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

That swishing sound you hear is Kleinman flailing as Taq hands him his ass.

Kleinman:

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I thought biologists are cloned.

Taq:

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You are flailing.

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Silly boy.

Kleinman:

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How many times do you want to do the Darwin's Finches example. They are doing selective sweeps to increase the frequency of adaptive alleles which increases the probability of an adaptive recombination event occurring. But the alleles have to exist in the first place.

Taq:

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The paper I gave you is studying de novo mutations. Unless you are trying to claim that mutations don't happen in finches I'm not sure what you are trying to argue. We all agree that natural selection is not mutagenesis.

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With an effective population size of 1e5 over 1000 generations, that give about 100 million replications, you would expect de novo mutations. They detect 44 de novo mutations, not all of which are adaptive in this constant single selection pressure experiment. You have about a billion replications for your human/chimp evolution argument but that is in a variable, multiple selection pressure environment. Do you think that adaptive evolution will work more quickly in a variable, multiple selection pressure environment? If so, give us a mathematical explanation with experimental verification.

Kleinman:

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So, take this process of selective sweeps based on your assumption that humans and chimps arose from the same gene pool and explain how recombination gives humans have such a large reproductive fitness advantage over chimpanzees.

Taq:

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It's the combination of de novo mutations and sexual reproduction that gave rise to the human genome.

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Do you mean descent with modification (DNA evolution) and recombination? Do you have a mathematical explanation for either of these processes?

Kleinman:

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Taq is now claiming that sexual replicators can't get adaptive mutations.

Taq:

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I never said any such thing. You are flailing.

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Oh really? So you admit that sexual replicators can get adaptive mutations. How do compute the probability of that happening?

Kleinman:

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When did I say that mutations can move toward fixation together? You are confusing the concept of a variant with multiple adaptive mutations moving toward fixation with multiple variants, each with different adaptive mutations moving toward fixation simultaneously.

Taq:

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A and B are two variants. That's multiple variants.
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You said that when the A and B variants are put into the same genetic background that the combination of the two variants are fittest, so they will be selected for as a combination and outcompete those with just the A or B variant. That's two variants (i.e. multiple variants) moving towards fixation together. That's what you said. You agreed that sexual reproduction combines beneficial variants into the same genetic background and moves them towards fixation. This is exactly what was seen in the Desai group's experiment.
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Remember the start of this whole conversation? You claimed that only the fittest mutation across the whole genome will move towards fixation, driving the rest of the mutations towards extinction. I told you this wasn't the case for sexual reproduction because multiple beneficial mutations can be combined into the same genome without competing with one another. This is exactly what was seen in the paper I gave. You asked for experiments where this happens, and you now have it. You also asked how this would alter evolution, and I gave you the paper that shows you exactly that.

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I need to make this more clear for you. Let's go back to the definition of fixation:
Fixation (population genetics)

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In population genetics, fixation is the change in a gene pool from a situation where there exists at least two variants of a particular gene (allele) in a given population to a situation where only one of the alleles remains.[1] In the absence of mutation or heterozygote advantage, any allele must eventually be lost completely from the population or fixed (permanently established at 100% frequency in the population).[2] Whether a gene will ultimately be lost or fixed is dependent on selection coefficients and chance fluctuations in allelic proportions.[3] Fixation can refer to a gene in general or particular nucleotide position in the DNA chain (locus).

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In the process of substitution, a previously non-existent allele arises by mutation and undergoes fixation by spreading through the population by random genetic drift or positive selection. Once the frequency of the allele is at 100%, i.e. being the only gene variant present in any member, it is said to be "fixed" in the population.[1]

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Fixation occurs when the frequency of that allele is 100%. So, in the case of two variants, A and B, fixation cannot occur without either A or B variants driven to extinction. So, in a population that is composed of A, B, and C (not A or B) variants, a selective sweep of that population that kills off the C variants will increase the frequency of the A and B variants, and the best frequency distribution for an adaptive recombination event would be half the population A variants and the other half of the population B variants. Understand rubberband? Now, take that principle and show us how you breed humans with a much higher reproductive fitness than chimps from the same gene pool.

Tanypteryx:

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That swishing sound you hear is Kleinman flailing as Taq hands him his ass.

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Tany, next time you bring up ERVs, please do your homework. And when will biologists learn the physics and mathematics of biological evolution? It would certainly help the medical and agriculture fields to understand why antimicrobial drug resistance evolves, how herbicide resistance evolves, how pesticide resistance evolves, and why cancer treatments fail. They really get their asses handed to them. Of course, I don't expect biologists to do this kind of science any time soon when their scientific training consists of a survey of physics and a survey of math courses.

We would expect every human to be born with 50 to 100 mutations, and about that for other primates. I would expect birds to be in the same neighborhood. Why are you acting as if the source of new alleles is some mystery? You still don't seem to understand how sexual reproduction, meiosis, chromsomes, or genetics in general works. Perhaps we should start there.You claimed that mutations stay in isolated lineages in sexually reproducing species. Do you agree that this is wrong? Do we need to go over the Desai paper some more until you are convinced that this is wrong? It would be a waste of time for people to give you mathematical models for processes you don't understand.

Why wouldn't I admit that? That's what I've been arguing the whole freaking time!!!!Also, there is no way to compute the general probability of a beneficial mutation, and you would know that if you understood genetics and biology. This is is what I mean. Your abject ignorance of genetics and biology leads you to ask asinine questions. That's not what happened in the Desai experiment for the sexually reproducing populations. How many times do we need to go over this? What good would it do to give you math equations if you can't even understand this basic concept?

Indeed. Maths is moulded to describe reality. It doesn't dictate reality.

That would be one of the main problems. Kleinman seems to think he can command reality to work differently by writing an equation.The second problem is not understanding the systems he is trying to model. Asking for the probability of a beneficial mutation is a bit like asking the probability of the number 42204 winning. Period. That's all the information you are given. How do you calculate that probability? Whether or not a mutation is beneficial depends on SO MANY factors that it is impossible to calculate a meaningful general probability, and Kleinman would know that if he understood the very thing he is claiming to model. Just a small change in environment can convert a neutral or deleterious mutation into a beneficial one. An otherwise neutral mutation in a specific individual can convert an additional deleterious mutation into a neutral or beneficial one, so the genetic background can matter. Will Kleinman understand any of this? I have my doubts.

Indeed. But we know he's a fervent Catholic, so nothing will convince him to drop his delusions. If he did, he'd end up doubting his belief he'll go to heaven when he dies. (Whilst ignoring all the child abuse his church has been covering up for decades).

Always meant to come back to this one: So let's do the actual math, in Python (written by me).

population = 100000
gentime = 25
time = 5000000
mutrate = 50
numgen = int(round(time/gentime, 0))

accumbirths = 0
accummutation = 0
for i in range(numgen):
    accumbirths += population
    accummutation += population*mutrate

print(f'{accumbirths:.2e} total births')
print(f'{accummutation:.2e} total mutations')
print(f'{round(accummutation/6000000000, 1)}x mutational coverage of human genome')

The code brackets should preserve the tab indentions, so a copy and paste into an online Python interpreter works just fine. (don't forget to scroll down in the code window)Online Python Compiler (Interpreter)I have a constant human population of 100,000, a mutation rate of 50 mutations per person per generation (which has been empirically verified), a generation time of 25 years, and a time span of 5 million years since common ancestry with chimps. These values can all be changed if you want, say to a constant population of 1 million individuals.The outputs give you the number of births, the total number of mutations, and the fold coverage for that number of mutations. The coverage represents the number of mutations that would have happened at each base if all mutations were spread evenly across the 6 billion base diploid human genome.With those numbers I get:2.00e+10 total births
1.00e+12 total mutations
166.7x mutational coverage of human genomeThose are a bit different from what Kleinman seems to be claiming. With just a constant population of 100,000 we get 20 billion births, and enough mutations to cover the human genome 166.7 times over, assuming even distribution.Kleinman, is my math right?

Kleinman:

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With an effective population size of 1e5 over 1000 generations, that give about 100 million replications, you would expect de novo mutations.

Taq:

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We would expect every human to be born with 50 to 100 mutations, and about that for other primates. I would expect birds to be in the same neighborhood. Why are you acting as if the source of new alleles is some mystery?

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Considering you don't have an explanation of how drug resistance evolves or why cancer treatments fail but think that you are explaining the evolution of humans and chimps from the same gene pool is the mystery. So which of these 50 to 100 mutations that humans get every replication are the ones that give humans the reproductive fitness advantage over chimps?

Kleinman:

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Do you think that adaptive evolution will work more quickly in a variable, multiple selection pressure environment?

Taq:

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You still don't seem to understand how sexual reproduction, meiosis, chromsomes, or genetics in general works. Perhaps we should start there.

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I'm the only one here that has presented a mathematical model for descent with modification (DNA evolution) and recombination. All you do is hand wave and say that sexual reproduction, meiosis, chromosomes, or genetics are the reason that humans and chimps evolved from the same gene pool. Why should anyone believe you when you can't even explain the evolution of antimicrobial drug resistance or why cancer treatments fail? And we will take your lack of an answer to my question about adaptive evolution working more quickly in a variable, multiple selection pressure environments as a "no". You know what the multiplication rule does to descent with modification (DNA evolution) in a multiple selection pressure environment.

Taq:

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You claimed that mutations stay in isolated lineages in sexually reproducing species. Do you agree that this is wrong? Do we need to go over the Desai paper some more until you are convinced that this is wrong?

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Don't be stupid, I'm the only one here that has presented a mathematical model of recombination. And you know it is correct, that's why you are arguing about multiple alleles fixing simultaneously. You don't even understand what fixation is. You can't have multiple alleles fixing simultaneously in a population. What is the definition of fixation that Desai is using in his paper?

Kleinman:

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Do you mean descent with modification (DNA evolution) and recombination? Do you have a mathematical explanation for either of these processes?

Taq:

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It would be a waste of time for people to give you mathematical models for processes you don't understand.

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And you do? Where's your mathematical explanation of the Kishony and Lenski experiments? When we started this discussion, you didn't even understand that the improvement in fitness with each fixation was decreasing for each adaptive step in the Lenski experiment. The same thing happens in the Desai experiment. So tell us Taq, how many adaptive mutations are required in the human lineage to give humans the reproductive advantage over chimps? And which mutations are they?

Kleinman:

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So you admit that sexual replicators can get adaptive mutations. How do compute the probability of that happening?

Taq:

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Why wouldn't I admit that? That's what I've been arguing the whole freaking time!!!!
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Also, there is no way to compute the general probability of a beneficial mutation, and you would know that if you understood genetics and biology. This is is what I mean. Your abject ignorance of genetics and biology leads you to ask asinine questions.

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So that's your excuse for failing to give the mathematical explanation for the Kishony and Lenski experiments. Biologists need to take more than a survey of mathematics and a survey of physics courses and then you might be able to figure that one out. Since you aren't able to explain the simplest laboratory experiments of biological evolution, what makes you think you can explain the more complex cases? Do you have any idea how descent with modification works (DNA evolution)?

Kleinman:

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So, in the case of two variants, A and B, fixation cannot occur without either A or B variants driven to extinction.

Taq:

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That's not what happened in the Desai experiment for the sexually reproducing populations. How many times do we need to go over this? What good would it do to give you math equations if you can't even understand this basic concept?

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You don't know how Desai defines fixation. Try reading his paper carefully. If you can't find it, I'll post the quote for you.

vimsey:

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Indeed. Maths is moulded to describe reality. It doesn't dictate reality.

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The math I presented predicted the behavior of the Kishony experiment before the experiment was performed. And it predicts the behavior of his 2 drug experiment if he ever gets it to run.

vimsey:

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Indeed. Maths is moulded to describe reality. It doesn't dictate reality.

Taq:

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That would be one of the main problems. Kleinman seems to think he can command reality to work differently by writing an equation.

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The math that I've presented correlates very nicely with the Kishony and Lenski experiments. And you know that the math I presented for random recombination is correct because you almost wrote the same equation. And that's why you keep arguing that multiple alleles can fix simultaneously which happens to be a mathematical impossibility.

Taq:

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The second problem is not understanding the systems he is trying to model. Asking for the probability of a beneficial mutation is a bit like asking the probability of the number 42204 winning. Period. That's all the information you are given. How do you calculate that probability? Whether or not a mutation is beneficial depends on SO MANY factors that it is impossible to calculate a meaningful general probability, and Kleinman would know that if he understood the very thing he is claiming to model. Just a small change in environment can convert a neutral or deleterious mutation into a beneficial one. An otherwise neutral mutation in a specific individual can convert an additional deleterious mutation into a neutral or beneficial one, so the genetic background can matter. Will Kleinman understand any of this? I have my doubts.

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Taq, you are so mathematically incompetent. The reason why it takes about 1/(mutation rate) replications for an adaptive mutation to occur is that math applies to every site in the genome. The population is sampling every possible mutation at every site. That's why it takes a billion replications in the Kishony experiment for each adaptive mutation for a mutation rate of 1e-9. In that billion replications will be members with a mutation at every possible site in the genome. In other words, an exhaustive random search is being done of the sample space. The selection conditions of the environment determine if any of those mutations are beneficial. You are such a slow learner, poorly trained in mathematics.

vimesey:

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Indeed. But we know he's a fervent Catholic, so nothing will convince him to drop his delusions. If he did, he'd end up doubting his belief he'll go to heaven when he dies. (Whilst ignoring all the child abuse his church has been covering up for decades).

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What?????? That's another one you are wrong on.