that’s creative thinking right there.
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The mutation rate isn’t the same throughout the genome, so there’s no reason to expect that pairs of LTRs from different ERVs should accumulate mutations at the same rate. The 5’ and 3’ LTRs of a single ERV will usually mutate at roughly the same rate though, which is why they can be used as molecular clocks successfully, as illustrated in this table, from the paper by Johnson and Coffin (1999) posted earlier in the thread.
That being said, I probably would expect there to be a general trend between ERV age and the total number of accumulated mutations, but you’d need a lot more than 9 data points to assess that rigorously.
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Looks like the paper explains some of the discrepancies. I don’t know that much about ERVs. Why should the 5’ and 3’ LTRs begin diverging at the point of insertion? Do they begin as identical? Why?
Based on the filename, I think it have something to do with Pokemon. 
The process of converting the single stranded RNA genome to a dsDNA genome results in identical LTR’s. It’s pretty complicated, and I won’t pretend to understand all of it, but it is covered in this paper:
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That’s complicated. And weird.
But it does explain why the 5’ and 3’ LTRs have to begin identical when the 5’ LTR serves as template for cDNA synthesis, and the 3’ LTR serves as a later binding spot for this same cDNA. Super weird process.
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Yeah, that’s what I’m discovering right now. My first foray into bioinformatics, as a total noob, is transcript discovery in an adenovirus strain. Putting shredded documents back together is child’s play compared to that. Retroviruses are very complex and weird, and much of it is probably due to the strict size constraints put on the genome by the viral capsid.
Looks like the 5’ and 3’ LTRs are both copied from the same template on the minus strand. The plus strand gets moved (in F) to the 5’ end and a new 3’ plus strand is then copied from the minus strand, while a 5’ minus strand is copied from the plus strand. Again: complicated, weird.
its a possible explanation, although the paper says:
“The distribution of an ERV among related species also reflects the age of the provirus: older loci are found among widely divergent species”
actually about 50% of the ERV’s they checked show a wrong phylogeny.
since they picked them randomly they should represent a true phenomenon.
No, you comparing different ERV loci to each other is not a “possible explanation” whatever that even is supposed to mean. What you did to try to argue against the line of evidence deriving from increasing divergence with age was incoherent, and does not actually constitute a meaningful rebuttal do that evidence.
Actually it’s 40%, not 50%, and for multiple reasons they’re not evidence against common descent. First of all some of them are still close to the canonical phylogeny, with several of them only having 1 misplaced branch. So their degree of mismatch is low. And then the authors of the paper also goes on to explain several issues with deriving phylogenies from these ERVs, for example that 12Q24 lack a 3’ LTR for outgroup rooting, in effect showing why they deviate and why this isn’t a problem. You should read it.
Another fundamental problem you need to wrap your head around is the concept of noise in data, which may result in loci that fail to provide evidence for common descent. But a locus that fails to provide evidence for common descent, isn’t evidence against common descent.
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6 out of 15 is not 50%, but as could be gleaned from simply reading the title of the paper, these can readily be explained by ectopic recombination.
That’s irrelevant. Even 9 randomly picked examples aren’t guaranteed to reproduce the general trend among thousands. Do you think if you polled 9 random Americans, you’d be able to predict something as simple as an election outcome, or anything else for that matter? Sample size matters.
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i actually meant that your explanation is possible. so we dont disagree here.
i refer to 2 papers on that topic. as far as i remember 10 out of 21 cases show a wrong phylogeny.
there are of course many problems with ERVS in general. for instance some ERVS lack any viral homologous. this make sense if retrovirus evolved from ERV and not the opposite. another point is that some creatures cant survive without some ERVS. again this make sense if retrovirus evolved from ERV. by the way there is also the possibility of convergent insertions among the entire genome.
This doesn’t make any sense. Could you explain this?
Why couldn’t an ERV be produced by an infection and then evolve a function afterwards?
What is the probability of this happening? Where did you get your info, and where’s the math?
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Very low, but not nonexistent. Not quite the same thing, but close enough, I think: there is one example of a retroelement insertion that seems to have happened identically and independently in two distantly related bird taxa. Still, definitely a low-frequency event.
Han, K.-L., E.L. Braun, R.T. Kimball, S. Reddy, R.C.K. Bowie, M.J. Braun, J.L. Chojnowski, S.J. Hackett, J. Harshman, C.J. Huddleston, B.D. Marks, K.J. Miglia, W.S. Moore, F.H. Sheldon, D.W. Steadman, C.C. Witt, and T. Yuri. 2011. Are transposable element insertions homoplasy free?: An examination using the avian tree of life. Systematic Biology , 60: 375-386.
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Those are my conclusions as well. I don’t know of any mechanism that would result in >99.9% of independent insertions occurring at the same loci. Could 1 out of 200,000 happen at the same base? Possible. I have seen creationists try to argue for independent insertions, but the references they use have all shown just the opposite. I think this is why they are trying to go down the “but a handful of ERV’s are function!” route because the other counterarguments have been thoroughly debunked.
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yes. if a retrovirus evolved from an ERV we might find an ERV without any viral homologous. since not all ERV evolved into retroviruses yet. this make sense if the viral origin was the genome itself.
but how the creature survived till it got that infection?
i dont know and i think that nobody know. thus i think that we cant realy reject this possibility. but here is something to think about: we do find at least few ERVS that are very close to each other in the genomes of several creatures. so its clear that many infections are not even close to random event.
Or the virus is no longer circulating.
The evidence for ERVs being the result of an exogenous retrovirus are two-fold. First, when you take the mutations out of the ERVs you get a functional retrovirus, as is the case for HERV-K insertions. If ERVs were giving rise to retroviruses then we shouldn’t need to remove mutations to get them to work. However, if ERVs did come from exogenous virus in the past then we would need to remove the mutations that have happened since insertion to get a functional virus. That’s exactly what we see.
Second, the flanking LTRs are consistent with insertion of an exogenous retrovirus. When the RNA genome of a retrovirus is reverse transcribed into a DNA provirus it has specific features at both ends of the genome, and ERVs have those features. This was discussed in my post (#24) above. The U3-R-U5 arrangement of the LTRs is what we would expect from an inserted virus.
The same way people survive retroviral infections now.
People do know. We can track retroviral insertions as they happen, and they don’t insert into the same position at the rate necessary to get greater than 99.9% of 200,000 insertions to happen at the same position in independent insertions.
Don’t forget, we can watch retroviruses making new ERVs right in the lab. It seems that the only reason you are rejecting this mechanism is that it leads to conclusions you don’t like.
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That was a confused answer, to a question that wasn’t asked. The answer of how a species survived without a retroviral insertion that’s now functional, even now necessary, is that it wasn’t necessary when the insertion happened but evolved to be that way. In other words, it’s the same answer as applies to irreducibly complex systems.
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unless they were degenerated because of mutations. another explanation is that these ERVs are actually protect from viral infections.
LTR has function related to gene regulation. thus it can be a functional part of a genome, just like any regular gene.
the problem is that there is no real evidence to show how such a system could evolve . on the same base that we dont have any evidence that the loch ness monster is real.
so lets try to calculate it. base on your calculations, what is the chance to get 2 independent insertions almost in the same location? (and when i say “almost” i refer to a chunk of about 100k bp). basically 100k bp is about 1\30,000 of the genome. so the chance should be one in 30,000. do you agree so far?