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

If you are going to use the H-D equation, you do. I already disproved this multiple times. You have admitted that the equation does not work with genetic loci that have an intersection, and the vast majority of comparisons of genes within the human genome have an intersection of the type you describe. In genetics, we call a lack of intersection a linkage disequilibrium and an intersection as being non-linked. Again, the vast majority of comparisons between genetic loci are non-linked because only genetic loci very close to one another on the same chromosome will display this type of linkage disequilibrium. There are also epistatic effects, but that muddies the waters a bit.

Kleinman:

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Recombination in some cases can get two beneficial mutations into the same individual, it can also cause the loss of two beneficial mutations in the same individual.

Taq:

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Recombination isn't even needed if the beneficial mutations are on separate chromosomes.
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And yes, we can get a case where offspring lack both beneficial mutations, and they will be selected against. This is where natural selection comes in, and why offspring with both beneficial mutations can be favored by natural selection which drives the fixation of both beneficial mutations in parallel instead of forcing them to compete as we see in asexual organisms.​

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The simple model I present assumes that if an A parent and B parent mate, an AB offspring will always occur. That gives the highest possible probability. You don't need natural selection for the parent with a diploid genome to not pass a beneficial allele to the offspring, just pass the chromosome without the adaptive allele. You should know that from your Mendelian genetics.

Kleinman:

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You are still not answering the question of how the shuffling of existing alleles creates new alleles (DNA evolution).

Taq:

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It doesn't. Mutations produce new alleles.

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Finally, a little bit of progress.

Taq:

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What I am trying to correct is your false claim that someone carrying beneficial mutation A must also have a new mutational event that produces mutation B in a separate, unlinked gene. This doesn't have to happen in diploid sexually reproducing species, does it? Instead, each mutation only has to happen once, and it can happen in separate individuals. In subsequent generations those beneficial mutations can be found in the same individual because of heredity, not because the mutation had to happen again.
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Do you agree with this or not?

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Certainly, I agree with this. But the probability of an A and B parents giving an AB offspring depends on the frequency of the A and B variants in the population. And you know this as well. That's why you have come up with this cockamamy idea that multiple alleles can fix simultaneously.

Just to be clear, these are the genotypes of the parents, and I will even put them on separate chromosomes. The Aa alleles are for gene X and the Bb alleles are for gene y:

Mom
chr1    chr2
AA       bb

Mom's gametes:
chr1     chr2
A          b

Dad
chr1    chr2
aa       BB

Dad's gametes:
chr1     chr2
a          B

Child:
chr1   chr2
Aa      Bb

Are we agreed on this?If so, where are you claiming there is recombination? All we need is segregation of the chromosome pairs during meiosis, don't we? If both are beneficial alleles then this frequency will increase for both over time, will it not? As the frequency of each increases so does the frequency of children carrying both beneficial alleles which is the intersection that ruins your addition rule.

Kleinman:

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You don't have to limit frequency calculations to a single genetic locus.

Taq:

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If you are going to use the H-D equation, you do.

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I'm not using the H-D equation, I'm considering the frequencies of different variants at multiple genetic loci simultaneously. In particular, I'm considering the loci that have beneficial allele A at one locus and beneficial allele B at a different locus.

Kleinman:

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But, no matter how many loci you want to consider, the sum of the frequencies of all variants must always equal 1.

Taq:

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I already disproved this multiple times. You have admitted that the equation does not work with genetic loci that have an intersection, and the vast majority of comparisons of genes within the human genome have an intersection of the type you describe. In genetics, we call a lack of intersection a linkage disequilibrium and an intersection as being non-linked. Again, the vast majority of comparisons between genetic loci are non-linked because only genetic loci very close to one another on the same chromosome will display this type of linkage disequilibrium. There are also epistatic effects, but that muddies the waters a bit.

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Taq, you are such a dumb cluck. The addition rule does work when there are intersections of the subsets. You just have to subtract off the intersection so that you don't count members twice. And if you sum up the frequencies of all the different variants in a population, it will always, always, always equal 1. It doesn't matter whether you are considering one genetic locus as with the H-D equation, two genetic loci that I use in the recombination model that I've presented, or every genetic locus in the entire genome. The sum of the frequencies of all the different variants will always equal 1 whether the subsets are mutually exclusive or whether the subsets intersect where you have to subtract off the intersection so that you don't count members twice.

Then your equation doesn't work.Then let's look at achondroplasia which is caused by mutations in the FGFR3 gene and cystic fibrosis which is caused by mutations in the CFTR gene. More than 99% of people have the healthy allele for both and only an extreme few have both cystic fibrosis and dwarfism. So let's do the math:
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0.99A + 0.99B + 0.0000001C != 1
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Just remember, this is the equation you gave:Define the following variables:
n – is the total population size.
nA – is the number of members in the population with beneficial allele A.
nB – is the number of members in the population with beneficial allele B.
nC – is the number of members in the population that have neither beneficial allele A nor beneficial allele B.
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In addition, we have the following condition: nA + nB + nC = n.
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And the frequency of each of the variants are:
f_A = nA/n
f_B = nB/n
f_C = nC/nNOWHERE DOES IT SAY TO SUBTRACT OUT ANY INTERSECTIONS!! NOWHERE!!!!!It flatly says the frequency of A. PERIOD.If you are going to make your equation work then you need to insert a term for those with both A and B, but then that equation will accommodate frequencies for both A and B that are above 0.5 which is what you claim can't happen. Again, nowhere does your equation have this function. We count the people with A, then we count the people with B. That's it. Nowhere does it say to count people with both A and B. If it did, then the frequency of each allele by itself can add up to more than 1 which is what you claim can't happen.If you are now saying that beneficial mutation A and B can both increase in parallel and near a frequency of 1 then we are in agreement.

Kleinman:

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The simple model I present assumes that if an A parent and B parent mate, an AB offspring will always occur. That gives the highest possible probability.

Taq:

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Just to be clear, these are the genotypes of the parents, and I will even put them on separate chromosomes. The Aa alleles are for gene X and the Bb alleles are for gene y:

quote:

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Mom
chr1 chr2
AA bb

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Mom's gametes:
chr1 chr2
A b

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Dad
chr1 chr2
aa BB

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Dad's gametes:
chr1 chr2
a B

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Child:
chr1 chr2
Aa Bb

Taq:

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Are we agreed on this?
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If so, where are you claiming there is recombination? All we need is segregation of the chromosome pairs during meiosis, don't we?
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What you call "a" and "b" alleles, I call "C" alleles (not A or B).And I'm working from this definition of recombination:
Genetic recombination - Wikipedia

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Genetic recombination (also known as genetic reshuffling) is the exchange of genetic material between different organisms which leads to production of offspring with combinations of traits that differ from those found in either parent.

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If you think the mechanism of how this reshuffling occurs affects the math, show us.

Kleinman:

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But the probability of an A and B parents giving an AB offspring depends on the frequency of the A and B variants in the population.

Taq:

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If both are beneficial alleles then this frequency will increase for both over time, will it not? As the frequency of each increases so does the frequency of children carrying both beneficial alleles which is the intersection that ruins your addition rule.

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You keep claiming that multiple beneficial alleles fix simultaneously but that's not what happens in the Lenski or Desai experiment (done with sexual replicating yeast). Is your claim something that is taught in biology textbooks because it isn't in my biology textbook? And why doesn't recombination cause combination therapy to fail for the treatment of HIV?

You take a million bacteria with mutation A in gene x and a million with mutation B in gene y and put them in the same broth. After one generation, how many offspring have both mutation A and B.You take a million people with genotype AAbb in gene x and y respectively and a million with genotype aaBB for the same genes and mix them together. After one generation, how many offspring have both mutation A and B? It doesn't happen in the Lenski experiment BECAUSE THEY ARE ASEXUAL ORGANISMS. My God man, how many times do I need to explain this?I have yet to see the Desai experiment, or I missed it in a previous post. If you link it we can discuss. There are a lot of things that aren't taught in your text book, apparently. It seems to include meiosis, the existence of chromosomes, meiosis, sexual reproduction, or linkage disequilibrium.

Kleinman:

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I'm not using the H-D equation, I'm considering the frequencies of different variants at multiple genetic loci simultaneously.

Taq:

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Then your equation doesn't work.
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Then let's look at achondroplasia which is caused by mutations in the FGFR3 gene and cystic fibrosis which is caused by mutations in the CFTR gene. More than 99% of people have the healthy allele for both and only an extreme few have both cystic fibrosis and dwarfism. So let's do the math:
​
0.99A + 0.99B + 0.0000001C != 1
​
Just remember, this is the equation you gave:
​
Define the following variables:
n – is the total population size.
nA – is the number of members in the population with beneficial allele A.
nB – is the number of members in the population with beneficial allele B.
nC – is the number of members in the population that have neither beneficial allele A nor beneficial allele B.
​
In addition, we have the following condition: nA + nB + nC = n.
​
And the frequency of each of the variants are:
f_A = nA/n
f_B = nB/n
f_C = nC/n
​
NOWHERE DOES IT SAY TO SUBTRACT OUT ANY INTERSECTIONS!! NOWHERE!!!!!
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It flatly says the frequency of A. PERIOD.
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If you are going to make your equation work then you need to insert a term for those with both A and B, but then that equation will accommodate frequencies for both A and B that are above 0.5 which is what you claim can't happen.

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My goodness! Is this so confusing to you? There are no AB variants until the recombination event occurs with the mating of A and B parents to give an AB offspring. The subsets are mutually exclusive until that happens.

Kleinman:

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The addition rule does work when there are intersections of the subsets. You just have to subtract off the intersection so that you don't count members twice.

Taq:

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Again, nowhere does your equation have this function. We count the people with A, then we count the people with B. That's it. Nowhere does it say to count people with both A and B. If it did, then the frequency of each allele by itself can add up to more than 1 which is what you claim can't happen.
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If you are now saying that beneficial mutation A and B can both increase in parallel and near a frequency of 1 then we are in agreement.

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After an AB recombination event occurs, there will be an intersection of the A and B subsets. But then the AB variant will be the most fit variant and in the biological competition, will drive all the A only and B only variants to extinction leaving only AB variants. Or perhaps you think that the frequencies of the AB, A only, and B only variants will all go to 1?

Kleinman:

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If you think the mechanism of how this reshuffling occurs affects the math, show us.

Taq:

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You take a million bacteria with mutation A in gene x and a million with mutation B in gene y and put them in the same broth. After one generation, how many offspring have both mutation A and B.

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That depends on the mutation rate. If the mutation rate is 1e-6, you will on average have one AB variant in that population.

Taq:

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You take a million people with genotype AAbb in gene x and y respectively and a million with genotype aaBB for the same genes and mix them together. After one generation, how many offspring have both mutation A and B?

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Now you want to have two subpopulations, one subpopulation with a frequency of 1 for the AAbb variant and the other subpopulation with a frequency of 1 for the aaBB variant, and then you mix the two subpopulations to give a frequency of 0.5 for each variant. Plug the numbers into the equation I've presented, which will give you the correct frequency distribution for the offspring.

Then what genetic variants do you think your equation applies to in the human genome? You seem to be claiming that it applies to all variants in the human genome, but I don't see how this can be given your newly invented qualification. You mean the A and B mutations will increase in frequency in parallel?

Yep ... dwise1 is an atheist, so he must be reeeal smart."The fool says in his heart, 'There is no God.'" (Psalm 14:1)ha ha ha ha ha ha ha ha ha ha ha ha ha ha ha ha ha ha ha ha ha ha ha ha!!!Good one, Phat!

It's a lot simpler than that. There are three possible mate pairs:aaBB : aaBB
AAbb : AAbb
AAbb : aaBBWithout even doing the math, we can see that a lot of mate pairings will be between AAbb and aaBB. All of their offspring will have both the A and B mutations. There are going to be hundreds of thousands of recombination events (as you describe it) between the A and B mutations.So you have about 1 in the bacterial populations and hundreds of thousands in the human population. That seems like a big difference, doesn't it?

Kleinman:

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There are no AB variants until the recombination event occurs with the mating of A and B parents to give an AB offspring.

Taq:

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Then what genetic variants do you think your equation applies to in the human genome? You seem to be claiming that it applies to all variants in the human genome, but I don't see how this can be given your newly invented qualification.

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This equation is applicable to any two genetic loci in any replicator, human or otherwise. And this mathematics is well known, not newly invented. Biologists just don't recognize how to apply this math and in your case, very slow to learn.

Kleinman:

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After an AB recombination event occurs, there will be an intersection of the A and B subsets. But then the AB variant will be the most fit variant and in the biological competition, will drive all the A only and B only variants to extinction leaving only AB variants.

Taq:

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You mean the A and B mutations will increase in frequency in parallel?

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The AB variants will increase in frequency because the AB variant will have greater reproductive fitness than either the A or B variants so those variants will decrease in frequency. That's how biological competition works. It still doesn't change how descent with modification works (DNA evolution). Are you going to explain to us how a member of the population with beneficial allele A from North Africa meets a member of the population with beneficial allele B from South Africa?

Kleinman:

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Now you want to have two subpopulations, one subpopulation with a frequency of 1 for the AAbb variant and the other subpopulation with a frequency of 1 for the aaBB variant, and then you mix the two subpopulations to give a frequency of 0.5 for each variant. Plug the numbers into the equation I've presented, which will give you the correct frequency distribution for the offspring.

Taq:

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It's a lot simpler than that. There are three possible mate pairs:
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aaBB : aaBB
AAbb : AAbb
AAbb : aaBB
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Without even doing the math, we can see that a lot of mate pairings will be between AAbb and aaBB. All of their offspring will have both the A and B mutations. There are going to be hundreds of thousands of recombination events (as you describe it) between the A and B mutations.
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So you have about 1 in the bacterial populations and hundreds of thousands in the human population. That seems like a big difference, doesn't it?

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So, why isn't everyone resistant to malaria, tuberculosis, influenza, covid, ... Don't the people that survive these diseases have beneficial alleles? And shouldn't all these alleles go to frequency 1 so that everyone has them by recombination?

I've already shown this isn't the case. You are now saying that as someone with a new mutation has offspring with any other person the equation no longer applies. I followed your equation exactly and it failed. The A only and B only variants can mate and have children that have both mutations, right?The A and B mutations are still on separate chromosomes and are being passed on as independent entities. They are not linked.As you yourself are now saying, A does not outcompete B. The frequency of B on chromosome 2 can increase in frequency alongside the frequency of A on chromosome 1. Both increasing in frequency even though they aren't on the same chromosome or closely linked on the same chromosome. What if both mutations are in North Africa?