You admit the ones I named do use the inane “it’s too improbable!!” argument, correct? Behe even wrote a whole book based on the claim.
As far as we can tell, chromosome 2 in human is the product of a fusion between 2 chromosomes. My question is the following: what is the likelihood of this type of event? I really don’t see what you don’t understand here?
Okay. But the criticism is they are determining probability incorrectly.
We know from experimental data that the likelihood of a chromosomal fusion is on the order of 1 per 1000 births.
If the question is rather “what is the likelihood of a chromosomal fusion becoming fixed in a population” then things become slightly more challenging. But the likelihood could be reasonably inferred by studying equids, which have numerous chromosome number changes in a fairly confined lineage.
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I understand what you are asking. I just don’t know why you are asking it. Just general curiosity? Or do you think the question has some bearing on whether humans descended from a common ancestor with chimps from undirected evolutionary processes?
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Just general curiosity
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Okay, I stand corrected and I’m glad to hear that.
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Okay thank you. So to be clear, your argument is that the 2011 repeats on 9 are or were part of 9’s centromere but mutated away? Why would a separation of 15Mb be believable and 38Mb not? Because of the heterochromatin?
I don’t know precisely how 2000 alphoid repeats ended up on the other side of the block of heterochromatin from chromosome 9’s centromere, but it’s actually irrelevant. If the claim is that these alphoid repeats are found all over the place, but in fact there’s only 2 blocks of repeats outside of the centromeric regions in the entire human genome, I think the claim is falsified, don’t you? Now, what do you suppose the odds are that 1 of those 2 blocks just happened to be located in the precise locus predicted by the fusion model?
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Ok. I’ll take that under advisement, but it’s not nearly as unlikely as some other things I could name.
You mentioned 2 other characterized examples of chromosomal fusions. What do you say to Tomkins’ argument that Chromosome 2 doesn’t look like other chromosomal fusion sites?
Quoting from his paper:
“All genetic data in living mammals up to this point shows that telomere-satelliteDNA or satelliteDNA-satelliteDNA are the hallmark signatures of naturally occurring but rare chromosomal fusion sites in nature, not telomere-telomere fusions (Chaves et al. 2003; Tsipouri et al. 2008; Adega et al. 2009).”
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Is this not data from three instances in three species? I see a sheep, a muntjac, and unspecified “domestic animals”. Where does the generalization come from? Or is this perhaps a case of misuse of sources?
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Of course not all chromosome fusions in nature are telomere to telomere, there are other types as well, but he’s flat wrong to suggest that there are no other examples of telomere-telomere fusions. I’ve got the sequence of the pig fusion site on chromosome 6 and it’s the spitting image of the human one, with (more) head-to-head telomere repeats.
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Forgive me for asking this naive question but why the difference in chromosome count would be an obstacle to common descent between apes and humans but not in Equus?
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I mean, they are both obstacles to the same extent and in the same way. There is overwhelming evidence for common ancestry of all equids, just as there is overwhelming evidence for common ancestry of all apes. But to make it work you do have to solve the chromosome count problems.
I suspect that it is a little more challenging with equids because there is so much diversity. You cannot make a single, simple, specific prediction about where fusions or splits occurred. With great apes, on the other hand, there is only one big difference and so we were able to predict with dramatic specificity exactly what sort of fusion we would see.
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By analogy…
Suppose you were teaching a typing class with four students. You gave them all identical stapled copies of a lengthy speech and told them to type it out exactly. When they turned in their work, three students produce nearly-identical 24-page copies of the speech while one produced a 23-page copy. You could tell at a cursory glance that the odd one began and ended with nearly the same words on each page as everyone else’s. It occurs to you that you don’t remember how many pages the original was.
Without knowing anything else, you can make a pretty clear prediction: the fourth student must have skipped a page. Even if it is as easy to duplicate a page as it is to skip a page, it’s much more likely that he merely skipped one random page than that all three of the other students duplicated the exact same page – in fact, it is about 530 times more likely.
In contrast, if you do this exercise with ten students and you end up with with seven different page counts – ranging from 32 up to 66 – then you really have no clear prediction. You can sit down and muddle through each submission and then come up with a reasonably likely model of how the different duplications and omissions happened, but because there are so many possibilities, there is no way to predict it in advance.
(This analogy breaks down a little because the four ape lineages are linearly nested and can be treated as independent for the purposes of chromosome count. However, the ten equus lineages are nested non-linearly and so this you can’t treat them as independent. To make the analogy work properly, you’d have to say that you had two TAs who copied down the assignment first, then each passed their copies to an intermediate group of students, who in turn passed their copies to these ten students.)
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The problem for Todd Wood is that nearly all epigenetic markers are wiped out during gamete production in primates (and the vast majority of vertebrates, as far as I am aware). Therefore, epigenetic markers are the product of genetics, and in order to have different epigenetics you need different genetics.
It also tends to collide with creationist claims that the entire human genome is functional.
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