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I am at heart didactic. A real teacher must either have infinite hope or give up immediately.You expect too much. holdon only asks questions. He doesn't answer them.
On the contrary, I have a great deal of evidence for that. We can predict theoretically what will happen to genetic variation under the effect of natural selection, and also under randomly accumulating new mutations. Most of the genome looks like the latter, about 5% looks like the result of selection against new deleterious mutations, and a small fraction shows clear evidence for positive selection for new traits.So, you say..... but you don't have any evidence for that. So, it's an assumption; a belief. That's all.
Then what did you say? What does Hardy-Weinberg say about anything at all that you're discussing?Nor did I say that.
Because the only ones I care about, and the only ones that we're counting, are the ones that we see in the offspring. We see new mutations all the time in offspring.How can you be so sure they are "all" passed on to offspring?
By reading the papers that describe the research. In the case of the gene M1CR1, variant that contributes to fair skin (and red hair) was completely absent in Africa; the variant that was in Africa was the same as that found in our close relatives. There was also strong genetic evidence that the gene was under purifying selection in Africa, i.e. selection against mutations that would disrupt the gene function. Outside of Africa (where there is much less need for skin pigmentation to protect against the sun), there were multiple variants in the gene.Really? How do you know?
Yup, holdon: how, in your view, does new genetic material emerge?
You expect too much. holdon only asks questions. He doesn't answer them.
Theoretically.On the contrary, I have a great deal of evidence for that. We can predict theoretically what will happen to genetic variation under the effect of natural selection, and also under randomly accumulating new mutations. Most of the genome looks like the latter, about 5% looks like the result of selection against new deleterious mutations, and a small fraction shows clear evidence for positive selection for new traits.
Because I think most geneticists would agree that Hardy-Weinberg is a good approach to allele frequencies in a population. And that approach shows that purely on a statistical basis, extremes have no chance of making it.Then what did you say? What does Hardy-Weinberg say about anything at all that you're discussing?
What exactly do you call "mutations", because I suspect there might be a difference.Because the only ones I care about, and the only ones that we're counting, are the ones that we see in the offspring. We see new mutations all the time in offspring.
And has it been established that this M1CR1 is solely responsible for the "fair skin" phenotype occuring in the population? Because you claimed "that the source population (all of sub-Saharan Africa) completely lacks the alleles for blue eyes and pale skin" and concluding that these alleles must be the result of mutations as they are not present in the "source population" which in itself is a BIG assumption. And even if certain alleles do not occur in one part of the species (homo in this case), it doesn't follow that the other part of the species must have mutant alleles, because selection does occur....By reading the papers that describe the research. In the case of the gene M1CR1, variant that contributes to fair skin (and red hair) was completely absent in Africa; the variant that was in Africa was the same as that found in our close relatives. There was also strong genetic evidence that the gene was under purifying selection in Africa, i.e. selection against mutations that would disrupt the gene function. Outside of Africa (where there is much less need for skin pigmentation to protect against the sun), there were multiple variants in the gene.
Theory tells you what you will see if certain conditions are true. Then you have to look at the empirical evidence to see whether the theory is supported or not. In this case the theory is supported. If you have an alternative theory to offer that would explain the evidence, by all means present it.Theoretically.
I'm sorry, but you don't understand Hardy-Weinberg. HW tells you (under idealized assumptions) what frequencies of genotypes to expect in a population, given an allele frequency. It has nothing to do with extremes "making it" or not. (Note: I am a geneticist.)Because I think most geneticists would agree that Hardy-Weinberg is a good approach to allele frequencies in a population. And that approach shows that purely on a statistical basis, extremes have no chance of making it.
A mutation is any change in genetic material. A germ-line mutation is a mutation that can be passed on to future generations, because it is in the reproductive cells..What exactly do you call "mutations", because I suspect there might be a difference.
I'm concluding that the alleles for fair skin in this gene are the result of mutation, based on the genetic evidence. As it happens, there are something like half a dozen genes implicated in human pigmentation that show evidence for positive selection; this type of evidence only appears when the allele in question starts out on a single chromosome.And has it been established that this M1CR1 is solely responsible for the "fair skin" phenotype occuring in the population? Because you claimed "that the source population (all of sub-Saharan Africa) completely lacks the alleles for blue eyes and pale skin" and concluding that these alleles must be the result of mutations as they are not present in the "source population"
These variants are not present in the sub-Saharan population; that's just a fact. That the sub-Saharan population is the geographic source of modern humans is not an assumption, but a conclusion drawn from a wide range of evidence.which in itself is a BIG assumption.
And even if certain alleles do not occur in one part of the species (homo in this case), it doesn't follow that the other part of the species must have mutant alleles, because selection does occur....
First: you confirmed my point: you also think HW is a good approach. Now, what is the difference between "expect" and "making it"?I'm sorry, but you don't understand Hardy-Weinberg. HW tells you (under idealized assumptions) what frequencies of genotypes to expect in a population, given an allele frequency. It has nothing to do with extremes "making it" or not. (Note: I am a geneticist.)
You said you see "mutations all the time in offspring". I guess you meant what you call "germ-line" mutations. How do you know what you see are mutations? That is: real changes in genetic material, that that genetic material didn't have before?A mutation is any change in genetic material. A germ-line mutation is a mutation that can be passed on to future generations, because it is in the reproductive cells..
It seems that MC1R varies quite easily thoughout the animal kingdom. Nothing proves that the variations of MC1R are "lighter skins" and that the "original" MC1R would be the dark one. It could as well be the other way around.I'm concluding that the alleles for fair skin in this gene are the result of mutation, based on the genetic evidence. As it happens, there are something like half a dozen genes implicated in human pigmentation that show evidence for positive selection; this type of evidence only appears when the allele in question starts out on a single chromosome.
Yeah, yeah.These variants are not present in the sub-Saharan population; that's just a fact. That the sub-Saharan population is the geographic source of modern humans is not an assumption, but a conclusion drawn from a wide range of evidence.
??? Why?No, but when you know that the first population lives in an environment where these alleles are selected against, as well as being absent (which is true for fair skin alleles in Africa), and when you know that the second population emerged from the first population and moved into a different environment, where the alleles are no longer selected against, you have good reason for thinking the alleles in the second population are indeed the result of mutation.
Huh? I think HW is a good approach to looking for experimental errors in genotyping, but it's just about useless for anything else. It says absolutely nothing about evolution: about where variants come from or about how or why they change in frequency.First: you confirmed my point: you also think HW is a good approach.
You ask very strange questions. Hardy-Weinberg tells you, for a given allele frequency, how many heterozygotes and how many of each kind of homozygote there will be, in the mean (= "expected value", hence "expect"). "Making it" for you seems to have something to do with whether an allele or a trait survives in the population. The two are unrelated concepts.Now, what is the difference between "expect" and "making it"?
Yes, I mean germ-line mutations. You can also see the other kind ("somatic mutation"), which are restricted to an individual, if you care to look for them. Cancers are loaded with them, for example.You said you see "mutations all the time in offspring". I guess you meant what you call "germ-line" mutations.
You examine the two parents' genetic material, see what they have for a gene, and examine the offspring's genetic material, and observe something different. Not very complicated, really. The mutations that attract attention, and are likely to be looked at, are those that cause disease, but mutations are happening in the rest of the genome all the time too.How do you know what you see are mutations? That is: real changes in genetic material, that that genetic material didn't have before?
From a genetic standpoint, since you are the geneticist here, how do explain the incredible amount of hereditary and beneficial mutations that are needed to explain "the origin of species" and at the same time that certain species never changed for an inordinate amount of time, although being subject to the same cosmic radiation and what not as the species that did evolve?
Certainly. The variation in MC1R causes variation in skin/fur pigmentation, which also vary a lot in the animal kingdom. Nearly hairless apes living in the tropics need a lot of pigmentation for protection from the sun, however, so the gene didn't vary much while we were still all in Africa.It seems that MC1R varies quite easily thoughout the animal kingdom.
Why do you make statements like this when you don't know whether there is anything that proves this or not? In fact there is quite a lot of evidence that variation in MC1R causes lighter skins and red hair in humans. See here for a summary of it.Nothing proves that the variations of MC1R are "lighter skins"
How could it be the other way around? Humans come from Africa. What happened to the variants in the African population in the last few ten thousand years?and that the "original" MC1R would be the dark one. It could as well be the other way around.
Yeah, really.Yeah, yeah.
Because the lighter-skin variants are strongly selected against in the parent population. That means that those mutations, when they occur, disappear very quickly, since they're bad for the individuals who have them. This is confirmed by the absence of the variants throughout Africa today. So if there weren't in the population that non-Africans descended from, they had to have come from somewhere, and the only only source is new mutation.??? Why?
HW simply predicts that if certain alleles are rare in P (parent generation), they will be equally rare in subsequent generations, selection not withstanding. In other words they will not be able to make it to the majority of the population, which means you will rarely "see" them.Huh? I think HW is a good approach to looking for experimental errors in genotyping, but it's just about useless for anything else. It says absolutely nothing about evolution: about where variants come from or about how or why they change in frequency.
You ask very strange questions. Hardy-Weinberg tells you, for a given allele frequency, how many heterozygotes and how many of each kind of homozygote there will be, in the mean (= "expected value", hence "expect"). "Making it" for you seems to have something to do with whether an allele or a trait survives in the population. The two are unrelated concepts.
Well to the tune of 1 in a 100 million bases! If you call that "lots" and "all the time", I don't know how you gauge thatMutations happes -- lots of mutations, all the time.
You mean this?: "one might expect mutations associated with red hair to be recessive (see 266300); most of the red-head and fair-skinned individuals in their study were either heterozygous or had no identifiable mutations."Why do you make statements like this when you don't know whether there is anything that proves this or not? In fact there is quite a lot of evidence that variation in MC1R causes lighter skins and red hair in humans. See here for a summary of it.
Sorry, wrong. HW says nothing about the action of selection, and only predicts future allele frequency for neutrally evolving infinite-sized populations. For finite populations (i.e. for all real organisms), genetic drift (which has been very well explored mathematically and experimentally) operates. HW is still of interest for finite populations, since it tells what the proportions of different genotypes will be, given the current allele frequency.HW simply predicts that if certain alleles are rare in P (parent generation), they will be equally rare in subsequent generations, selection not withstanding. In other words they will not be able to make it to the majority of the population, which means you will rarely "see" them
No, I meant all of the studies showing the causal link betwen variations in MC1R and red hair. Did you skip those? Red-headedness is not solely determined by a single gene, but mutations in this gene are clearly one of the causes.You mean this?: "one might expect mutations associated with red hair to be recessive (see 266300); most of the red-head and fair-skinned individuals in their study were either heterozygous or had no identifiable mutations."
Of course I almost forgot. "The scientific journals" and "scientists".
Well documented how? What newly developed species has been well documented? And how?
Of course. Really? Then please explain to me how it is possible that organisms that have not evolved since "millions of years" are still here today exactly the same and unaltered (at least from what we can tell) despite all the environmental selective pressures they must have gone through like all other life forms.
What you call "science" assumes that all life forms must have evolved through an infinite number of mutations, requiring therefore an infinite space of time.....
Or maybe start first with: what is genetic material precisely?
What exactly do you call "mutations", because I suspect there might be a difference.
And even if certain alleles do not occur in one part of the species (homo in this case), it doesn't follow that the other part of the species must have mutant alleles, because selection does occur....
From a genetic standpoint, since you are the geneticist here, how do explain the incredible amount of hereditary and beneficial mutations that are needed to explain "the origin of species"
the species that did evolve?
HW simply predicts that if certain alleles are rare in P (parent generation), they will be equally rare in subsequent generations, selection not withstanding.
In other words they will not be able to make it to the majority of the population, which means you will rarely "see" them.
Well to the tune of 1 in a 100 million bases! If you call that "lots" and "all the time", I don't know how you gauge that
No, I meant all of the studies showing the causal link betwen variations in MC1R and red hair. Did you skip those? Red-headedness is not solely determined by a single gene, but mutations in this gene are clearly one of the causes.
But I didn't say that it did.Sorry, wrong. HW says nothing about the action of selection
Of course genetic drift must now explain everything. But it doesn't, because it assumes.and only predicts future allele frequency for neutrally evolving infinite-sized populations. For finite populations (i.e. for all real organisms), genetic drift (which has been very well explored mathematically and experimentally) operates. HW is still of interest for finite populations, since it tells what the proportions of different genotypes will be, given the current allele frequency.
Actually, the number should be increased by a factor or 2, yes. Anyway, who knows what the number really is? Nor does it account for the even lower likelihood of persistance: hereditary.Nor for supposed repeated "beneficial" ones.1 per 100 million bases (which is probably low by a factor of two) is 60 per person, or 360 billion new mutations in the current population. .
That explains it.Looking backward, my copy of the genome has seen ~10 million mutations since it was the same as the chimpanzee genome.
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