It wouldn’t be less miraculous, but it would be more in line with the actual evidence. That’s why guided evolution is preferable to separate creation.
But it isn’t the same signature. It’s different signatures, organized in a special way, the way that common descent would be expected to produce.
Who says they’re better than chimps? Are humans better than frogs? Better than maple trees? That’s the same sort of question. Now why don’t we see transitional forms today? Many possible explanations: some populations could be directly ancestral to humans and could all have transformed (through ordinary processes of mutation, gene flow, etc.); some populations could have been in competition with better-adapted populations and have gone extinct; some populations could just have been unlucky, in the volcano’s path at the wrong time. The point is that we do see such populations in the fossil record. What do you think they’re doing there?
No, as you’ve been told several times, it doesn’t. Most protein differences between chimps and humans are probably neutral or nearly so. And it isn’t even 80%. Why can’t you get that one simple point, if nothing else?
That parenthetical comment is one of the better indications here of how profound is your misunderstanding of evolution. By what objective criteria would a particular phenotype be defined as an “abomination”?
It is obvious that @Ahmed_AbdelSattar has a repertoire of pre-written responses that he just copy/pastes when he feels he needs to say something, whether or not it pertains to the current discussion. The 80% is probably included in them, and he can’t be bothered to edit it.
I just rejected a couple snarky posts. I try to be fairly light-handed with the moderation but this thread is getting a bit aggressive and we don’t want it to get nasty.
So let me just remind everyone of some our community guidelines and expectations.
Especially as this is in the Conversation category, please try to keep the professionalism up and be hospitable as you engage with those you disagree. As much as possible try to keep criticism constructive. Posts should include questions, information, or otherwise move the conversation forward. You can be honest and to the point without being uncivil.
By tolerance , we mean to create space for those with whom we disagree, where we can engage larger questions together, even as we explain our own point of view.
By patience , we mean endurance with one another across our disagreements, where we seek to understand others, and help them understand us.
And many of those residues can be substituted by others with little to no functional effect.
That a protein’s amino acid sequence determines it’s structure and function does not mean many alternative amino acids can not do the job equally well, which as @John_Harshman also told you about, is revealed by the variants that exist in the human population.
Speaking of proteins more generally, biochemical experiments have routinely revealed that variant sites in proteins (those that aren’t conserved) also have little to no functional effects if substituted. Just to pick an example, check this reference on biochemical characterizations of mutations on a human G-protein coupled receptor:
Here they experimentally characterize the functional effects of almost all possible single amino acid substitutions in all positions on the protein, and the result is revealed in Figure 4c:
The residues colored pale green tolerate all possible amino acid substitutions:
Unsupervised learning reveals functionally relevant groupings of residues
Given that our data spans thousands of mutations across several treatment conditions, we used unsupervised learning methods to reveal hidden regularities within groups of residues’ response to mutation. In particular, we applied Uniform Manifold Approximation and Projection (UMAP) (McInnes and Healy, 2018) to learn multiple different lower dimensional representations of our data and clustered the output with density-based hierarchical clustering (HDBSCAN; Figure 4—figure supplement 1; Campello et al., 2013). We found residues consistently separated into six clusters that exhibit distinct responses to mutation (Figure 4A,B). Clusters 1 and 2 are globally intolerant to all substitutions, whereas Cluster 3 is vulnerable to proline and charged substitutions. Cluster 4 is particularly inhibited by negatively charged substitutions and Cluster five by proline substitutions, while Cluster 6 is unaffected by any mutation.
As the paper also states, the tolerance to mutations of individual positions in the protein well predicted by comparative genetics:
Results like these are not at all unusual, so the burden of proof is on you to explain why your non-sequitur has any merit. I remind you that you are the one who attempted to derive the conclusion that the very few amino acid differences between proteins shared among human and chimp must have a functional consequence simply because the majority of proteins have a tiny handful of such differences.
Again I have to say you seem to have a difficult time with the concept of evidence. Evidence does not MAKE anything be true. Something is either true or it is not, regardless of what we happen to have evidence for. But evidence is what should guide our beliefs about what is true.
But what conclusions we, as human beings, should draw about what is true about the world(what should we believe and why?), depends on what evidence we have available to us when we have searched for and collected it.
Given that we have a pattern in the data supporting a hypothesis that explicitly predicts that pattern, and we do not have any competing hypothesis that predicts that same pattern of data, the fact that we do have a hypothesis that predicts it then becomes a reason to accept the hypothesis as likely being true. The data is expected given the hypothesis.
So no, there is no argument from ignorance going on. I am appealing to the fact that we have a hypothesis that makes a whole lot of sense of the data.
No, because I am not saying it’s true just because no alternative hypothesis is known. I’m saying evidence should guide our beliefs, and the evidence only supports one hypothesis.
I can’t make sense of that statement. What is a “general homoplasy”?
So, if the difference between the processing power of the basic desktop PC and the largest cray computer is way larger than the difference between the PC and a calculator… does that make a calculator a computer??!
You reasoning is quite flawed.
You don’t do intra-category comparisons versus inter-category comparisons and reach to anything.
The problem is circular logic again. You start by presupposing common descent, so humans and chimps are great apes, and them you give yourself a green card for doing such a comparison.
I have to tell you it is irrelevant and misleading.
That the Y-chromosome is fast-evolving compared to the rest of the genome, and therefore the prediction that if humans and chimps share a common ancestor, the Y chromosome should be more different on average, than the rest. The authors explain why the chimpanzee Y is more different from human and gorilla with a rather straightforward inference based on observation, and that explanation makes logical sense.
My TI-89 calculator is literally a computer. So are many calculators. Depending on one’s definition of computer, so are most calculators.
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!
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.
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…
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.