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

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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You still can't address it.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? Now you have to lie about what I have said. I never said those things, and the papers I cited never said those things. Why do you lie on a regular basis?Read the citations. They clearly state that recombination is factor in the evolution of multidrug resistance in HIV. If all you can do is lie about what those papers say, then what does that say about your argument?

Kleinman:

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You think this causes UCD, so go for it, explain how a phage makes this possible.

Taq:

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I think it proves your claim about 1 adaption per 1 billion replications wrong. You still can't respond to this????

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Go tell Kishony and Lenski they are wrong. And then explain how a phage make UCD possible.

Kleinman:

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You think that combination therapy doesn't work because of recombination, there is far more literature that says it does work. It works for HIV, weeds, and insects. You are wrong.

Taq:

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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.

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Tell everyone treating HIV with combination therapy and everyone using combination herbicides and pesticides they are wrong.

Kleinman:

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Show me the paper that explains how drug resistance evolves.

Taq:

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I already did that.
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Sexual recombination and increased mutation rate expedite evolution of Escherichia coli in varied fitness landscapes | Nature Communications

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Tell Kishony, Lenski and Desai, I'm sure they would be interested. Of course, you have no idea how drug resistance evolves.

Kleinman:

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Only in a single selection pressure constant environment and that only gives a slight improvement in fitness. In a multi-selection pressure environment with multiple selection pressures, it's a different game even if you think that evolution works the same in a constant single-pressure environment as in a varying multiselection pressure environment.

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...Clearly, Haldane’s scenario does not explain our simulation results as shown in Fig. 2...

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Wow, you have a simulation, try doing an experiment with real populations and real selection conditions.

Kleinman:

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Tell Kishony and Lenski to use a phage and their experiments will evolve instantly.

Taq:

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You still can't address it.

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I have, you want me to explain your reference and I tell you to explain how a phage makes UCD possible. Do you want me to explain non-target site resistance to you?

Kleinman:

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So nobody should use combination therapy for the treatment of HIV, weeds, and insects because Taq says he read it.

Taq:

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Now you have to lie about what I have said. I never said those things, and the papers I cited never said those things. Why do you lie on a regular basis?
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Read the citations. They clearly state that recombination is factor in the evolution of multidrug resistance in HIV. If all you can do is lie about what those papers say, then what does that say about your argument?

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Don't be silly, you are the one claiming that recombination makes combination therapy fail. But now you are claiming something different. Do you think that combination therapy impairs evolution and if so, why?

Ouch! You really know how to hurt a bloke ...

There's probably not much difference between a dozen verified ERVs and 200,000 questionable ERVs.Everyone knows that Darwinist scientists can't be trusted and that they exaggerate the evidence for their cherished beliefs.It's a bit like how the media reported that "300,000" spectators lined the streets to watch the Sydney Gay Mardi Gras, but the police reported a crowd of considerably less - about 30,000.

I don't know who you think is "everyone" but it sure looks like the kind of exaggeration of your cherished belief, that you are talking about. It's interesting that you couldn't provide an example of scientists exaggerating anything, but rather a completely unrelated example.

A classic example is evolutionary scientists claiming that they "know how evolution works" ... which is actually worse than an exaggeration ... it's a flat-out lie. It's impossible to know what process was responsible for producing the changes in life-forms evident in the fossil record."The deceit is sometimes unconscious, but
not always, since some people, owing to their sectarianism, purposely overlook reality and refuse to acknowledge the inadequacies and falsity
of their beliefs."Pierre-Paul Grassé, EVOLUTION OF LIVING ORGANISMS, TRANS. FROM FRENCH (ACADEMIC PRESS: NEW YORK, NY, 1977) P.8 NOV 30 . 1977Another source of Darwinist exaggeration is transitional fossils .... Archaeopteryx, is a classic example.In short, anyone who trusts what Darwinist scientists say is a fool.

It's interesting that you couldn't provide an example of scientists exaggerating anything, but rather a completely unrelated example.

Taq:

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The chimp genome paper is 17 years old. Six years before McLatchie tried to claim that there are less than a dozen ERV's shared by humans and chimps there was a chimp genome paper that demonstrated how chimps and humans share over 99% of the 200,000 ERVs found in the human genome.

Dredge:

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There's probably not much difference between a dozen verified ERVs and 200,000 questionable ERVs.
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Everyone knows that Darwinist scientists can't be trusted and that they exaggerate the evidence for their cherished beliefs.
​
It's a bit like how the media reported that "300,000" spectators lined the streets to watch the Sydney Gay Mardi Gras, but the police reported a crowd of considerably less - about 30,000.

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This claim about ERVs has to be one of the worsts that biologists come up with. Retroviruses kill most of the cells they infect. Just look at what happens to people with HIV and what it does to their immune systems. Taq then brings up an example of koalas and retroviruses, and it is ruining their immune system and possibly driving them to extinction. And then they expect you to believe them that a germ cell line can have 200k retroviral infections. Maybe a moron like Tany thinks that but he also doesn't know how descent with modification works and antibiotic resistance evolves based on the Kishony experiment which is repeatable and measurable. This happens when you chase bugs and think it teaches you about biological evolution.

Tanypteryx:

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It's interesting that you couldn't provide an example of scientists exaggerating anything, but rather a completely unrelated example.

Dredge:

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A classic example is evolutionary scientists claiming that they "know how evolution works" ... which is actually worse than an exaggeration ... it's a flat-out lie. It's impossible to know what process was responsible for producing the changes in life-forms evident in the fossil record.
​
"The deceit is sometimes unconscious, but
not always, since some people, owing to their sectarianism, purposely overlook reality and refuse to acknowledge the inadequacies and falsity
of their beliefs."
​
Pierre-Paul Grassé, EVOLUTION OF LIVING ORGANISMS, TRANS. FROM FRENCH (ACADEMIC PRESS: NEW YORK, NY, 1977) P.8 NOV 30 . 1977
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Another source of Darwinist exaggeration is transitional fossils .... Archaeopteryx, is a classic example.
​
In short, anyone who trusts what Darwinist scientists say is a fool.

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Tany is the worst kind of example. He takes an observation whether it be fossils or genetic sequences he calls ERVs and draws any kind of conclusion he wants but ignores the Kishony and Lenski experiments which are repeatable and measurable. It would never enter his mind that these are sequences that control the expression of coding genes so that he doesn't have hair growing out of his eyeballs and fingernails growing from his nose.

Tanypteryx:

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It's interesting that you couldn't provide an example of scientists exaggerating anything, but rather a completely unrelated example.

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No one can claim that you are exaggerating the Kishony and Lenski experiment. You don't know anything about them or how they work. But you are an expert on retroviruses and how a germ-cell line can have 200k infections and not cause any harm and how a single fossil shows how reptiles evolve into birds and fish evolve into mammals. You are a very smart bug chaser that knows everything about biological evolution except how it works.

Right, you are avoiding it. Here it is again.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? That is a lie. It is the authors of peer reviewed papers that are saying recombination is an important factor for developing multidrug resistance in HIV.

Yes, it is an example of a circulating retrovirus producing endogenous retroviruses, something you claim can't happen. Reality trumps your empty claims.

We seem to be in a liars for Jesus phase again.