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

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I'm not summing the frequencies of alleles for any locus

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According to Message 930 it seems that you are:

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I'm summing the frequencies of alleles at 2 loci. And the sum of the frequency of allele A at locus 1 plus the frequency of allele B at locus 2 plus the frequency of allele C (neither A nor B) at either locus must equal 1.

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As written that is nonsense. Maybe you are making additional assumptions - beyond the assumption that alleles A and B never occur in the same individual - but you don’t mention any.

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here is no intersection of the A and B subsets until either an adaptive recombination event occurs or a mutation occurs on allele C that transitions into an A or B allele when that member has the B or A allele already

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If one locus has alleles A and C (and no others) and the other has B and D the frequencies of A and C must sum to 1. Adding the frequency of B is pointless. (Indeed, if no individual has A and B the overlap of B and C must be every individual with B).This is pretty simple math, Kleinman. Do you understand it yet?

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I'm assuming homogeneity of the alleles, that is, for a diploid, A if it occurs, it occurs in both genomes, and if B occurs, it occurs in both genomes and if A doesn't occur at that locus, it is C (in both genomes) and if B doesn't occur at the second locus, it is C (in both genomes). All this does is eliminate Mendelian Genetics from the computation where the genomes are not homogenous. That would reduce the probability of an AB variant occurring.

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You have to assume more than that.

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It is simple math. The problem is that you are assuming heterogeneity.

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That is incorrect - in fact I completely ignored that issue, just as you did.

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Nope, that's all I'm assuming.

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Well it seems very confused. Aside from mixing up alleles and genomes you need some explanation of how you can have C at both loci. A recent gene duplication?

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Nope, I only assume that whatever gene is at a given locus, is homogenous. You assume they are not homogenous.

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I certainly did not make any such assumption. But just to make you happy I will write it out again with homozygosity explicitly assumed,If one locus has alleles A and C (and no others) and the other has B and D and all individuals are homozygous, the frequencies of AA and CC must sum to 1. Adding the frequency of BB is pointless. (Indeed, if no individual has AA and BB the overlap of BB and CC must be every individual with BB).

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C is any allele that is not A or B. C doesn't have to be all the same allele, they just have to be different than A and B.

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Then I suggest that you use less obfuscatory terminology.

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Sure you do. You do that when you say one locus has A and C alleles and a second locus has B and D alleles.

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In the same way that you “assume heterozygosity” when you say that the first locus can have A or C. I.e not at all.And it should be perfectly clear that nothing in the following text supported your misinterpretation at all. It was just a straightforward explanation of the rule of 1.

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I'm sorry that this simple concept confuses you. I wrote the following in the published paper

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Since the explanation is rather critical to understanding it, leaving it out is your failure,

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I'm not misinterpreting anything

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So you really do think that the rule of 1 only applies if we assume heterozygosity.

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You just don't read very carefully

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Oh, I get it. This is where you attribute your faults to others. You didn’t read carefully and misunderstood so you have to pretend that the writer didn’t read carefully.

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That's why you screw up such a simple concept.

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I’m not the one that screwed up. But again, you have to attribute your faults to others.

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Demonstrating your scientific rigor by denying that evidence exists is a good look for you.

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Apparently Kleinman doesn’t know what a retrovirus does to a cell.

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Don't blame your confusion on me. Your confusion is your problem.

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Your unclear writing is your problem. If A and B are alleles then the natural readings is that C is also an allele.

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You are still confused.

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You object to a simple example of the rule of 1 on the grounds that it supposedly assumes heterozygosity (even though it doesn’t) You claim to understand what you are saying. The implication is obvious.

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You are the one blaming me for your confusion. Why don't you take responsibility for your own confusion?

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You claimed that a simpler application of the rule of 1 assumed heterozygosity when it did not. That is your problem, not mine.

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Still confused, aren't you?

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Oh no. I just know something you don’t.

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The peer reviewers had no trouble understanding my meaning and they published this work. You just don't read very carefully.

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They had no problem because you explicitly explained what you were doing.

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You assumed heterozygosity,

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Wrong. And I even rewrote the example with assumed homozygosity, just for you. It shingled nothing of significance because it is just a simple application of the rule of 1.

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I didn't claim heterozygosity, you did. Why don't you accept the blame for your own blunders?

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I didn’t claim heterozygosity, nor did I claim that YOU claimed heterozygosity. Those blunders are yours.

I guess you still don’t know what retroviruses do to a cell.Too bad.

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I listed the link to the paper many times. You just never bothered to read it.

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That’s not much of an excuse. If you choose to use unclear notation it shouldn’t require following a link to see what it means.

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Sure it is a simple example of the rule of one because there the subsets are mutually exclusive. Is it that hard for you to understand?

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You were the one objecting to it on spurious grounds. That’s not my fault.

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Sure you did, you didn't understand that C simply represented all the non-A and non-B alleles. That's why you introduced a, b, c, and d alleles.

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Which does not in any way make my point incorrect. You choose to confuse the issue with your arrogant bluster, and that is entirely your fault.

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You made a blunder

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A minor error, due to your use of unclear notation. The point made was still correct. You’ve made far worse blunders. Your mistaken claim that I was assuming heterozygosity was at least as bad.

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The probability of an adaptive recombination event depends on the frequencies of alleles in the population.

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And those frequencies will not be static. Indeed, if the alleles are adaptive they will tend to increase.

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They certainly don't make UCD possible and the idea that there are 100s of thousands of these in the human genome is nonsense

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Nobody has said that they make UCD possible. But the presence of ERV fragments in the human genome - and in the genomes of other apes is evidence of common ancestry. And if you knew what ERVs do to a cell it wouldn’t be surprising to find them in the human genome.

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That's as smart as the idea of junk DNA. That was a really smart idea of biologists.

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Junk DNA is a fact. You may not like it, but that is your problem.

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I don't need much of an excuse for something so simple. Why it confuses you is really a mystery.

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There is no mystery at all. You chose to use unclear notation and didn’t explain it in the posts here,

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Whose fault is it that you don't see the obvious?

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It’s your fault that you failed to see the obvious. That’s the problem.

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You make the error and you should get the credit for your error, it's only fair enough.

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Funny how you expect everyone else to accept the blame for your errors then.

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My notation was clear enough to anyone who can read, perhaps your problem is that you can't read.

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Only to those who read the explanation - which you didn’t post here.Of course it was perfectly clear that my point didn’t depend on heterozygosity but you somehow missed that.

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That's correct in a constant environment. What happens when the environment is changing? An allele might be advantageous in one environment but disadvantageous in another environment

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Might be is hardly a guarantee. Many environmental conditions are relatively constant, or changing in a way that makes the advantageous allele more advantageous. Human intelligence is obviously useful in a wide range of terrestrial environments. Malaria maintains the frequency of sickle cell and doesn’t seem to be going away any time soon - for all our efforts. Hospital conditions are constant enough to make multiply-resistant bacteria a problem.That something might happen is not proof that it did or would.

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Of course, they don't make UCD possible. It also is a demonstration of biologists wrongly doing non-random sampling and introducing bias into their math. But if that is all you have, what else can you do.

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I guess that lies and scorn for science are all you have.

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So anything you don't understand is junk. No wonder you are so slow in understanding.

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The evidence for junk DNA is rather more than that it isn’t understood. But of course you can’t be bothered to understand that. So you call it junk.

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It's only unclear to you. To the peer reviewers, it was obvious

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Because you explained it in the paper. The only mystery is how you fail to see the obvious.

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I think you should take responsibility for your own errors. Why don't you take responsibility for your own errors?

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I do. I just won’t take responsibility for yours.

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Now that's a claim. When is the environment constant over the lifespan of a human?

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I guess that you can’t read. I said that aspects of the environment can remain sufficiently constant. I even offered an example - the presence of malaria in some regions seems quite constant, for instance.

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And hospital conditions include a population that is immune compromised. In case you didn't know, they have sick people in hospitals. That's why there is a higher concentration of drug-resistant infections in hospitals than out in the community.

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By which you mean that I was correct. The environment in hospitals is sufficiently stable to permit the evolution of multiply resistant bacteria. Which is all I said on the subject.So please, please take responsibility for this gross error on your part.