Your evidence demonstrates how rare they are. Your evidence supports our argument.
Remember, you need a mechanism by which 99.9% of 200,000 retroviral insertions can insert into the same orthologous base in multiple species, all through independent insertions. Finding a handful out of hundreds of thousands won’t do it.
Next, you have to explain the pattern of overall ERV sequence divergence and divergence of the 5’ and 3’ LTRs within the same ERV.
its not. they are talking about host part (retrotransposon) that becoming a retrovirus.
here (figure 3):
It is.
Transcription is not function. RNA polymerase is more than capable of transcribing non-functional DNA.
The figure isn’t about transcription? It’s pointing out the correlation between the proportion of non-coding DNA in genomes with the number of cell types in an organism (a crude proxy for “organismal complexity”).
It does nothing to demonstrate that all or most of the genome is functional @scd.
A distinction without a difference, perhaps. Immagonna call it progress! 
I got caught up in the abstract instead of focusing on the specific figure. Good point.
I think this is the same paper we have discussed in several other threads, and the consensus was that the data is cherry picked. Include species like the bladderwort, amoeba, salamander, lungfish, and puffer fish and you will get very different results.
It looks like a slightly more sophisticated version of the dog’s-ass plot. Cherry-picked data to create a false impression.
how is that relevent to the paper who talks about how non viral part becoming a retrovirus?
actually the opposite is true. the author checked many species and we can see a general correlation. the species that dont fit that correlation (amoeba, salamander, lungfish etc) are the exceptions, not the rule.
Prove it.
You get quite a different picture if you look at the genome size database rather than just the species whose genomes have been sequenced, which were mostly chosen for their small size.
how it will make any difference? the point here is the correlation. the size should be irrelevant.
The sizes do not correlate well with indices of complexity, which is the point. Do you know what the C-value paradox is? The onion test? I swear we’ve been over this before.
That’s not evidence that all, or the majority, or even that any significant fraction of retrotransposons are functional.
Even if there was some correlation between some measure of organismal complexity(such as number of distinct cell types, however you decide to define that), and the amount of non-coding DNA in an organism’s genome, that says nothing about the direction or magnitude of causality involved.
For example, it could be that 99% of the non-coding DNA owing to retrotransposons are nonfunctional, yet that remaining 1% are functional retrotransposons, and that those 1% of retrotransposons are required for that additional complexity.
That’d still leave 99% of retrotransposons nonfunctional. And of course, whatever the fraction of retrotransposons that are functional in transcriptional regulation, says nothing about the extend to which putative ERV insertions evolve into viruses.
So we’re still left with the inference that ERV insertions are much, much, much more likely to constitute nonfunctional derivations of ancient retroviral insertions, than retroviruses deriving from ERV-like sequences independently created for no reason to exhibit the attributes of a retrovirus genome.
I have yet to see such a paper. Retrotransposons are not retroviruses, if that is what you are talking about.
this figure shows otherwise:
again you are talking about the exceptions, when im talking about the rule.
the figure isnt about the function of retrotransposons. i gave it to show that the chance to get the same insertions in two different species is much higher. if the whole genome is functional then there are only few places where a retrovirus can insert into the genome and be fixed.
see here:
I have to say that it looks like you keep losing track of the preceding discussion. I highly, highly recommend you go back and read what your own words were, that we are responding to.
That way you can at least understand what point is being made and how it is supposed to constitute a rebuttal to your own.
“The figure isn’t about retrotransposons”. I know, I’m not saying it was. Please try to undertand the context of what is being said. That means understanding and remembering what you said earlier, and then understanding what people respond with.
I shouldn’t have to do this, and it’s getting extremely tiresome to have a conversation with someone who can’t follow his own train of thought, but here is that context, please at least try to follow the reasoning:
You: if the whole genome is functional (as some scientists claims) then there are only specific spots in the genome that we can get viral insertion without any problematic result to the creature. thus if this scenario is true we should find viral insertions only in specific spots.
T_aquaticus (responding to that): You need evidence, not bare assertions.
So here you are making a claim about the functionality of the genome. You refer to some scientists postulating that the entirety of the genome is functional, to try to argue against viral insertions being tolerated. You infer that if the whole genome is functional, there would probably not be many places that could tolerate a retroviral insertion.
TAQ responds that you need to provide evidence that the whole genome is functional, not just say that it is.
So then you respond to that, with this:
You: here (figure 3) A meta-analysis of the genomic and transcriptomic composition of complex life - PubMed
You with me so far? So here you appear to believe that you have provided evidence that the whole genome(including retrotransposons, and all non-coding DNA) is functional. TAQ asked for it, and you then provided it. Right?
I then proceed to explain to you that you have not succeeded in meeting that burden of proof. That what you provided does not constitute evidence that the whole genome is functional. I use the example of retrotransposons for the sake of argument, both because a huge fraction of non-coding DNA actually derives from transposons, and because you keep insisting that retrotransposons are functional(“it’s an integral part of the genome”), and because you are proposing that it is from these functional retrotransposons that retroviruses evolved(instead of retrotransposons ultimately deriving from ancient retroviruses).
So then what do you respond with?
You: the figure isnt about the function of retrotransposons. i gave it to show that the chance to get the same insertions in two different species is much higher. if the whole genome is functional then there are only few places where a retrovirus can insert into the genome and be fixed.
Yes, I know it’s not about retrotransposons per se, that it is about the fraction of the genome that is functional. And that is exactly what my explanation argues against. I’m just using the example of transposons. So you have still not provided evidence that the whole genome is functional, much less that we can infer anything about what the odds of chance parallel retroviral insertions are.
Do you understand any of this or are we all just wasting our time?
That’s just repeating your previous citation. Note that it’s cherry-picking a few species out of the millions that exist and out of the thousands that have had their genome sizes determined. Do you think it was a representative sample of those millions or thousands?
To repeat myself: limiting the sample to well-annotated complete genomes biases toward organisms with small genomes, since those were the most frequently sequenced. The major exception would be humans and close relatives. No wonder they’re at the top of the graph.
That doesn’t cast the origin of the ERVs in doubt. Transposons also insert randomly within the genome, so you have the same issue as before.
ok so here is the original claim:
ok, but even if it was true it doesnt explain the correlation of the non coding sequence and complexity. if 1% of the genome is functional why it has a correlation with the rest 99%? this is the problem after all for these who reject the idea that most of the genome is functional.
of course. do you think that the author just ignored the results that dont fit with his idea? because if so we can throw any scientific paper to the garbage can.
the genome size is irrelevant in this case since we see that correlation in different genomes size. so the issue isnt about the genome size but about the correlation.
That’s literally what I just did. It’s in that last sentence there after the 3rd comma.
Try to wrap your head around this scenario:
Less complex organism has genome with less non-coding DNA, a large portion of which is transposons, and a small fraction(say 1%) of these transposons are functional, and among their functions they help to determine the level of complexity of the organism by participating in the regulation of distinct cell types.
More complex organism has genome with more non-coding DNA, a large portion of which is also transposons, and a small fraction(say 0.9%) of these transposons are functional, and among their functions they help to determine the higher level of complexity of the organism by regulating more distinct cell types.
So what happened was that:
So suppose it went from 10.000 transposons, 1% of which were functional and helped produce distinct cell-types, to 15.000 transposons, with 0.9% of these being functional, which also help produce more distinct cell-types.
So now it went from 100 to 135 functional transposons, and from 9900 nonfunctional to 14865 nonfunctional transposons. And those functional transposons help give it more distinct cell-types, which gives it greater complexity. But the proportion of functional transposons have gone down, from 1% to 0.9%, while the proportion of non-coding DNA has gone up a lot by mostly constituting dead transposons.
So it got more complex (by the number of distinct cell-types measure), while also getting more junk-DNA. That would then explain the correlation without it at all implying the whole genome is functional.
And just to drive this point home: Most of the genome for complex organisms with large genomes, are actually made of dead transposons.
Nope, not a problem at all, for reasons just explained.
