Human Evolution Discussion with Ahmed

You’ve made at least two massive errors here:

  1. My TI-89 calculator is literally a computer. So are many calculators. Depending on one’s definition of computer, so are most calculators.
  2. The range of human intelligence includes the average chimpanzee intelligence. So in your example you should ask ‘The most basic desktop PC is less powerful than the average calculator, does that make calculators computers’. Worded like that, the answer is obviously ‘Yes’.

You can learn that the two categories are fully continuous. Given that the original question is ‘Are these two things fully continuous’, I’d say that’s something relevant.

Let’s ignore the fact that humans and chimpanzees are both great apes for a moment: Is the range of human intelligence still fully continuous with the range of chimpanzee intelligence? Yes? Guess I didn’t need that ‘assumption’ after all!

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The calculator being a computer (which it is) depends on what the definition of a computer is, not how different PCs, supercomputers, and calculators are from each other.

You can have rocks of wildly different sizes, yet they are still rocks despite their colossal range of volumes.

Humans are primates because we have all the traits that meet the definition of primates. We are also mammals, because we have the traits that meet the definition of mammals. We are also amniotes, tetrapods, vertebrates, craniate, chordates, bilateria, deuterostomes, and so on, all the way to eukaryotes. Yes, humans are a mammalian life form, and a type of eukarotic cellular life.

You’ll be surprised to find we also have mass and volume, and must eat to survive.

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I have made notes about this before, but lets take it on one more round:
Judging by result we have the 80% difference (you insist on 71% and it is not the point at all).
The human proteome can be as big as 400,000 proteins; you might like to attribute them to 20K genes, yet, we only understand 1.5% of the genome… so, as I mentioned few times in other discussion threads, I would rather count on what is directly observable as a result of the measurement, rather than something we (as humans) do not really understand.
Hence, saying that the result of the mutations is not predominantly neutral, judging by result, is fair.
If you want to claim otherwise, then once human understanding of human genome and epigenome is expanded, you can make an argument from DNA!

Apart from mentioning above why I think that this calculation is separated from the measurable reality, it once again ignores the so-called “non-coding” regions, and the 5 million indels!

And then once you accept that there are plenty of non-neutral mutations, that work together to cause the difference in function, morphology, and proteome, then you need to consider coherence (mutual constructiveness) and we can talk about fitness (or lack thereof), fixation times, generation length, and number of offspring and the rest of it. If you want to solve this with neutral theory or coalescence, you can’t because they become irrelevant… you need to do the real stuff, and a proper simulation… (which I made some approximations for it by hand and is miserable - you run out of the age of the universe after few mutually constructive mutations)!
As I said in the video, even if the hardcore mutations are few thousands and they are some-how responsible for all of it (which I obviously think is highly unlikely), still to get them to occur and line up needs absurd probabilities and unimaginable time…

Cheers.

It is not the availability of replies from the “evolutionary biology” community that is the issue.
The issue is whether those replies are appropriate answers.
I am afraid they are not.

I don’t see where this is going really… though the video was fun!

There is a whole series of PC computers going back through time, and processing power gradually increases over that time.

However, if you were only able to pick 3 of those computers over the last 50 years you would probably say that the changes in processing power were sudden instead of gradual. That’s the fossil record.

We have mountains of evidence for common descent. It isn’t assumed.

More importantly, Linnaeus was a creationist who lived 100 years before Darwin. Linnaeus didn’t believe in evolution or common descent. Linnaeus listed humans as primates. You may want to think about that for a second.

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Are you aware that an SNP is responsible for sickle cell disease?!

No further comments!

I think we are all aware that a mutation is responsible for different hemoglobin alleles. That doesn’t mean every mutation causes a change in phenotype.

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I’ve already explained this, if you were paying attention.

Gaussian?

What result? You have cited a paper that itself gets its information from a much older paper that predates the publication of the chimpanzee genome. And the chimp genome paper has a much better value, based on the entire genome rather than just 100 or so genes. You’re right that it’s a trivial point, but the fact that you refuse to correct it is not at all trivial.

No, it can’t. I presume you refer to alternative splicing, but functional alternative splicing is quite rare, and most such splicing is probably just noise, as is much transcription.

Not at all true. We understand most of the genome, and most of it is junk. I must suppose that you have been selectively reading only what you want to be true. Though it’s true that the popular press is a bad source for science, and creationist web sites are worse.

Then you should pay attention when people cite actual data to you, as has happened many times, all of which you have ignored. This is not good practice.

Judging by result, most mutations are neutral. Judging by result, most protein differences between humans and chimps are neutral. You have been shown publications to that effect. Have you noticed them?

Most of the non-coding regions are junk. Most indels are in junk DNA and affect nothing.

I expect you made some faulty assumptions. If you would run it by here, someone might be able to point out those assumptions. I’m guessing a combination of requiring sequential mutations and assuming a particular target (the Texas sharpshooter fallacy).

I’d be interested in your reasons for thinking that a few thousand mutations couldn’t do the job and your reasons why they would have to “line up”, whatever that means.

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Are you aware there are literally millions of SNPs in my genome (and yours) and most have little or no effect on my (or your) fitness. Most are selectively neutral.

No further comments!

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12 posts were split to a new topic: Comparing chimp and human intelligence: overlap or apples and oranges

It seems as though your argument is as follows:

  1. We only understand the 1.5% of the genome that codes for proteins, so let’s just look at differences in proteins.
  2. All changes to proteins are non-neutral.
  3. Therefore most mutations are non-neutral.

Can you spot any flaws in that line of logic? Perhaps a non-sequitur, invalid premises, and some circular reasoning?

Mutations are changes to the DNA, these may or may not result in changes to protein sequences. Changes to protein sequences may or may not be neutral. I already pointed out to you that most of the nucleotide differences in humans and chimp protein-coding genes are synonymous - they don’t change the protein sequence.

We know the specific value isn’t the point, but why use an outdated value after you’ve been provided with a more correct one? If you just want to use a nice round number, use 70%, it’s closer to the true value than 80%. It’s frustrating seeing you constantly reference the outdated figure as though all of our comments are just falling on deaf ears. It doesn’t inspire confidence.

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Alternative splicing Cancer Pubmed. @Ahmed_AbdelSattar

9,081 results

Cancer cells are often formed when embryonic pathways are unregulated. Alternative splicing is active during embryo development.

We don’t have an “80% difference”, rather 71% of human-chimp orthologous protein sequences (that is, protein sequences inherited from the common ancestor of humans and chimps) differ by at least one amino acid. The remnant 29% are identical, that is, if we see “A” in the human version, we also see “A” in the chimp version: this happens for every amino acid position in the protein sequence.

We know that 8% of the human genome is composed of ERVs which is way above your 1.5% mark. We know a lot more of course, but this is sufficient to show the inaccuracy of your statement.

If we read the same primary literature on this topic, then you would know this is an empirically false claim. You are really insensitive to actual evidence.

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Yes, but Gaussian with respect to what? Location? Gaussian would be particularly odd with respect to location.

Base substitution rates are higher in closed chromatin regions compared to open.

I was using the statistical definition of random normal, as in a Gaussian distribution.

Incomplete lineage sorting. It is one example of the noise that is expected in a stochastic biological process.

Nota bene: the existence of noise does not cancel the signal of common descent, which is quite strong.

Regards,
Chris

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I do. And it’s not where you think it is, or want it to.

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:nerd_face:
This reminds me of New Testament Textual Criticism, where among manuscripts and manuscript text-types there are thousands of textual variants, but most variants are meaningless since they only affect orthography (spelling of words) and syntax, but not the overall meaning of most of the NT text. It’s all basically the same, although there are some passages that account for the small percentage of very important variants that affect the meaning of the text. Just because there are thousands of differences doesn’t mean they are meaningful, and lay-people can misuse “thousands and thousands” of variants to mean that the text is highly unstable all throughout, which is not accurate. There are important variants only in certain places like Mark 16:9-20; John 7:53–8:11; and 1 John 5:7 [in King James/Textus Receptus].

Of course, this is just an analogy, I know it doesn’t all completely translate analogously to these issues of “orthologous protein sequences” coming DNA transcription…but just saying.

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Gene deaths, per the paper, seem to be the main factor contributing to that noise, but ILS might be significant as well.

@thoughtful based on the paper, gene deaths were highest in the lineage leading to chimps and bonobos, hence, explaining why the gene content in humans and gorilla are more similar relative to chimps. Imagine there were 30 genes on the Y-Chr of the ancestral population (AP) that gave rise to chimps, humans and gorillas. When all three split from that ancestor, two genes from the AP “died” in humans and gorillas, but ten of those genes died in chimpanzees. This means if you examine present-day Y-Chr gene content among the great apes, the gorilla gene content would be similar to that of humans, and both of their gene contents would be less similar to that of chimps.

Absolutely.

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