How closely have you followed the fusion argument? Would the argument even exist if common ancestry was not assumed?
Yes it would. Even RTB thinks it’s a fusion (engineered by God), and they don’t assume CD. It just really looks like a fusion.
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Fusion events happen I agree. Do you have any papers that show how it would get fixed in the population?
There are modern examples of people walking around with new chromosomal fusions.
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I don’t, offhand. But drift seems like a reasonable answer. Does that work for you?
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I’m not sure how you would get all those different gametes from the fusion heterozygotes. In meiosis, both chromosomes 14 and 15 ought to pair with the fused 14/15, so the gamete would get either 14 and 15 or 14/15, never just 14 or 15. There should be a minimal loss of fertility. And the fusion homozygote should be able to reproduce just fine with a normal human to get all heterozygote children.
I agree it is most likely drift but it also appears to be a rare mutation per Tompkins analysis below. There are also 1500 inversion mutations between chimps and humans in the paper @David_MacMillan cited.
Genetic bottlenecks (real ones, not the 6-person nonsense of YEC) are good at fixing novel mutations.
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Sorry Bill but what peer-reviewed scientific journal was that YEC “analysis” published in?
It isn’t clear what point you’re trying to make by posting that execrable “analysis”. Of course chromosomal fusion is a rare mutation. But still they do happen frequently enough that occasionally one of them gets fixed, and it happened once in the human lineage.
Which paper are you talking about? Yes, inversions are more common than fusions. So?
Incidentally, how long are those 1500 inversions? The commonly noticed ones, historically, have been multiple megabases long. More recently, through sequencing, inversions as short as 5 bases have been found.
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You pick up hundreds of inversions (mostly rare) just by sequencing 10 - 20 thousand people. Every human genome contains dozens of inversions on average. See this recent paper for example:
Mapping and characterization of structural variation in 17,795 human genomes.
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This particular fusion includes a transcription cite. What do you think the odds are are of it getting fixed in a human population if it only occurs once or twice? @David_MacMillan idea of a bottle neck is a necessary condition but is it sufficient?
Whatever is a “transcription cite”?
Extremely low. If it’s strictly neutral drift, the probability of any particular mutation becoming fixed is 1/(2N), where N is the effective population size. And in fact most mutations are lost within a generation or two. But occasionally one does become fixed. Millions of chromosomal fusions have likely happened in the history of the human lineage, but only one of them became fixed.
It’s not necessary at all. You are misinformed. The only effect of a bottleneck is that N is smaller. But that bottleneck would have to extend over many generations in order to have any significant effect on fixation rates.
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Doesn’t matter what the odds are Bill. The evidence shows it already happened so the probability was 1.0.
What are the odds of you winning the lottery if you buy just one ticket? What are the odds of someone winning the lottery if 100’s of millions of people each buy one ticket?
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As others have said, a bottleneck is not necessary (nor is it my “idea” because there is strong genetic evidence for multiple bottlenecks in human history, though those two are too recent to have been associated with the fixing of the Chromosome 2 fusion). They can also become fixed in the population by simple drift. A bottleneck simply helps because the smaller the population, the more easy it is to fix a mutation by drift, per 1/(2N) as noted above.
Also, your question is malformed. Chromosomal fusions do not happen only “once or twice” in human history. They are extremely common – one in every 1000 births, or about 360 per day. Of course the human population is very large now, but even so that is very, very common. Billions of chromosomal fusions have happened in the history of the human lineage.
Neanderthals and Denisovans also had the chromosome 2 fusion. The point of fixing is most likely very close to the human-chimpanzee common ancestor.
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Then again, the smaller the population, the less likely a chromosomal fusion will occur in any individual. It all comes down to the mutation rate.
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This event if fusion is really the cause is rare as there is a high level of function where the fusion occurred if Tomkins article is correct. If the fusion was a random event we would not expect a high level of function at the site as Tompkins has argued.
Tompkins is completely wrong.
First off, Tompkins has not provided a valid argument that there is function, let alone a coding sequence, at this particular site. There is in fact no coding sequence at this site.
But even if there was function at this site, it would not prove what Tompkins thinks it proves. The whole point of evolution is that the genome evolves. How do you think we get genes and chromosomes in the first place? If a coding sequence evolves at the location of vestigial telomeres or a vestigial centromere, that’s not at all strange or uncommon. It just means that’s one of the many, many genes that has evolved since the fusion became fixed.
Most of the phenotypically-manifested differences between humans and chimpanzees have been the result of “gene switch” mutations in both lineages, rather than novel genes. However there have been 689 new genes added to the human genome since the LCA: an average of thirty per chromosome. So even if Tompkins was right, it wouldn’t be surprising to see a novel gene evolve near the fusion site.
This is nonsense. The “randomness” of the fusion is not related to anything. There IS a fusion here. That is painfully obvious. But how random or nonrandom it is has no bearing whatsoever on what type of genome change takes place after it becomes fixed.
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Yawn. These kinds of a priori probability calculations are, for the hundredth time, meaningless. You can pick out any one mutation of those that occurred and eventually went on to become fixed and ask how likely it was that that mutation would have occurred and become fixed, and you’ll get some unimaginably small probability.
Take some particular substitution with a probability of 1 in 10 billion, then ask what it’s probability of fixation is, which if ~neutral is about 1 in 50.000 for the human population, which means the probability of that mutation occurring and becoming fixed for a population with an effective size of 10.000, is 1 in a quadrillion. 10^-15.
That’s a very low probability, and we seem to have calculated that the occurrence and fixation of neutral substitutions are impossible? But somewhere on the order of 50 to 100 of those are fixed every generation.
Of what use is it then, to calculate the prior probability of a particular of one of them? It doesn’t tell you that what occurred didn’t occur, or was implausible to occur, or couldn’t occur. It does not even weakly indicate it in any way. It is a useless and meaningless probability. Why can’t ID proponents fathom this elementary concept?
It’s like rolling a handful of 10 dice 50 times in a row, then picking out one particular throw of that handful of 10 dice, after having thrown it, and calculating the odds of that particular throw occurring. Does the number you derive somehow show you didn’t actually throw that result? Obviously not. It’s a meaningless calculation to do. It can’t possibly show you that what you just did, did not plausibly occur. Then why would you do that for some historical mutation occurring when the exact same principle applies?
How can this inane question keep coming up? It’s a pointless calculation that cannot possibly rationally inform your beliefs about whether history occurred.
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