Population Genetics

None whatsoever. Haldane himself later recognized the errors in his own model, and was more than confident that subsequent information would render his calculations pointless (he was right, of course). In particular:

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Haldane's "cost of natural selection" stemmed from an invalid simplifying assumption in his calculations. He divided by a fitness constant in a way that invalidated his assumption of constant population size, and his cost of selection is an artifact of the changed population size. He also assumed that two mutations would take twice as long to reach fixation as one, but because of sexual recombination, the two can be selected simultaneously and both reach fixation sooner. With corrected calculations, the cost disappears (Wallace 1991; Williams n.d.).

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ReMine himself introduces a number of errors into an already invalid model:

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* The vast majority of differences would probably be due to genetic drift, not selection.
* Many genes would have been linked with genes that are selected and thus would have hitchhiked with them to fixation.
* Many mutations, such as those due to unequal crossing over, affect more than one codon.
* Human and ape genes both would be diverging from the common ancestor, doubling the difference.
* ReMine's computer simulation supposedly showing the negative influence of Haldane's dilemma assumed a population size of only six (Musgrave 1999).

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from CB121: Haldane's DilemmaTo assert that there's any tooth to Haldane's so-called "dilemma" is to assert that the entire field of population genetics hasn't gone anywhere since Haldane's work in the late 50's. (Where did you get the idea that Haldane was a "19th century biologist"? He was born in 1892.)He misstates Gould as well, I suspect. Statis isn't the cessation of genetic change; it's the cessation of morphological change. Indeed, periods of rapid change are only possible because of the genetic changes occuring "under the radar" during periods of stasis.

Haldane is wrong. It's that simple. Not only does every population geneticist know that Haldane is wrong, Haldane himself knew he was wrong.What wasn't clear about my post? To the extent that ReMine bases his arguments on Haldane, he's wrong. Because Haldane was wrong. You don't seem to have spoken to that point at all.The rest of the ReMine material you post is just a hand-waving accusation of fraud among evolutionists with absolutely no evidence to support it. He claims that evolutionists somehow "didn't tell the public" about Haldane's Dilemma, but that's obviously false - Haldane published in the peer-reviewed journals just like everybody else. He didn't toss his manuscript into a file cabinet that ReMine discovered, or something. Haldane's research has been publically avaliable since he published in 1957. No, he didn't. As I told you, he used assumptions that invalidated his own model. He used assumptions that are contradicted by reality. In fact, as a student of genetics, I can tell you that this is absolutely false. Mendelian genetics is the sole staple of a high school genetics program simply because that's the only genetics a high school student can be expected to understand.In truth, very, very few genes operate in a strictly Mendelian way. The greatest advance in genetics, of course, came well after Haldane - the elucidation of the molecular structure of DNA and the confirmation of its role as the mechanism of gene expression and heredity.The backbone of genetics is DNA, and the research on DNA was in its infancy in 1957. And you're really going to try to tell me that we've learned nothing new since 1957? Really? Funny; I've been to all the garage sales but I can't seem to find a PCR-RFLP kit from back then. Or a gel electrophoresis setup. Or a list of primer sequences and restriction enzymes from 1957.I wonder why that might be? I just told you how. What wasn't clear about my post? Strawman argument. Nobody's saying that, given a finite stretch of time, an infinite number of mutations is possible. Clearly, that's not something we should expect to see.But 1667 is far, far too few. Haldane knew it; everybody seems to know it but ReMine. Most importantly, it's contradicted by direct observation so clearly any model that predicts so few possible mutations is structurally flawed. We conclude that it is flawed in the same way we conclude that any equation where 1 = 0 is flawed. When the outcome is contradicted by the reality we know the model is flawed, simple as that.

Because everybody knew Haldane was wrong. Just like everybody but ReMine seems to understand that ReMine is wrong. His work is consistently rejected in peer review. There's nothing at all straightforward about it to me. Could you elaborate? Usually people say "this is obvious" when they don't understand a step in the reasoning but they're hoping no one will ask them to explain it.Look, it's pretty obvious to me that in a sexual reproducing species, you can fix a large number of beneficial mutations simultaneously. In fact sexual reproduction makes this a lot more likely to occur, which is part of the evolutionary advantage of sexual reproduction. So this idea that you can only fix one gene at a time, and only over 300 generations, simply doesn't hold up for me. It's prima facie ridiculous. Open a phylogenetics text. It's well-understood that, in mammals (for instance), we can expect roughly one uncorrected nucleotide substitution during DNA replication per every ~3 billion base pairs. That means that every new individual mammal should have somewhere between 5 and 100 mutations. (6 gbp genome, two copies of each genome per offspring, plus mutations that may occur during the very earliest stages of cell cleavage, which would have a similar effect as germline mutations inherited from parental gametes.)So I don't see 86 mutations as a really large amount. You almost certainly have way more than 86 mutational differences between the genes you had as a zygote and the genes you should have inherited on your parent's chromosomes.ReMine operates from the ridiculous assumption that multiple genes can't be fixed at a time; that beneficial mutations have to be fixed in linear chronological order, one at a time. Neither he nor you seem to have offered any support I can detect for this position. Please correct me if I'm mistaken.

I thought I was as clear as I could possibly be. ReMine and Haldane are wrong because 300 generations to fix a gene doesn't mean only one gene fixed every 300 generations. Multiple genes can fix simultaneously - in fact, sexual reproduction makes this a given. No, that's not true. Bruce Wallace answered it in 1991 in his book Fifty Years of Genetic Load - An Odyssey. When you correct Haldane's misapprehension that two genes take twice as long to fix as one, the genetic cost of fixation disappears entirely. It has been. ReMine has simply ignored it, and so have you. That's why you keep avoiding the rebuttals, and why ReMine can't publish except in the vanity press. It is child's play. That's what I'm telling you - we teach it to children because it's a lot easier than molecular genetics, because it applies to so many fewer cases.Most genes are not strictly Mendelian. (Mitochondrial genes are not at all Mendelian.) Phenomena like penetrance and epistasis are regularly observed, but Mendel had no explanation for them.Molecular genetics is the true understanding of inheritance, and more importantly, the mechanism of inheritance, not simply it's pattern. Mendel simply observed a pattern of inheritance that he could not truly explain. Molecular genetics explains both Mendel's patterns and the non-Mendelian patterns, like epistasis. I never said it wasn't. Crick and Watson figured out what it did and how it did it, which proved that DNA was the molecule of heredity. This was suspected but not confirmed until their work. Sure. But nobody knew how that worked, or why some traits were inherited but some were not. Even Mendel didn't know; he just observed the patterns of inheritance of four specific characters in one specific species. Even his attempts at developing an explanation were clumsy. It took Thomas Morgan to develop the chromosomal theory of inheritance; the first steps into molecular genetics. Why would we need to? I told you that even Haldane himself eventually rejected his own "dilemma". A rebuttal to what? Look, you're hopelessly confused. Let me spell out this portion of our exchange. You quoted ReMine saying that Gould's punctuated equilibrium proposed long periods of genetic stasis.This is false. Punctuated equilibrium does not propose genetic stasis, it proposes morphological stasis. Genetic changes continue during the morphological stasis, that's how sudden morphological change occurs when stasis ends - because of genetic changes that had been occuring the whole time.That's how ReMine misrepresents Gould. Maybe you're simply not clear on the difference between morphology and genetics? You need to get back to Mendel, I guess. Yes. It's why the argument is wrong.What exactly is unclear, here? ReMine's model predicts fewer fixations in a population than we observe. Hence, his model is wrong. You can't use a model to disprove what's right in front of your face. That's such a basic idea of epistomology that it shouldn't even have to be made explicit. Name you one? I'll go much better than that - all organisms have beneficial mutations that are the result of point substitutions. Huh? No, there's plenty of mutations that are fatal to prokaryotes. Seriously. "Bound to do something good"? Where do you get this stuff? Er, well, now you're leaving behind ReMine's argument, which was an argument from population genetics, to delve into the actual molecular chemistry of proteins, genes, and mutations. That wasn't the scope of ReMine's argument. Are you sure you're ready to leave that behind? You should probably open a new thread if you want to talk about how a mutation could be beneficial, even in a human. No. A point substitution won't change the read frame. You have to have an addition or a deletion to affect the read frame. And even if you do, a subsequent addition or deletion down the line restores the read frame anyway, leaving the disruption limited to the space between the two mutations. Anyway you can usually alter up to 60% of the primary structure of a protein with little to no effect on its function.Look, until you're up to speed with molecular genetics, you're not going to be able to deal with the evidence from genetics. And the fact that you think any change at all in a gene "garbles" the gene shows me that you have no idea what's going on, here.

Because every individual is the result of two genetic heritages.Thus, fixation happens at least twice as fast as Haldane's model. ...ok, you've lost me. I thought we were talking about Haldane's dilemma, not speciation. Speciation isn't the topic of this thread and it doesn't have anything to do with Haldane's dilemma. Are you just not interested in pursuing this topic? Or did you just not understand the topic before you posted on it, and so now you don't know how to respond to rebuttals except to bring up irrelevant, off-topic subjects? Right. Where's the dilemma? Eventually, every member of a sexual population can trace it's ancestry back to two single shared individuals; one male and one female. (No, this isn't proof of Noah's Ark or some such nonsense.) You seem to have misunderstood. I was referring specifically to germline mutations, not somatic mutations. In fact, you'll pass on half of the mutations you were born with (statistically; it depends obviously on which of your chromosomes are passed on to your offspring) to each of your children. If it occurs in a germline cell, it has an equal chance of being passed on, so I don't know where you're getting this idea that they'll "go away when you die." If your offspring get that chromosome it'll live on long after you. Again, you apparently didn't read closely. I was not referring to the somatic mutations you've accrued from decades of living in an environment with mutagens, etc. I was referring specifically to the germline mutations you aquired from your parents (or just after) at conception. You have between 5 and 100, maybe more, and since your own germline cells are decendants of your original single cell, your offspring will get some of them too. (Have gotten, I think you mentioned before you have children.)I mean, counting all mutations, you surely have billions by now. I was just talking about the germline mutations since they're the evolutionarily relevant ones.

It's up there, farther back in the tree, at the spot where the branch containing the dog and the branch containing the cat meet. That convergence is their most recent common ancestor from which they're both descended.

You learned all the wrong lessons, I guess. I was trying to teach you to stop posting nonsense with the assumption that we're all too stupid to tell the difference.