Did Darwin get anything correct and what did Darwin get wrong?

I wonder if Dan Eastwood (@EastwoodDC) might reply here. He is a biostatistician, and you couldn’t snow him with your misperceptions (not that you have anyone else, only yourself).

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It’s a very basic mistake:

@amkleinman is painting the targets around the bullet holes.

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Ah, the Hawaiian sharpshooter. :grin: (I don’t want to be statist.)

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@Randy: His clothing is a bit of a non sequitur for Hawaii – I probably should have said Wyoming (Wyomingite?) sharpshooter. There are way more cowboys there.

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I realize. I was jumping ahead to what happens with these mutations. It certainly is not that chimpanzees turn into humans because humans evidenced larger populations, which is where this seemed to be going.

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Are chimpanzees a branch living on a branch? Why haven’t they branched out like humans?

Steve, you will only confuse Ron with the facts. What do you think of T_aquaticus’s claim that if a random event happens, its probability is 1?

Does your first-year biology textbook tell you that you can’t compare the reproductive fitness of different species? What if a farmer asks a biologist whether he should grow apples or oranges on his farm? Does the biologist say, sorry, I can’t tell you which would have better reproductive fitness because they are different species.

I don’t recall saying that. Post the quote where I said that. And you still haven’t told us what gene polymorphism is or what a selective sweep is.

Do you realize that Desai is trying to duplicate the Lenski experiment except with sexual replicators? How exactly does Desai perform his experiment to get improved fitness to reproduce from his population?

Do you think that humans got improved fitness to reproduce over chimpanzees by neutral evolution? If so, explain how.

So, how did the 17 mutations from your chimp/human example fix?

Why would drawing any two cards be highly improbable? It is only when you draw specific cards that the probabilities become a factor.

You are half right that I’m not predicting which mutations will occur before the happen. When a replicator does 1/(mutation rate) replications (actually slightly more because multiple different mutations can occur at a given site), it is doing an exhaustive search of the sample space, that is, a mutation occurs at every site in the genome. That’s how the Kishony experiment works. In that colony of a billion, there is at least one member in that colony with a mutation at every site in the genome. That lucky member with an adaptive mutation at the correct site can grow in the next higher drug concentration region.

Descent with modification does not depend on combinatorial math. Recombination does.

Maybe he can correct T_aquaticus’s strange idea that when an event happens, its probability goes to 1. He can check out the math I had published which was peer-reviewed by experts in Probability theory and Statistics. He can try and find an error in the nath, which I doubt he will.

Good luck with your Texas sharpshooter argument because that’s exactly how descent with modification and adaptation works. Only when the population does 1/(mutation rate) replications do you get a reasonable probability that at least 1 adaptive mutation occurs. That’s how the Kishony experiment works, that’s how the Lenski experiment works and that is why humans and chimps did not descend from a common ancestor. You don’t have nearly enough replications.

I’m still waiting on your experts in biology and mathematics to explain how drug resistance evolves and why cancer treatments fail.

That’s exactly what it does. You are mistakenly thinking about the probability of the next event.

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“Read carefully, I wrote selective, not beneficial mutations.” --@amkleinman

I’m not your dictionary.

Desai introduces rounds of sexual reproduction in some populations and only asexual reproduction in others. He got different results in the different populations. Why do you think he got different results?

No, I don’t. I am showing you the math for how many mutations we would expect to see if humans and chimps evolved from a common ancestor. You continue to ignore it.

I don’t even know if all 17 are fixed since it is only a comparison of two genomes.

I just showed you.

It is only when you SPECIFY AHEAD OF TIME that probabilities become a factor. You aren’t doing that with mutations. You are specifying AFTER THEY HAVE APPEARED. It is absolutely guaranteed that there are going to be DNA differences between two primate species if they have evolved for 5 million years from a common ancestor. The differences that do result after evolution are always going to be extremely improbable. The very act of evolution guarantees that we will get a mixture of mutations that are extremely improbable in the very same way that drawing 5 cards guarantees that I will have a hand with a probability of 1 in 2.6 million.

Also, you keep using the mutation rate in bacteria to model humans. This is wrong. The mutation rates are different by a factor of about 10. You also assume that there is only one mutation at any one time that can be beneficial. This is wrong for the vast, vast majority of cases in nature. The paper I gave you for human skin color is a perfect example of this, as is the multiple different beneficial mutations for lactase persistence.

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Yes my first year biology textbook told me that. And I have taught the same to my own university students for the last 25 years. And it appears even in Wikipedia so apparently is pretty universally known.

The question you pose about the farmer contemplating his choice of crops, is a question of which species is better adapted for the prevailing environmental conditions (best able to exist in a certain ecological niche) and is also a question of economics and the markets. Adaptations to different niches is different than “quantitatively comparing the fitness of two species” which is impossible.

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it is absolutely ridiculous to think that there is only 1 possible beneficial mutation in the human genome across all of the environments that humans live in.

There are plenty, as shown by the math for the fixation of neutral mutations.

That’s completely irrelevant to human evolution.

Another paper showing the math:

Simulations of asexual and sexual populations show that in asexual populations just a few of the beneficial alleles can reach fixation because of clonal interference. However, sexual reproduction allows for the shuffling of mutations across the genome which can fix all 100 beneficial loci.

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Are you really? By now we’ve seen you pour forth a multitude of ‘questions’ - every one of which seems to have been answered (many repeatedly) by mainly @T_aquaticus, @klw, and others too. And I thank you for those questions - even if poorly motivated -, because they do make an excellent springboard for knowledgeable people here to continue to educate many of us (like me) who would not be able to answer your questions, and might otherwise be cowed into thinking that perhaps there are problems, where in fact there are none.

It does seem that a want of humility on your part may be preventing you from really benefitting from the answers supplied you here, though. It is the same scourge that reveals so much ideological fruit today for what it really is, and this does not go unnoticed by the observant young. You could be advancing your own knowledge instead of sacrificing it to the service of an ideology that has not served you or others well.

Do you think that claiming the probability of an event happening makes that probability go to 1 is a rational answer? Perhaps that is why T_aquaticus can’t explain the evolution of drug resistance and why cancer treatments fail. Doesn’t anyone post on this forum that understands basic probability theory? After all, descent with modification and adaptation is a stochastic process. I’m waiting for a scientific answer, not some weird misunderstanding of well know mathematical principles.

Lots of people do, but apparently you don’t. You actually think you can apply mutation rates in bacteria to human populations. You also think you can apply the probability of antibiotic resistance occurring in bacteria to primate populations. This is all wrong. You act as if one beneficial mutation per billion replications is some sort of physical law. It isn’t. You also can’t understand that drawing a 3 of clubs and a 5 of hearts has the same probability as drawing an ace of spades and an ace of clubs.

You can’t even understand the difference between sexual and asexual reproduction. You can’t understand how there is more than one gene in a genome and how those genes are shuffled in sexual reproduction. Nope. For you, beneficial mutations can only happen in one gene, and one gene only. And no matter what, the rate at which those beneficial alleles appear has to be once in 1 billion replications, no matter what. Never mind you that even the rate of evolution for different single selective pressures in E. coli can differ 1,000 fold.

That’s a 1,000 fold difference in the rate of resistance to phage and antibiotic in just one species of bacteria.

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That question is not even constructed properly. You just said a probability of an event makes the probability go to 1. Talk about irrational. The probability of an event happening is 100%… when it has already happened. That’s what you’re not getting (among manifold other things). The probability of the next event is not 1. But like all the rest, the question has already been asked and answered, and more than once. I think the probability of this happening again is high.

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@amkleinman: Let’s try this. If you have a 3 of clubs and a 5 of hearts in your hand, what’s the probability of your having a 3 of clubs and a 5 of hearts in your hand? Or what’s the probability of your having already drawn a 3 of clubs and a 5 of hearts?