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

You didn't address what I said. Here it is again.The Lenski experiment had a constant environment for 10's of thousands of generations. Are you saying that a constant environment does not disqualify an experiment?As to the Kishony experiment, what would the dynamics of adaption to chloramphenicol look like if the E. coli in the experiment were undergoing sexual recombination? How would it compare to a population of asexual E. coli adapting to the same environment?Imagine if scientists published a paper on that very experiment? Well we don't have to imagine.

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From the evolution experiments in each fitness landscape, we find that increased mutation rate expedite adaptation in some environments tested, and that sexual recombination further speed up adaptive evolution in some environments. We also observe strong evidence of an in situ recombination event that help to alleviate clonal interference and generate a superior genotype in a sexual E. coli.

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Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes

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Look at the title of that paper. Wouldn't you know it, sexual recombination speeds up adaptation, and it does so by alleviating clonal inteference. More from the paper:

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The results suggest that sexual recombination facilitates a more swift increase in resistance, probably by combining compatible determinants of CM tolerance.

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CM tolerance is chloramphenicol resistance. Sexual recombination combines different beneficial mutations in different genes into the same genetic background, thereby speeding up adaptation to chloramphenicol. Yes, it is sexual recombination that alleviates clonal interference. Why wouldn't those same beneficial mutations increase in frequency if there was sexual recombination in every generation? The experiment was already run. It helps.

The Peabody et. al. (2017) paper mentioned earlier has a great illustration of how adaptation differs in asexual and sexual populations:
from the paper:
Theoretical impacts of mutation rate and sexual recombination on population structures. a Mutationally limited fitness landscape, where most mutations fix in a single sweep with very little inter-clonal competition. b Increased mutation rate over (a), more competition and faster evolution observed, but some mutations are lost due to inter-clonal competition. c Adding sexual recombination to (a), due to few available beneficial mutations, no strong influence on evolution is observed. d Both sexual recombination and increase in mutation rate from (a), more rapid evolution is observed and fewer beneficial mutations are lost due to clonal interferenceThe two variables here are mutation rate and recombination. The two plots on the left are with the lower mutation rate. The two plots at the bottom are with sexual recombination.a. low mutation, asexual
b. low mutation, sexual
c. high mutation, asexual
d. high mutation, sexualEven at low mutation rates, you can see that the sexual population gets all 5 beneficial mutations which the asexual population is limited to 4 because clonal interference drove the ABD lineage to extinction. In the sexual population, recombination between the ABC and ABD lineages put all 5 beneficial mutations into the same background. When mutation rates are even higher, the differences can be even more stark.

You still haven't addressed what I said.The Lenski experiment had a constant environment for 10's of thousands of generations. Are you saying that a constant environment does not disqualify an experiment?
​ The adaptive alleles would increase in frequency if there was sexual reproduction in every generation. How does recombination work differently in varying environments? The Lenski experiment used a constant environment of 10's of thousands of generations."The Kishony and Lenski experiments demonstrate exactly how descent with modification operates."--Kleinman

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It doesn't work with HIV, weeds, and insects.

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Yes, it does.

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These findings emphasize that recombination can participate in the adaptation of HIV to changing selective pressure, both by generating novel combinations of resistance mutations and by maintaining diversity in genomic regions outside those implicated in a selective sweep.
Just a moment...

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So says the person who extrapolates the Kishony/Lenski experiment to all of evolution. You are really mixed up now. You were saying that Desai had to asexual reproduction in a constant environment in order to increase the frequency of beneficial alleles. Why wouldn't those same alleles increase in fitness with sexual reproduction in every generation and a constant environment? Why did Lenski use 10's of thousands of generations of constant selection? Why don't you show us the principle. Show us a real world example that compares asexual and sexual reproduction in a changing environment. Show us the math.Put up or shut up.

Except that it does. Peabody et al. observed those same effects in their experiment. Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapesBeneficial mutations for CM resistance can occur in different genes which makes it a candidate for studies on sexual recombination. They found that the combination of a faster mutation rate and sexual recombination increased the speed of adaptation to CM resistance.The genderless are the sexual reproducers, and higher mutation rates were induced with arabinose (ara). Therefore, the sexual reproducers with high mutation rates are the genderless ara+, and they adapted to CM the fastest.

The more you look around the more examples you can find of sexual recombination increasing the efficiency of adaptation.

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The findings presented above indicate that multiple beneficial mutations were present in the evolving populations and that, as required by the FM model, in the absence of recombination, competition between these mutations was associated with slower fixation times. Indeed, this competition was so strong that in the rec− lines, the relative effect of the focal spoTEv mutations became negative, such that additional beneficial mutations must have occurred on the same background in order for the focal mutation to fix. The possible existence of linked deleterious mutations cannot explain this result by itself, because the deleterious mutations would impose a constant cost to the focal mutation. By contrast, in the rec+ lines, the relative advantage conferred by the spoTEv mutations showed no overall change, indicating that recombination effectively reduced the effect of competition between beneficial mutations. This reduction in competition is consistent with recombination bringing competing beneficial mutations together into one lineage, the mechanism proposed by the FM model.
Recombination Speeds Adaptation by Reducing Competition between Beneficial Mutations in Populations of Escherichia coli | PLOS Biology

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The rec+ populations were recombination positive. Wouldn't you know it, recombination alleviated clonal interference and sped up adaptation by putting beneficial mutations from different lineages into the same genetic background. Seems to be a repeating theme.

The Lenski experiment used a constant environment and a single selection pressure for 50,000 generations."The Kishony and Lenski experiments demonstrate exactly how descent with modification operates."--Kleinman

Joshua and Esther Lederberg published a hallmark paper in 1951 titled, "Replica Plating and Indirect Selection of Bacterial Mutants", which can be found here:REPLICA PLATING AND INDIRECT SELECTION OF BACTERIAL MUTANTS - PMCLuria and Delbruck went on to explain the processes that undergirded the Lederberg's results which later won Luria and Delbruck a Nobel Prize.There is one interesting observation in the Lederberg paper:"The culutre is fully sensitive to the phage T-1, as well as to streptomycin, and like most E. coli strains gives rise to resistant mutants at rates of approximately 10E-7 and 10E-10 per division, respectively."In this example we saw a beneficial mutation rate of 1 in 10 million and 1 in 10 billion to two different selection pressures using the same strain of E. coli.Kleinman is telling us that one beneficial adaptation every billion divisions is some universal constant, or something of the like. It is so universal that it can even be applied to human evolution. However, in another experiment using E. coli we see beneficial mutation rates that are quite different than what Kleinman claims.If Kleinman's math can't even apply universally to evolution in E. coli, what hope does it have of applying to any other species? Reduces the probability of what, and compared to what?Would a changing environment cause clonal interference in a sexually reproducing population? NO.Would beneficial alleles in the new environment increase in frequency in the new environment in sexually reproducing populations? YESWould you get a combination of beneficial alleles faster in a changing environment with a sexually reproducing population compared to an asexual population? YES In a constant environment, why wouldn't beneficial alleles increase in frequency in a sexually reproducing population? I do know the answer. Sexual recombination doesn't change in a changing environment. It works the same way. When humans move to a different environment their gametes still work in the very same way. You said the Lenski experiment demonstrates exactly how descent with modification works, and it had 50,000 generations in the same exact environment. You reject the Desai experiment because it had a constant environment for 90 generations.Hypocrisy much? I'm not the one rejecting published science. You are. Then show it in a real population. Show how an asexual and sexual population evolve in changing environments with multiple selection pressures. All of which increase their rate of adaptation through sexual recombination.

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The acquired inheritable trait of plants to survive and reproduce under herbicide exposure is defined as resistance. Herbicide resistance is an extraordinary example of adaptive evolution in weed species infesting agroecosystems with clear detrimental consequences on agriculture sustainability around the globe (Palumbi, 2001; Llewellyn et al., 2016). Multiple herbicide resistance is a compelling evolutionary process in which distinct survival mechanisms are present in a population or are combined within single plants, each endowing resistance to dissimilar site of action herbicides (Hall et al., 1994; Gaines et al., 2020). These multiple mechanisms may involve either target site (TSR) or non-target site resistance (NTSR) mechanisms or any combination endowing multiple resistance. Multiple resistance can evolve through unique events that sequentially select for resistance alleles within single plants and/or genetic exchange of independently evolved resistance mutations through pollen outcrossing among plants within or between populations.
Frontiers | Editorial: Multiple Herbicide-Resistant Weeds and Non-target Site Resistance Mechanisms: A Global Challenge for Food Production

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Wouldn't you know it, recombination can speed up the acquisition of multi-herbicide resistance.

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Multidrug-resistant (MDR) HIV-1 presents a challenge to the efficacy of antiretroviral therapy (ART). To examine mechanisms leading to MDR variants in infected individuals, we studied recombination between single viral genomes from the genital tract and plasma of a woman initiating ART. We determined HIV-1 RNA sequences and drug resistance profiles of 159 unique viral variants obtained before ART and semiannually for 4 years thereafter. Soon after initiating zidovudine, lamivudine, and nevirapine, resistant variants and intrapatient HIV-1 recombinants were detected in both compartments; the recombinants had inherited genetic material from both genital and plasma-derived viruses. Twenty-three unique recombinants were documented during 4 years of therapy, comprising ∼22% of variants. Most recombinant genomes displayed similar breakpoints and clustered phylogenetically, suggesting evolution from common ancestors. Longitudinal analysis demonstrated that MDR recombinants were common and persistent, demonstrating that recombination, in addition to point mutation, can contribute to the evolution of MDR HIV-1 in viremic individuals.
https://www.liebertpub.com/doi/10.1089/aid.2011.0383

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Recombination is an important factor in evolving multidrug resistance in HIV.

So your only response is to quiz people on terminology? That's it?

Joshua and Esther Lederberg published a hallmark paper in 1951 titled, "Replica Plating and Indirect Selection of Bacterial Mutants", which can be found here:REPLICA PLATING AND INDIRECT SELECTION OF BACTERIAL MUTANTS - PMCLuria and Delbruck went on to explain the processes that undergirded the Lederberg's results which later won Luria and Delbruck a Nobel Prize.There is one interesting observation in the Lederberg paper:"The culutre is fully sensitive to the phage T-1, as well as to streptomycin, and like most E. coli strains gives rise to resistant mutants at rates of approximately 10E-7 and 10E-10 per division, respectively."In this example we saw a beneficial mutation rate of 1 in 10 million and 1 in 10 billion to two different selection pressures using the same strain of E. coli.Kleinman is telling us that one beneficial adaptation every billion divisions is some universal constant, or something of the like. It is so universal that it can even be applied to human evolution. However, in another experiment using E. coli we see beneficial mutation rates that are quite different than what Kleinman claims.If Kleinman's math can't even apply universally to evolution in E. coli, what hope does it have of applying to any other species? It isn't exponential in sexually reproducing populations. Haven't you been paying attention? Beneficial alleles for each of those challenges can be combined into a single genetic background through recombination.You still don't understand how sexual reproduction works.

I am citing published science which demonstrates recombination is an important factor in evolving multidrug resistance.

Still no response to the actual material????Joshua and Esther Lederberg published a hallmark paper in 1951 titled, "Replica Plating and Indirect Selection of Bacterial Mutants", which can be found here:REPLICA PLATING AND INDIRECT SELECTION OF BACTERIAL MUTANTS - PMCLuria and Delbruck went on to explain the processes that undergirded the Lederberg's results which later won Luria and Delbruck a Nobel Prize.There is one interesting observation in the Lederberg paper:"The culutre is fully sensitive to the phage T-1, as well as to streptomycin, and like most E. coli strains gives rise to resistant mutants at rates of approximately 10E-7 and 10E-10 per division, respectively."In this example we saw a beneficial mutation rate of 1 in 10 million and 1 in 10 billion to two different selection pressures using the same strain of E. coli.Kleinman is telling us that one beneficial adaptation every billion divisions is some universal constant, or something of the like. It is so universal that it can even be applied to human evolution. However, in another experiment using E. coli we see beneficial mutation rates that are quite different than what Kleinman claims.If Kleinman's math can't even apply universally to evolution in E. coli, what hope does it have of applying to any other species? I'm not speculating. The scientific literature demonstrates that recombination is an important factor in multidrug resistance in HIV and multi-herbicide resistance in weeds. Apparently, you haven't been reading the papers I have cited for you.

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As stated above, Haldane (1957) argued that the costs of natural selection accumulate over loci, i.e., the reproductive cost of allele substitution at two loci would be twice the cost at a single locus. Consequently, the time required for substitution should be twice as long. In general, if it takes t generations for a gene substitution at a single locus, it should take Lt generations for substitutions at L loci. Applying this logic to our model, given that it takes 400 generations for allelic substitution at one locus, it should take 40 000 generations for substitutions at 100 loci. This prediction is in stark contrast to our finding that it takes only 400 generations for allelic substitution at all 100 loci (see Fig. 2F). How can we explain this major difference between Haldane’s prediction and our findings?
Clearly, Haldane’s scenario does not explain our simulation results as shown in Fig. 2. The reason for the discrepancy is, we believe, that Haldane’s argument assumed that the optimal genotypic combination had to be already present in the initial population and that genotypes could be considered as fixed entities that reproduce themselves from one generation to the next. But these assumptions do not hold for a sexually outbreeding population. First, the population is usually not large enough to contain even a single individual with the vanishingly rare optimal genotypic combination; this fact has already been pointed out by Ewens (1972) and Maynard Smith (1976). Second, specific genotypes are broken down by recombination each generation and replaced by other genotypic combinations (Hickey and Golding 2018). The process of recombination involves the continual disassembly of existing genotypes and reassembly of new genotypes from one generation to the next. Because of this process, however, those genotypes that are expected to be vanishingly rare when the allele frequencies are low will be automatically generated through recombination once the allele frequencies begin to rise in response to selection (Muller 1964; Hickey and Golding 2018). Consequently, there is no need for the massive culling that would be required in a very large initial population that contained an extremely rare optimal genotype. Thus, in an outbreeding sexual population, recombination solves the perceived problem of costs that are cumulative over different genetic loci. In Haldane’s scenario, it is necessary to “grow” the optimal genotypic combination from an initial, vanishingly rare frequency to fixation. In practice, however, this optimal combination is produced by recombination only near the end of the process. This avoids the huge cumulative cost of natural selection.
Canadian Science Publishing

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Sexual recombination allows multiple beneficial alleles to move towards fixation simultaneously. You keep forgetting that.

I think it proves your claim about 1 adaption per 1 billion replications wrong.Joshua and Esther Lederberg published a hallmark paper in 1951 titled, "Replica Plating and Indirect Selection of Bacterial Mutants", which can be found here:REPLICA PLATING AND INDIRECT SELECTION OF BACTERIAL MUTANTS - PMCLuria and Delbruck went on to explain the processes that undergirded the Lederberg's results which later won Luria and Delbruck a Nobel Prize.There is one interesting observation in the Lederberg paper:"The culutre is fully sensitive to the phage T-1, as well as to streptomycin, and like most E. coli strains gives rise to resistant mutants at rates of approximately 10E-7 and 10E-10 per division, respectively."In this example we saw a beneficial mutation rate of 1 in 10 million and 1 in 10 billion to two different selection pressures using the same strain of E. coli.Kleinman is telling us that one beneficial adaptation every billion divisions is some universal constant, or something of the like. It is so universal that it can even be applied to human evolution. However, in another experiment using E. coli we see beneficial mutation rates that are quite different than what Kleinman claims.If Kleinman's math can't even apply universally to evolution in E. coli, what hope does it have of applying to any other species? IT'S ALREADY PUBLISHED!!!

I think it proves your claim about 1 adaption per 1 billion replications wrong. You still can't respond to this????Joshua and Esther Lederberg published a hallmark paper in 1951 titled, "Replica Plating and Indirect Selection of Bacterial Mutants", which can be found here:REPLICA PLATING AND INDIRECT SELECTION OF BACTERIAL MUTANTS - PMCLuria and Delbruck went on to explain the processes that undergirded the Lederberg's results which later won Luria and Delbruck a Nobel Prize.There is one interesting observation in the Lederberg paper:"The culutre is fully sensitive to the phage T-1, as well as to streptomycin, and like most E. coli strains gives rise to resistant mutants at rates of approximately 10E-7 and 10E-10 per division, respectively."In this example we saw a beneficial mutation rate of 1 in 10 million and 1 in 10 billion to two different selection pressures using the same strain of E. coli.Kleinman is telling us that one beneficial adaptation every billion divisions is some universal constant, or something of the like. It is so universal that it can even be applied to human evolution. However, in another experiment using E. coli we see beneficial mutation rates that are quite different than what Kleinman claims.If Kleinman's math can't even apply universally to evolution in E. coli, what hope does it have of applying to any other species? I cited the scientific literature which clearly stated that recombination is an important factor in multidrug resistance in HIV. Ignore it all you want, it's still there. I already did that.Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes | Nature Communications

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As stated above, Haldane (1957) argued that the costs of natural selection accumulate over loci, i.e., the reproductive cost of allele substitution at two loci would be twice the cost at a single locus. Consequently, the time required for substitution should be twice as long. In general, if it takes t generations for a gene substitution at a single locus, it should take Lt generations for substitutions at L loci. Applying this logic to our model, given that it takes 400 generations for allelic substitution at one locus, it should take 40 000 generations for substitutions at 100 loci. This prediction is in stark contrast to our finding that it takes only 400 generations for allelic substitution at all 100 loci (see Fig. 2F). How can we explain this major difference between Haldane’s prediction and our findings?
Clearly, Haldane’s scenario does not explain our simulation results as shown in Fig. 2. The reason for the discrepancy is, we believe, that Haldane’s argument assumed that the optimal genotypic combination had to be already present in the initial population and that genotypes could be considered as fixed entities that reproduce themselves from one generation to the next. But these assumptions do not hold for a sexually outbreeding population. First, the population is usually not large enough to contain even a single individual with the vanishingly rare optimal genotypic combination; this fact has already been pointed out by Ewens (1972) and Maynard Smith (1976). Second, specific genotypes are broken down by recombination each generation and replaced by other genotypic combinations (Hickey and Golding 2018). The process of recombination involves the continual disassembly of existing genotypes and reassembly of new genotypes from one generation to the next. Because of this process, however, those genotypes that are expected to be vanishingly rare when the allele frequencies are low will be automatically generated through recombination once the allele frequencies begin to rise in response to selection (Muller 1964; Hickey and Golding 2018). Consequently, there is no need for the massive culling that would be required in a very large initial population that contained an extremely rare optimal genotype. Thus, in an outbreeding sexual population, recombination solves the perceived problem of costs that are cumulative over different genetic loci. In Haldane’s scenario, it is necessary to “grow” the optimal genotypic combination from an initial, vanishingly rare frequency to fixation. In practice, however, this optimal combination is produced by recombination only near the end of the process. This avoids the huge cumulative cost of natural selection.

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