Yes, I knew that when I replied, but a Gaussian distribution w.r.t. what exactly?
And why should mutations be Gaussian distributed???
Thanks for that clarification. I should have read the paper before I responded!
Well, to do the calculation you need to introduce some assumption about the distribution of the mutations among the genes. We would expect some genes to have very few, some very many in a stochastic process. Assuming a random normal distribution seemed like a plausible, but admittedly imperfect, assumption.
Best,
Chris
Your point doesnāt make as much sense in light of the entire section I quoted.
Despite a recent divergence of these species (ā¼7 million years ago [MYA]) (9), their Y chromosomes differ enormously in size and gene content, in sharp contrast to the stability of the rest of the genome. For example, the chimpanzee Y is only half the size of the human Y, and the percentage of gene families shared by these two chromosomes (68%) that split ā¼6 MYA (9) is similar to that shared by human and chicken autosomes that split ā¼310 MYA (7). Puzzlingly, in terms of shared genes and overall architecture, the human Y is more similar to the gorilla Y than to the chimpanzee Y even though human and chimpanzee have a more recent common ancestor (8).
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Iām not a prophetess 
but I think it very likely that small things like this will continue to stack up and evolution via common ancestry may start to āstink.ā All of the evidence you all have shown me on this forum has an alternate explanation which waits on research to uncover certain things to become part of a stronger model, imo. I continue to be amazed at scientistsā faith (especially here in this forum) that the current evolutionary model will never be overturned. Since arguing about it then is somewhat a waste of time, I will bow out of this discussion for now. Iād rather pop in with my questions from time to time than argue anything.
I donāt anything about textual criticism but this sounds like a reasonable analogy.
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It can? According to the human proteome mapping project weāve only found 30,000 proteins so far, which is an order of magnitude less.
Where did your figure come from?
P.S. Whether the actual percentage of human-chimp identical proteins is 71% or 80% may not be the central point, but your insistence on continuing to use a value that is demonstrably incorrect is seriously marring your credibility.
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The section you quoted doesnāt contradict anything Michael or Chris said. Youāre quoting the introduction, while the rest of the paper goes on to solve that puzzle. See the abstract:
The Y chromosomes of great apes represent a particular puzzle: their gene content is more similar between human and gorilla than between human and chimpanzee, even though human and chimpanzee share a more recent common ancestor. To solve this puzzle, here we constructed a dataset including Ys from all extant great ape genera. We generated assemblies of bonobo and orangutan Ys from short and long sequencing reads and aligned them with the publicly available human, chimpanzee, and gorilla Y assemblies. Analyzing this dataset, we found that the genus Pan, which includes chimpanzee and bonobo, experienced accelerated substitution rates. Pan also exhibited elevated gene death rates.
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Hi thoughtful,
You seem to be unfamiliar with stochastic processes and stochastic models.
A good example of a stochastic process is radioactive decay. Take the C14 ā N14, which has been modeled mathematically as a logarithmic function with a half-life of approximately 5700 years.
Now suppose this morning you start observing one atom of C14. Tomorrow morning, you detect the emission of an electron and an electron antineutrino.
But wait, the half-life of this decay is supposedly 5700 years! Has your experiment proven that the standard physics textbooks are completely wrong about the half-life of C14?
Best,
Chris
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In order for the things you quote to constitute a problem for common ancestry youād have to assume that the different chromosomes evolve at a constant and similar rate in all separate lineages. But we just donāt have any reason to assume that(the real world is just more complicated than that), and in fact we have experimental observations that show evolutionary rates vary over time, vary between chromosomes, tissues, and organelles, and vary between species. Why should we ignore such observations when trying to test predictions of common ancestry? That doesnāt make sense.
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Youāre not a prophetess, and whatās more relevant, you know nothing about the science involved, so your prophecies have no basis other than your wishing them so. Your mistake in the current situation is your misunderstanding of evolution, notably the idea that phylogeny is based on mere similarity. Y chromosomes evolve much more quickly than do autosomes, and chimpanzee Y chromosomes would be expected to evolve more quickly than human or gorilla Y chromosomes due to heavy sperm competition in the chimpanzee population. Thatās all. This isnāt faith, just familiarity with the subject.
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Iām not a prophetess 
but I think it very likely that small things like this will continue to stack up and evolution via common ancestry may start to āstink.ā
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āStinkā? You are misinterpreting that paper and ignoring the data for the explanations that account for the disparities between the human and chimp Y-Chr.
Letās try this again because I know at times you get these things but need sometime to figure it out. There are two talking points here according to the section you quoted, āpercentage of shared gene familiesā and āoverall Y-Chr architectureā.
First, the phylogeny of the great apes (including us) derived from the Y-Chr agrees with the phylogeny derived from their autosomes, further confirming our shared ancestry
Second, despite our closer evolutionary relationship to chimps based on the Y-Chr phylogeny, the percentage of gene families we share with them are less, but more with gorillas. Why? The answer is a higher rate of gene loss in the Pan lineages (chimps and bonobos) relative to humans and gorillas. According to the paper, the common ancestor of us, chimps and gorillas had 25 gene families and you can see it in this tree diagram (from the paper, Fig 2):
That common ancestor is the root of the tree and you can clearly see the 25 gene families it had. Evolution starts and gets to us, but a lot of changes had happened to that collection of ancestral gene families in the different lineages. Out of the 25 ancestral gene families, chimps lost 8, bonobos lost 7, while we and gorillas lost 1. From the figure, the common ancestor of chimps, bonobos, humans, gorillas and orangutans lost one ancestral gene family, while the common ancestor of only chimps and bonobos lost 6 gene families, giving a total of seven ancestral gene family deaths: after splitting from their common ancestor with bonobos, chimps went on to lose one more ancestral gene family, raising its gene family loss to eight. This beautifully explains why the percentage of gene families shared between chimps and humans relative to that shared between humans and gorillas is lesser, despite our closer relationship to chimps.
Third, the overall architecture of the chimp Y-Chr differs from that of humans despite their recent shared ancestry. Is this surprising? No, as per the data in the paper. For instance, chimp Y-Chr is half the size of human Y-Chr, but this is expected considering the significant number of gene loss events (some of which are deletions and gene deletions shrink genome sizes), for example. In general the evolutionary rates of Y-Chrās (be it in humans, chimps or other great apes) is higher relative to the autosomes and X-Chrās, explaining why they are much smaller size relative to the aforementioned chromosomes. Since this rate is much higher in the chimp Y-Chr, its not surprising that is smaller in size than that of humans.
Then you have a strawman perception of scientists.
Whatās more amazing is your ignorance of the data right in front of you from the paper you cited.
You are right that it is pointless arguing about it because the data is right there in front of you and it settles the challenges but you choose to ignore it.
Looking forward to that, but I hope you take your time to understand the data and come to a conclusion supported by that data.
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Alternate splicing is always occurring in all cells. The real question is how many of those alternately spliced transcripts are functional.
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The diversity of human proteins includes, but is not limited to, alternate splicing, modifications of proteins after they are translated into proteins, and V(D)J recombination that produces tons of different antibodies. However, these protein species are not relevant to the question of evolution and comparative genomics.
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It may not be a central point. What is more notable from this though is that you keep on using this figure and not even acknowledging the correction, even after multiple people have repeatedly pointed this out to you.
Where did you get that number from?? From what I can see, we produce an estimated amount of 19,778 proteins (of which 18,357 are known), very close to the estimated number of genes in the human genome (FYI, not all of which are protein coding). HUPO - HPP Progress to date
What youāre likely referring to is the idea we can produce many more unique proteins from our gene through alternative splicingā¦but your figure would suggest the average gene produces ~20 alternatively spliced protein-coding transcripts, which is very unrealistic. The best estimations I have seen are between 40,000 to 80,000 proteins (or 2-4 alternative splicing on average). But I am not even convinced of that, since these estimations hinges on whether the alternatively spliced mRNAs actually produce (functional) proteins. Itās most likely the case that this is the result of splicing error, and the vast majority of protein coding genes in the human genome codes for just one unique functional protein.
[The implications of alternative splicing in the ENCODE protein complement]
[Alternative Splicing May Not Be the Key to Proteome Complexity]
But ALL of this is not relevant to our discussion. We were talking about how different humans and chimps are with respect to their genome, specifically and I (as well as other) have repeatedly pointed out why the fact that 71% of the proteins being different by at least one amino acid:
1. Does not tell you how identical the protein coding genetic sequences between humans and chimps are (which is about 99%), and
2. Neither does this mean that in coding regions 71% of mutations are not neutral (not even āby resultā whatever that means).
Try to stay on topic.
First of, we actually do know quite a lot about the genome besides the 1.5% that is protein coding. We know of regulating DNA, like cis regulatory elements and promoters. I think what you meant to say is that YOU donāt understand. Please donāt project your ignorance onto others.
NO!! Even assuming that you are right and we can only rely on 1.5% of the genome, you canāt make a āfairā result by analyzing just 1.5% of the data. Thatās asinine. But itās even worse, since you are still using the 80% (actually 71%) figure as if it tells you anything about the percentage of mutations are not neutral, which - as we have all pointed out to you, many times - it does not (not even just the ones tat that occur within the protein coding regions).
This response just reveals that you have missed the point on multiple levels no less. Where to even begin?
First, this particular point was about the AMINO ACID differences between the PROTEINS of humans and chimps specifically. The question was about how different the proteins are between humans and chimps actually? Hence, non-coding DNA is NOT relevant when it comes to this particular point.
Second, the fact that you pointed out that this calculation is separated from the measurable reality - as if it was a rebuttal against me - while this was the whole point of that calculation!! The reason for this calculation was to point out how far separated from measurable reality YOUR claim is. See my previous comment to see the context (emphasis mine):
To abbreviate, in order to draw your conclusion of ātoo many millions of mutationsā from the fact that 71% of proteins are different from that of chimps, these protein would have to be different by 140 amino acids on average. But this is false. You canāt make this conclusion from the 71% (or 80%) figure. Do you now understand the point?
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Just returning to the original topic of this thread, I found the section of the video from 1:41:30 to about 1:43:00 quite amusing, where Ahmed claims to have run a simulation showing that human evolution is impossible:
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I split off the, I donāt even know quite what that was, off-topic āconversationā about who knows more than whom and what knowledge is ā¦ 
This topic is is for discussing the conversation between @swamidass and @Ahmed_AbdelSattar about human evolution.
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@Ahmed_AbdelSattar has decided to teach an online course on evolution. He has released the following introductory video:
I noticed a few errors that I have brought to his attention:
Itās misleading to say that natural selections means that the āweakerā members of a population are ākicked out.ā Much evolution involves the increasing frequency and ultimate fixation of particular alleles in a population.
Fish gills did not become lungs and fish scales did not become skin. Fish already had skin.
It is not true that if one human parent has black hair and the other brown, their offspring can only have either black or brown hair. They could have shades of colour in between, and they could even have blond hair
That phylogenetic tree you show at the end is very weird, in that it shows archaea and bacteria joining to form eukaryotes. That is very very wrong.
I guess that last one was supposed to depict endosymbiosis, but itās still a weird way to show the three domains.
Iām sure he would appreciate further feedback if anyone notices something I missed.
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Iām equally sure that he would not.
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