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Sure I have. Mutations accumulate after species diverge. That's why the genetic differences between humans and chimpanzees look exactly like lots of accumulated mutations. I know I've pointed that out to you before, too. You didn't have an explanation for it, and you don't seem to care.
I have no idea what that's supposed to mean. As you are quite well aware, I did my bit to determine what the difference was between humans and chimpanzees. The observed difference is, again, quite consistent with being the result of lots of accumulated mutations.
What obvious problems?
You've never understood that genes can be highly conserved under some circumstances and free to evolve under others. (I believe I've also pointed out that HAR1 shows evidence of having been in a high-mutation-rate recombination hotspot, which makes rapid evolution more likely.)
What problem? They've identified 5000 sites in the genome that have started undergoing transcription. If 1% turned out to be useful, that would not be a shock. Why is it that new genes always turn out to have an obvious mechanistic origin? They're either the result of gene duplication, previously noncoding DNA (which can still be seen in other species), or a transposable element.
You frequently get facts very wrong. Just in this thread, you've once again gotten the number of ERVs in chimpanzees completely wrong
I like you too, Mark, but you consistently get genetics wrong. I tried, repeatedly, to give you detailed explanations about why you were wrong, but eventually I gave up. Life is too short.
No, it isn't Mark. I am saying that common ancestry is evidenced because the distribution of orthologous ERVs matches the expected phylogeny.
Quite true. Chimpanzees are the species most similar genetically to humans in about two-thirds of the genome. In roughly one-sixth of the genome, we're more closely related to gorillas, and in one-sixth chimpanzees and gorillas are more closely related than either is to humans. This is an expected result with a (relatively) short time between the divergence of gorillas and the human/chimpanzee split. The process is known as incomplete lineage sorting.
That's not talking about orthologous ERV insertion points. It's talking about a virus that infected multiple species and inserted into the genomes of each, but in different places. Key sentence: "First, there is virtually no overlap (less than 4%) between the location of insertions among chimpanzee, gorilla, macaque, and baboon..."Lineage-Specific Expansions of Retroviral Insertions within the Genomes of African Great Apes but Not Humans and Orangutans
"It is interesting that one of the three main branches of Old World monkey PTERV1 may actually share a monophyletic origin with the gorilla and chimpanzee elements. One possible scenario may be that this retrovirus was introduced into the great ape lineages by horizontal transmission, perhaps from contact with an ancient Old World monkey specie"
Quite true. This is an expected result with a (relatively) short time between the divergence of gorillas and the human/chimpanzee split. The process is known as incomplete lineage sorting.
That's not talking about orthologous ERV insertion points. It's talking about a virus that infected multiple species and inserted into the genomes of each, but in different places. Key sentence: "First, there is virtually no overlap (less than 4%) between the location of insertions among chimpanzee, gorilla, macaque, and baboon..."
And you still haven't told me why. You have never acknowledged the genomic divergence with regards to over all genomic divergence, rationalizing away the fact that it's reported at 96% the same at best.
Never addressed the obvious problems with the causation regarding gross structural changes in protein coding genes required. No explanation of how HAR1f and the other highly conserved genes suddenly undergo dramatic changes. Then there is the problem with the 60 de novo genes that must have originated some 2 mya. You just keep saying I'm wrong and all I keep doing is reminding you of the facts.
They match the actual expectations from the phylogeny, which is surely what's important, right?so loudmouth claim that : "distribution of orthologous ERVs matches the expected phylogeny" isnt always true.
Huh? They found that the vast majority (96%) of insertions were clearly not orthologous. The remaining ones were probably not orthologous either. Those ones don't match the expected phylogeny for the simple reason that they're independent insertions.not according to this:
"We performed two analyses to determine whether these 12 shared map intervals might indeed be orthologous. First, we examined the distribution of shared sites between species (Table S3). We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates [5]. This is particularly relevant for the human/great ape lineage. For example, only one interval is shared by gorilla and chimpanzee; however, two intervals are shared by gorilla and baboon; while three intervals are apparently shared by macaque and chimpanzee. Our Southern analysis shows that human and orangutan completely lack PTERV1 sequence (see Figure 2A). If these sites were truly orthologous and, thus, ancestral in the human/ape ancestor, it would require that at least six of these sites were deleted in the human lineage. Moreover, the same exact six sites would also have had to have been deleted in the orangutan lineage if the generally accepted phylogeny is correct. Such a series of independent deletion events at the same precise locations in the genome is unlikely"
and still they conclude that this finding contradict the accepted phylogenetic tree.
You have again got it wrong. Here they're comparing the phylogeny of the virus with the phylogeny of the primates; they're not looking at the phylogeny suggested by viral insertions. Once again, the conclusions is that the virus moved between species, which is mildly interesting but not at all surprising, since we know viruses do that. They're not reporting anything odd about the viral insertion points.this is not a single case:
Distribution of baboon endogenous virus among species of African monkeys suggests multiple ancient cross-species transmissions in shared habitats.
"This viral evolutionary tree does not follow host phylogeny, indicating the cross-species transmissions and multiple germ line fixations of the virus must have occurred in the past"
so loudmouth claim that : "distribution of orthologous ERVs matches the expected phylogeny" isnt always true.
not according to this:
"We performed two analyses to determine whether these 12 shared map intervals might indeed be orthologous. First, we examined the distribution of shared sites between species (Table S3). We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates [5]. This is particularly relevant for the human/great ape lineage. For example, only one interval is shared by gorilla and chimpanzee; however, two intervals are shared by gorilla and baboon; while three intervals are apparently shared by macaque and chimpanzee. Our Southern analysis shows that human and orangutan completely lack PTERV1 sequence (see Figure 2A). If these sites were truly orthologous and, thus, ancestral in the human/ape ancestor, it would require that at least six of these sites were deleted in the human lineage. Moreover, the same exact six sites would also have had to have been deleted in the orangutan lineage if the generally accepted phylogeny is correct. Such a series of independent deletion events at the same precise locations in the genome is unlikely"
and still they conclude that this finding contradict the accepted phylogenetic tree. and this is not a single case:
Distribution of baboon endogenous virus among species of African monkeys suggests multiple ancient cross-species transmissions in shared habitats.
"This viral evolutionary tree does not follow host phylogeny, indicating the cross-species transmissions and multiple germ line fixations of the virus must have occurred in the past"
Maybe he didn't want a serious discussion after all.No, I'm offering to have a serious, honest, adult discussion with you about why evolution explains the diversity of life.
Maybe he didn't want a serious discussion after all.
Those ones don't match the expected phylogeny for the simple reason that they're independent insertions.
Oh for crying out loud. These are sites that we've already discussed, ones that mapped to more or less the same part of the genome but that couldn't be definitively shown to be in the same or different spots. The authors are quite explicit: "Within the limits of this BAC-based end-sequencing mapping approach, 24 sites mapped to similar regions of the human reference genome (approximately 160 kb) and could not be definitively resolved as orthologous or non-orthologous (Table S3)." Why didn't you quote that bit? Or the title of the Table S3, "Retroviral Map Intervals That Potentially Overlap between Species"? What do you think "potentially" means in that title?but they actually do talking about shared sites:
"First, we examined the distribution of shared sites between species (Table S3)"
and their conclusion:
"We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates"
Just stop and think about what you are saying for a moment.
What is evolution? Isn't evolution the process of accumulating mutations over time, resulting in descendants that are modified versions of their ancestors?
Divergence between lineages is exactly what we should see if evolution is true.
How are evolving genes a problem for evolution?
Yea and then there is this:but they actually do talking about shared sites:
"First, we examined the distribution of shared sites between species (Table S3)"
and their conclusion:
"We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates"
Still waiting for some atheist to tell me what evolved first DNA or Protein , I asked once my bio teacher and he was bullying me for rest of year .
Oh for crying out loud. These are sites that we've already discussed, ones that mapped to more or less the same part of the genome but that couldn't be definitively shown to be in the same or different spots. The authors are quite explicit: "Within the limits of this BAC-based end-sequencing mapping approach, 24 sites mapped to similar regions of the human reference genome (approximately 160 kb) .
In fact Darwin (1809-82) was 50 when The Origin of Species was published (November 1859).It is interesting to know that Darwin, in later life, regretted writing his book and said that his theory was "the unborn idea of a young man." If that is what the founder of Evolution said, then that must put a bit of dent in it.
The spots aren't that tiny; they're ~160,000 bp in size. Yes, we would only expect independent insertions in the same region very rarely -- if insertion probability is uniform across the genome. Since retroviruses and transposons both tend to have substantial biases in what parts of the genome they insert into, however, we shouldn't have any particular expectation of how clustered these insertion points should be. To tell that, you'd have to do a detailed analysis of insertion biases for this virus. Have you done that?even if those ervs are in a similar spot in the genome and not identical, it's almost the same. what is the chance that in a 3bilion bp we will get the same ervs in a tiny spots in that genome?
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