Alu and LINE-1 are transposons, not ERVs. Transposons are bits of DNA that copy themselves and insert elsewhere in the genome, but they are not viruses and are not infectious. The numbers we are after are the ERV class 1 and 2.
On a side note, we could also use shared transposon insertions as evidence for common ancestry in the same way that ERVs are used due to the fact that transposon insertion is close to random, but including them here would only confuse the discussion.
In my experience, a nested hierarchy is synonymous with phylogeny or cladogram.
“Evolution predicts that living things will be related to one another in what scientists refer to as nested hierarchies — rather like nested boxes. Groups of related organisms share suites of similar characteristics and the number of shared traits increases with relatedness.” Understanding Evolution
The cladogram you showed earlier has lineages which have the ability to produce shocks. This is showing convergent evolution of an ability in those lineages.
This seems a bit odd to throw gene duplication and whole genome duplication into the dependency model as the entire point is that they are very intelligently designed in the first place or am I mistaken?
Do you mean in these models or in the field as a whole? I would be very curious to hear how you imagine DG for example engaging ERV evidence for evolution like we had in a recent thread:
My apologies on the slight outdated OP in regards to data, but we are looking at hundreds of thousands of such ERVs that must have been inserted independently by the designer where he only gave a handful of unique ones to say humans and chimpanzees after he made the first couple of us.
OK, so the point of that video is that the ERV evidence makes evolution overwhelming–an “Irrefutable truth.” The powerful conclusion comes from their calculation that the probability of the evidence (without evolution) is 1 in 2 * 10^138. IOW, two times a 1 followed by 138 zeros. It is a really huge number, so you can imagine my surprise to see you citing this video, given your earlier comment that:
I guess when the big number is in support of evolution it is OK.
In any case, it is important to understand that these ERVs do not help evolution. ERVs (at least according to the usual account, and as implied in the video), are non functional. They impose a cost on the genome, and are not exactly the sort of thing an evolutionist should be claiming as strong evidence. (continued …)
Yeah I don’t like big numbers. As a physicist I generally tend to believe they are indicative of a model not accurately describing reality. None the less, I’m almost sorry you watched that video. I started to post to ask you to stop but you did none the less. So thanks for that.
So what is going on in the video? Why does it claim “Irrefutable truth” for something without selective value? Well for this, we need to look at their calculation. How do they get 1 on 10^138 anyway?
The underlying calculation is that there is a 1 on 10^138 chance of the ERVs landing there by chance. Of course, “:by chance” is a very common notion in evolutionary thought. “By chance” is the way evolution works. So this notion is not too surprising to see in evolutionary thinking. But they are using that assumption in an evolution apologetic. Do you see the circularity?
IOW, the underlying argument is that we have two alternatives: Either the ERVs landed there by chance, or evolution is true. And since the former is ridiculously unlikely, the latter must be true, regardless of how unlikely evolution actually is, according to science.
See how evolution works? This is how the strong arguments work.
This is nonsense. In fact, what the video doesn’t mention is the ERVs that don’t fit the pattern. That is, the ERVs the line up in different species, but the species are too distant, and so the ERVs must have gotten there by independent events (not common descent). In those cases evolutionists admit it must not have been by chance. It must have been common mechanisms, not common descent.
But if ERVs can land in the same place via common mechanism when evolution cannot explain it, then why must we assume ERVs must have landed there by chance in those other cases?
We can observe where the ERVs are today. But we need to be careful in assuming how they got there.
Yes I know. It’s quite obvious when ERVs get there via one of two methods (either common descent or seperate lineage insertions). We discussed quite extensively a paper by Yohn et. al. from 2005 that let us know that:
When there is a viral infection of this nature that infects two populations independently, you might see less than 5% in the same spot in the genome.
In humans and chimpanzees, there are 203,000 ERVs and less than 300 are in different spots… meaning that we see 99.86% in the same spot. This cannot be explained by separate viral infections and the most parsimonious explanation by a long shot is common descent.
(note going to move this over to the other thread so as not to go on a rabbit trail from this new paper you are discussing)
Changed it so it is less internet debatey- I was copying some of the text of a post I had made after many hours of typing and the same paper being used to reject CD and so I apologize you caught some of that.
So the question is, how to reconcile the uncooperative homologous ERVs (e.g., same location, but more distant species) which require a common mechanism and are too unlikely to have occurred by chance. If they can occur by common mechanism, how can we be sure the others did not? Here’s a question: What confidence would evolution be held with if there were even more uncooperative homologous ERVs. Even if all were uncooperative? To forestall the obvious, there would be no change–evolution would still be a fact.
That will indeed be “the question” (or at least “a question”) when and if such ERVs are discovered. Those ERVs, like all interesting genomic elements and mutations, will be studied carefully, with attention paid to what is known about their behavior. To date, I know of zero examples of ERVs in “same location, but more distant species” that defy explanation via testable and even well-known mechanisms of molecular biology and population genetics.
Like the unsupported claims of Ewert about gene families missing from intervening lineages (see my comment here), ERVs in distant lineages in the same genomic location are phenomena that will require specific and robust explanation. First, of course, someone has to show that the phenomena are real. My hunch is that this will be difficult, because the phenomena are fictional.
Another one was found absent in chimps and gorillas:
Another problem is that humans do not have endemic infectious retroviruses:
There are explanations for these (which I think was Stephen Matheson’s point in his post below). So it is not as though these defy explanation. But they can get complicated and questionable (by questionable, I merely mean vague, or not well supported), I don’t mean impossible.
So yes, aside from cases that do not fit, the retroviruses do provide supports for CD. You brought these data up in the spirit of taking a larger view. That is, in response to the DG model, what about ERVs?
That’s a good point, but you know that works both ways, as there are many more problems with evolution and CD. There are a great many specific examples you can look at. I also like this meta study (Klassen, 1991) of 49 studies. Figure 6 shows how the empirical data consistently do not fit CD:
Again, one can always come up with explanations for the empirical data, and that’s fine, but it is important that we’re not talking about anomalies. The data, on the whole, do not fit CD, so you have an enormous parsimony cost with CD (like geocentrism, it works, but you need a lot of extra mechanisms). That’s why it is difficult to answer Ewert’s paper merely by saying, “well, we add more mechanisms,” as I mentioned above.
Also, in the spirit of stepping back and taking a larger view, in addition to the patterns, there are also process problems with evolution. With your ERV question you brought up primate evolution, so I’ll stick with that.
One interesting problem here is the chimp-human DNA similarity or ~99%. As you know this often is taken as powerful evidence for evolution and CD. It also presents a challenge, because what we know from biology indicates this isn’t going to work. What I mean is, you can make all kinds of changes to a genome, and get little or no phenotype change. The mapping is pretty robust. But a 1% change to get you from a primitive, rudimentary primate to a human being? That really seems far out.
It does not seem very credible, given the science, to expect such a tiny genetic change to produce such enormous quantum leaps in phenotypic improvement.
But I appreciate your ERV point, it is a good one.
Not sure that qualifies for ‘uncooperative homologous ERVs (e.g., same location, but more distant species)’ but it is very interesting- I wish it were more common but I think this is a lone case of a nested ERV that is homologous in 3 primates but not homo sapiens! That still seems to support CD, with plenty of reasons why it is not in a homologous spot in humans. I don’t see why any ERV ever should be in a homologous spot without CD, let alone hundreds of thousands of them for chimps/humans.
Good eye. I wasn’t aware of such. So there isn’t even the option for the hundreds of thousands in humans to be inserted after the human lineage began but rather inherited through ancestry.
That’s what I would say with ERV evidence.
So the figure is interesting, but it in itself is not particularly helpful or earth shattering as the paper is moreso about highlighting the flaws of the CI vs. anything else- it is certainly not a knockout of any sort against CD! Seeing how the community interacted with this paper was useful for me (just looking at the papers that have cited this work) as the paper helped improve statistical analysis of cladograms.
Here is a recently accepted paper that outlines many potential methods to assess tree support: