Substitutions are mutations.
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This is quite absurd.
I am having a hard time reconciling it with some of howls I got when “Dr” was dropped from Carter and Sanford in a title…
My experience with Sanford is that he does not talk down to people quite that way. I get the sense that most the article was written by @PDPrice. Is that the case?
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To what extent is the genome destroyed by a mutation that increases the femur length by 0.01%? If you can’t answer this, genetic entropy is necessarily false.
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Mutations don’t destroy genomes. Mutations change genomes, the results of which may be neutral, deleterious, or beneficial depending on the local environment. Your nonsense GE claims still assume a static, never changing environment where new local fitness maxima can never appear. Like the rest of your layman’s misunderstanding of basic biology that is demonstrably wrong.
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The more “destroyed” the fitness-contributing parts of the genome gets, the lower fitness gets, and lower fitness is selected against. As the DFE shifts gradually more and more towards being mostly neutral and beneficial (because destroyed functions can only evolve neutrally or regain function), you are no longer accumulating deleterious mutations because they get purged by selection(the fewer fitness-contributing functions remain, the stronger their loss is felt), and countered by the more frequent and larger magnitude beneficials.
No, the other way around.
At very low fitness levels, the fitness impacts of individual mutations are much larger. Taking away 2 ATP molecules per second from the organism that can only make 100 per second matters much more than taking away 2 ATP molecules per second from the organism that can make a million per second.
The fitness-effects of deleterious mutations near the floor are huge, and so are beneficial mutations in turn. Adding 2 ATP molecules to the 100 per second organism is hugely beneficial, but is almost invisible to the million ATP per second organism.
The organism with ten thousand fitness-contributing functions, losing one may matter very little. To the organism with only a few hundred fitness-contributing functions, losing one is felt strongly.
The genome with 100 gene copies of a gene feels very little when one is lost, the genome with 3 copies feels it strongly when one is lost. Etc.
And strongly deleterious and strongly beneficial mutations, which are more frequent at very low fitness levels (where we are at when many functions are near their bottom or destroyed) are selectable.
I’m not convinced this is true, but since already destroyed functions can’t be destroyed even more, further changes to them have become neutral, so don’t contribute to GE, and hence change simply accumulates until functions are gained.
We aren’t inventing computers from scratch, but considering how molecular genetics of reproducting organisms actually work at the biochemical level.
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Please tell @Joe_Felsenstein who made that distinction not me. Maybe it was a typo. I was trying to figure out what he meant.
Certain fields use slightly different terminology. I believe he is referring to the mutation causing an amino acid substitution. The probability of which is not the same as the mutation rate alone due to codon redundancy and mutation bias.
Substitution can also mean a base pair change. Because of ambiguities like these in many fields, there has been an effort to standardize nomenclature in human genetics and reduce the stigma associated with “mutation.” For example, the common usage of SNP should really be replaced by SNV 
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In this case, the term “substitution” is not referring, I think, to any particular type of mutation but to the process of substitution in which a mutation rises from some initial frequency to the point where it is “fixed” (i.e., has a frequency of 1.0 or thereabouts) in the population.
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If you’re implying I wrote the words being attributed to Dr Sanford, you’re definitely not correct. Dr Sanford’s words are his own.
Can’t be answered. You could ask the same about any one typo in isolation, looking at a whole series of progressively added typos in a computer program. Nonetheless, if you add enough typos to a computer program, eventually it will be completely destroyed. The problem is, fundamentally, that engineering is hard. You don’t get it by randomly throwing changes together.
Same old mistake that was directly addressed in the article. The difference in relative fitness is too small to be selectable.
This is your fundamental, fatal problem. You have to be convinced of the obvious.
The human body is vastly more complex and functional than the most complex computer humanity has ever devised. So fundamentally, yes, we’re talking about inventing computers from scratch, one tiny piece at a time, with no designer at all.
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Congrats, you’ve confirmed that genetic entropy is necessarily false.
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Perhaps! I would simply to refer to that process as fixation rather than substitution, personally. But who knows, populations of haploid lights are strange creatures.
No, that is not what I am implying. Rather I am observing that the parts not directly attributed to Sanford likely were written by you. Sanford is much more respectful than the writing in the parts not attributed to specifically to him.
Is that not the case?
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Nature is unified.
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Yes, “fixation” is certainly a less ambiguous term, but “substitution” is sometimes used as well, particularly in the context of molecular evolution analyses where sequences from separate species are compared.
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Genomes aren’t tightly coupled computer code which can be destroyed by typos. Once again you rely on an inappropriate analogy when you can’t provide any scientific evidence to back you specious claims.
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The parts not directly attributed to Dr Sanford were co-written by me and Dr Carter. Dr Sanford only wrote what has been directly attributed. All three of us were in full agreement on the content of the article.
Nature is unified.
Of course it is. We were talking about the speculations of scientists, not nature itself. One field should never take for granted that the speculations of another field must be accurate, such that it interferes with the full exploration of their own field. Sadly, that’s what Dr Felsenstein was saying in his textbook. Don’t bother looking for widespread function in DNA because, essentially, it would mean we should all be dead by now from mutational meltdown.
Don’t you know, the haemoglobin we have today is absolutely destroyed?
Our haemoglobin today is only 43% identical to the reconstructed ancestral haemoglobin. Since this gene is ~150 aa in length, it means there are about 95 differences.
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The “speculations” of astronomy and geology. And of course we gotta steer clear of all that physics stuff.
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Was Sanford in agreement with the claim that @Joe_Felsenstein is not an expert in population genetics?
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And that I am not an expert in virology?
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