Rebuttal To Creationists - "Since We Can't Directly Observe Evolution..."

The Kishony and Lenski experiments are not descent with modification? You are the one who is saying that we shouldn't use these treatments. Don't look at me.

So this whole time you've been going on and on about those experiments, and they aren't even descent with modification. Go figure. Don't you have google?

There goes all of your papers. Guess they are all wrong. None of them actually refer to descent with modification.

. . . in asexual populations. Your title is incomplete.

The one sentence that disqualifies Kleinman from commenting on evolution.

That's my suspicion. Even worse, he doesn't seem inclined to learn about sexual reproduction. It's almost as if he is trying to play the plausible deniability card. If he doesn't understand sexual reproduction then he can "plausibly" deny that his papers don't apply to all situations. That's probably why he refuses to engage with anything outside of his usual hobby horses. He can't venture outside of his own echo chamber. He can't even deal with a paper that discusses a beneficial mutation rate in E. coli of 1 in 10 million replications. His mind glitches and he does whatever he can to never address it. That's not part of the echo chamber, so he can't even begin to admit that it exists.

New alleles are created by mutation. Where asexual and sexual populations differ is how those beneficial mutations interact within the population.

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To investigate how sex improves the efficiency of selection, we analysed the dynamics of adaptation. As in earlier studies21,22, asexual populations exhibit signatures of hitchhiking and clonal interference (Fig. 2a–d). Groups of functionally unrelated mutations, linked within the same genetic background, change in frequency together as clonal cohorts. The outcomes of evolution are determined by competition between these cohorts. In contrast, sexual populations are not characterized by cohorts of linked mutations (Fig. 2e–h). Instead, the dynamics of each mutation is largely independent of other variation in the population. In these populations, mutations that occur on different backgrounds fix independently, while others briefly hitchhike to moderate frequencies where they persist or are eliminated from the population.
Sex speeds adaptation by altering the dynamics of molecular evolution | Nature

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Your math is wrong because it does not incorporate sexual reproduction.

It's how those beneficial mutations move towards fixation that differs between sexual and asexual populations. That's the part you keep getting wrong. Just like the Lenski experiment which you claim is a valid experiment for demonstrating descent with modification.Also, you keep skipping the fact that the sexual and asexual populations were in the same exact environments. However, there was no clonal interference in the sexual populations, contrary to your papers on the math of evolution. So says the person who generalizes to all of evolution based on two experiments using asexual populations. I already did that. Here it is again. Do I need to walk you through that paper?

Then why do you keep claiming that clonal interference is a problem in human evolution? Except that it does.

If that is what you think then you know nothing about biology. It isn't a changing environment that causes clonal interference. I never said that.You claimed that multi-drug resistance does not evolve in HIV, and that it definitely doesn't do so by recombination. In reality, it does. Reality wins. You are wrong.

So says the person who can't measure the entropy of a DNA sequence, and a person who thinks changing environments cause clonal interference in sexual organisms.

Then you don't understand what either is. You are missing a big part of the probability which is the total number of possible beneficial mutations in a given genome in a given environment. That is why adaptive mutations for different phenotypes will occur at different rates, such as in the case of the Lederberg experiment where beneficial mutation rates differed by a factor of 1,000 for different adaptive phenotypes.This is the part you keep getting wrong. It's like claiming the odds of guessing heads on the flip of a coin is 1 in 150 million because those are the odds of winning the Powerball. Why would a changing environment cause clonal interference in a sexual population? Explain. The asexual populations were in the same exact conditions, and they had clonal interference. The sexual populations did not. Can you explain this or not? Guess what, it has nothing to do with the constant environment. If it did, then there wouldn't have been clonal interference in the asexual populations. I ALREADY HAVE!!!!! Notice the bit about beneficial mutations moving towards fixation independently of other alleles? That's how it works.added in edit . . .If you need a more obvious explanation:

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Because the availability, frequency, and strength of beneficial and deleterious mutations vary depending on the environment, ALE [adaptive laboratory evolution] in different environments can yield different intra-population dynamics. In many environments, clonal interference shapes population structure during microbial adaptive evolution, wherein many beneficial mutations co-arise and compete as subpopulations (Fig. 1)19,20. The presence of sexual recombination is theorized to have two advantages for an evolving population: reducing clonal interference thereby speeding evolution (Fig. 1d) and to break apart hitchhiking (deleterious or neutral) mutations from strong beneficial mutations. Additionally, an increased mutation rate is expected to expedite the rate of fitness improvement by increasing the availability of beneficial mutations (Fig. 1c), but also increase the accumulation of deleterious mutations.
Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes - PMC

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You can't tell us how drug resistance evolves. You get it wrong at every turn.For example, why does chloramphenicol resistance evolve faster in sexual hypermutating strains of E. coli than it does in standard and hypermutating strains of asexual E. coli? Why does sexual reproduction fail to speed up evolution of trimethoprim resistance?Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes - PMC

So you admit that you can't do it. In order for you to claim that you would need to calculate the entropy of the different DNA molecules. What about the change in entropy for the process of reproduction? Going from one strand of DNA to two strands of DNA? Is that a decrease or increase in entropy? You are the one who thinks a constant environment is what reduces clonal interference in sexual populations, not me.