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Author | Topic: The Great Debate: Molecular Population Genetics and Diversity in Evolution | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Genomicus Member (Idle past 1178 days) Posts: 852 Joined: |
This is the Great Debate thread on genetic diversity and the limits of evolution, between myself and Faith.
The purpose and scope of this topic is the material and overarching themes I discussed in the OP of "Molecular Population Genetics and Diversity through Mutation". Instead of regurgitating our few exchanges on that thread and posting them here, here I've listed the relevant messages to look at in order to get caught up. Message 1, OP, by Genomicus. Message 4, response by Faith. Message 18, response by Genomicus. Message 27, response by Faith. Message 38, response by Genomicus. Message 39, response by Faith. If this topic gets approved, I will simply start by responding to Message 39 and perhaps adding a bit of material on the key points I intend to demonstrate. Moderator, let me know if there's anything that needs to be changed with this.
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Genomicus Member (Idle past 1178 days) Posts: 852 Joined:
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In this discussion, I intend to demonstrate that the limits to evolution as perceived by Faith are non-existent in the real world of biology. While it is indeed true that evolutionary forces and dynamics can sometimes lead to morphological, physiological, or biochemical dead-ends, this is in no way a necessary outcome of evolutionary development and emergence. Thus, I intend to show that Faith's argument is not a viable critique of the plausibility of the modern evolutionary synthesis or the theory of universal common ancestry.
Here I will marshall an array of observations, evidence, and arguments from phylogenetics and phylogeography, molecular population genetics, bioinformatics, and functional genomics, which collectively refute Faith's argument. ***
Then let's compare your expectation of an overall trend in increasing homozygosity to biotic reality -- to what really see in nature. For this example, I will look to the classic case of a ring species: the Larus gulls. A phylogenetic tree of mtDNA sequences of various Larus gull taxa (Liebers-Helbig et al., 2010, Figure 7, page 11) has established the "ring order" of these gulls. By "ring order," I simply mean which gulls are representative of the original population, and which arose later in a ring-like manner. This phylogenetic analysis shows that: 1. Larus canus are the oldest, or "original" population, that represent the very "start" of the ring species formation. 2. L. argentatus and L. hyperboreus are slightly younger taxa than L. canus, but are still considerably old, so they also represent the early parts of the formation of this ring species. 3. L. schistisagus, L. glaucescens, L. glaucoides, are all considerably younger taxa than those in #1 and #2, and so represent the latest "end" to the ring species. Thus, by your expectation, Faith, there should be an increasing trend of homozygosity from L. canus to L. argentatus and L. hyperboreus to L. schistisagus, L. glaucescens, and L. glaucoides. Significantly, this trend should "show up clearly." But does it? Answering that question a decade ago -- when you first floated this argument -- may have been difficult, but progress in biotechnology has yielded an explosive amount of genomic data. A study by Sonsthagen et al. (2012) examined levels of heterozygosity in all of the above gull taxa (see Table 1 in their paper). Here are the averaged observed heterozygosity values observed in the previously mentioned taxa: Larus canus: 61.04 L. argentatus: 50.4 L. schistisagus: 59.5 Interestingly, the only part of your expectation that holds up is that L. canus (representing the earliest part of the ring species formation) has the highest level of heterozygosity, at 61.04; but after that, your expectation completely falls apart. First, L. schistisagus, one of the latest-evolving species at the end of the ring, has a heterozygosity value (59.5) well above the heterozygosity values of either of the older, earlier-evolving gull taxa (L. argentatus and L. hyperboreus). In fact, all of the later-evolving gull species have more heterozygosity within their populations than the earlier-evolving L. hyperboreus species. Second, these later-evolving taxa also have greater heterozygosity than the earlier-evolving species L. argentatus, with the exception of L. glaucoides. This completely upends any notion that there is some kind of "trend" here, wherein "the overall trend would be to increasing homozygosity, which would show up more clearly after a series of population splits such as in ring species." Importantly, this data on heterozygosity was acquired from microsatellite sequences. The study also looked at heterozygosity values from nuclear introns and mitochondrial DNA. So what kind of trend does your model predict we should find in these genomic regions? And why, if your argument is actually biologically valid, do we not see the trend toward homozygosity exactly where you say we should find this trend -- in ring species?
Well, clearly in the gull ring species, mutation, gene flow, and population growth is sufficient to overcome any trend towards increased homozygosity. So we have biological evidence that this trend doesn't actually do much to impede a reversal towards heterozygosity and genetic diversity.
And the answer to that question is a resounding "yes." To further bolster this answer, I will draw an example from human genomics. In particular, let's look to a small island in the Mediterranean, Sardinia. The human population in Sardinia has grown in size generation over generation, without immigration (so it's been an isolated population), as evidenced by sequence analyses of the D loop region of the mitochondrial genome and nuclear DNA polymorphisms (see references 18 and 19 in Di Rienzo et al., 1994). So to re-quote you: "...the question, again, is whether this increase in heterozygosity could occur in a geographically / reproductively isolated daughter population to any extent to offset the trend to homozygosity or reduction of alleles." In fact, there is an excess in the number of alleles in the population (this is known as "allelic richness," and is another measure of genetic diversity), compared to the proportion of individuals who are heterozygous at a given site (see Cornuet and Luikart, 1996). In other words, while there isn't a striking degree of heterozygosity, there is a high prevalence of the number of different alleles in the population at a given chromosomal locus, which in turn means that mutation -- coupled with population growth -- has fueled the rise of new alleles. And that means that far from witnessing a decrease in genetic diversity, this geographically isolated human population has seen an increase in genetic diversity.This makes sense, of course, from a population genetics perspective -- for if the population steadily grows over time, then mutation plays an increasingly major role in shaping genetic diversity than genetic drift or selection does. That mutation has increased genetic diversity in the Sardinian population is evidenced by the high ratio of allelic richness to heterozygosity. This is exactly what we would predict if the Sardinian population has grown over time, without immigration, as other lines of independent evidence demonstrate. And this uncovers a lethal blow to your argument: namely, population growth is a very simple mechanism that can relatively easily offset an increase in homozygosity in a reproductively isolated population. Both the equations of population genetics, and real-world observations, demonstrate this. Put differently, a reproductively isolated population might initially have a low amount of genetic diversity, but by growing in size generation after generation, the number of different, diverse alleles steadily increase (due to mutation) -- providing the increase in genetic diversity that can further drive evolution.
See the microsatellite heterozygosity data from the gull ring species, above, which is contrary to the expectations of your idea. That being said, you have yet to demonstrate that (1) population growth, and (2) mutation is not sufficient to reverse any trend towards homozygosity. There is absolutely no reason why these processes cannot, under any biological or evolutionary circumstances, increase genetic diversity in a reproductively isolated population (as measured by heterozygosity, nucleotide sequence divergence, or allelic richness).
Sure, the fixation of a novel phenotype in the population does mean that the competing alleles are lost. So what? There's still plenty of other chromosomal loci which will be increasing in diversity due to mutation, and this provides a "fresh batch" of diversity which natural selection can operate on when the environment changes. And this increase in genetic diversity in the numerous chromosomal loci which are not under strong selective pressure means that further population splits can recover genetic diversity simply through mutation and population growth.
So if there can still be great diversity for other characteristics that aren't relevant to the phenotype that's being fixed in the population, then what's the problem here? Why can't this increased genetic diversity also happen in daughter population that successively split off from each other?
Are you willing to stake your idea on the notion that a few thousand years ago human heterozygosity was as high as 50%? What about overall nucleotide sequence diversity? Do you think there has been an increase or decrease in nucleotide sequence diversity over the course of human history?
Nope, because the trend can become reversed by mutation and population growth.
You state this as if it is an empirical observation. It is not; quite the contrary, in fact -- human genetic diversity, on the whole, has increased over time. Would you like me to provide the consilience of independent lines of biological evidence for an increase in human genetic diversity over time? In the meantime, you can present your evidence that human genetic diversity has been decreasing. If you do not have such evidence, then your argument is little more than an anti-evolutionary fantasia.
Do you have any evidence that this "trend" cannot be reversed or counterbalanced by sufficient mutation or population growth?
Well, we have evidence that speciation can occur followed by an increase in genetic diversity. See the microsatellite heterozygosity data on the gull ring species, above. And, of course, there's nothing stopping mutation and population growth from adding genetic diversity to a population, even while a few phenotypes are being fixed. There will still be plenty of chromosomal loci which will see an increase in heterozygosity or allelic richness, and there's nothing stopping that.
No, because plenty of loci won't be under any significant selection pressure.
Speciation doesn't amount to a "genetically compromised" population. Cheetahs underwent a significant population bottleneck; but if a founding population is sufficiently large, then there is nothing of necessity preventing mutation and population growth from replenishing the genetic diversity of the population. Sometimes the population is too small, and the mutation rate to small, that extinction results. Other times the population size is not too small, and the mutation rate is sufficiently large, that genetic diversity can increase. This not only makes perfect sense from the mathematics of population genetics, but it's also what we see in biology. Your error is in assuming that all founding populations are equal, all mutation rates are equal, and all selective pressures are equal. They are not. Your argument not only makes a failed prediction (see ring species example of gull taxa), it also ignores perfectly valid and demonstrated principles of genetics. Edited by Genomicus, : No reason given.
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Genomicus Member (Idle past 1178 days) Posts: 852 Joined:
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Well, yes, if you want to verify that what I'm saying is accurate.
I've concurred that selection at a locus under consideration reduces the genetic diversity of that locus. That there is a variety in heterozygosity in daughter populations in ring species is exactly what we'd expect if genetic diversity is determined by a combination of mutation rate, population size, genetic drift, and selection. Population growth and mutation rate are sufficient to add genetic diversity to daughter populations.
I also expect you to have to spend a fair amount of time on this, inasmuch as I spent a considerable amount of time assembling various lines of evidence. However, the intention is not to swamp you, but rather to be thorough -- as all too often threads turn into nitpicking back-and-forth from a lack of comprehensiveness. Take all the time you need, of course.
And that right there is a concession that this trend you speak of can be overcome by counteracting biological processes, such as gene flow. Or mutation. Or population growth combined with mutation. Or horizontal gene transfer. In other words, there are so many "exceptions" that this so-called trend doesn't become a problem for the Neo-Darwinian synthesis. And, as a side note, you do realize that there will almost always be a degree of gene flow among the taxa of a ring species, yes?
Yes, there is that evidence, right in the paper I cited. Here's a look at the mean values ofnucleotide diversity of the various gull taxa (the closer these values are to 1, the greater the amount of nucleotide diversity): Larus canus: .00380 L. argentatus: .00418 L. schistisagus: .00300 Once again, this pattern reveals absolutely no trend towards decreased genetic diversity in daughter populations. But why do we think this diversity is the result of mutation after the origin of the species? Because: 1. This nucleotide diversity data comes from nuclear intron sequences, and there is no evidence that there has been significant gene flow among nuclear DNA genes in various Larus species (see Pons et al., 2014). 2. If this nucleotide diversity was the result of significant gene flow, then it would totally confuse any molecular phylogenetic construction of the Larus species. For if there has been significant gene flow among nuclear regions -- enough to account for this diversity -- then that gene flow would result in multiple shared polymorphisms among divergent Larus taxa. And, this in turn, would lead to weird, conflicting branching patterns in molecular phylogenies of these taxa -- which we don't observe. In other words, the best explanation for this nucleotide diversity is mutation.
Yes, actually, these numbers very nicely demonstrate the real phylogenomic history of these taxa. Edited by Genomicus, : No reason given. Edited by Genomicus, : No reason given.
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Genomicus Member (Idle past 1178 days) Posts: 852 Joined: |
No, we see particular processes of evolution more clearly with reproductively isolated populations. Other evolutionary processes are better captured by, e.g., ring species.
So basically gene flow refutes your whole notion that evolution is necessarily limited under all biological circumstances.
I'm not going to get into a debate about the nuances of mutations quite yet. That may be an interesting discussion for the future, however.
For evidence that genetic diversity can increase in reproductively isolated populations, see the genomics data I reference in Message 3 regarding the human population on Sardinia.
No, these processes are evolutionary change. *Gene flow increases the heterozygosity of a population, which in turn means that there are a greater number of variants possible which can elevate the fitness of the population. A.k.a., evolution. *Mutation adds new variants in the population, and increases the genetic and therefore morphological distance between a daughter population and a parent population. A.k.a., evolution. *Horizontal gene transfer can completely alter genomes which are better suited to a new environment, so these new genomes spread throughout a population. A.k.a., evolution. And so on.
Honestly, I'm pretty sure you're the only one who's confused. Anyhew, if you want a fancy lab setup, then the short generation time of bacteria would seem to offer an excellent way to test your idea. Now, you will object here likely because you know bacteria refutes your idea. So you're going to say that the organisms used need to be animals. But why is that the case? If your argument were actually valid, it would apply equally well to "reproductively isolated" bacteria (that is, bacteria which are not exposed to other bacterial populations) and reproductively isolated Metazoa. So why shouldn't we test your idea with bacteria? Edited by Genomicus, : No reason given.
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Genomicus Member (Idle past 1178 days) Posts: 852 Joined: |
That isn't evolution according to someone with little more than a high school level of understanding of biology or according to the relevant experts?
Sure it is. These are all factors that contribute to the formation of new species. Mutation + positive selection + genetic drift all work together to create new species. A population need not be geographically isolated from its parent population in order to become a novel species. The population merely must occupy a somewhat different ecological niche; genetic divergence (through mutation, drift, selection) from the parent population then, over the course of generations, leads to the emergence of reproductive barriers which define the new species.
No, that's not true. It is the genetic divergence between a daughter population from its parent population that eventually gives rise to reproductive barriers (as characterized by morphology or molecular/cell biology) between the two populations, and this is speciation. And what creates genetic divergence between two populations? Mutation. Genetic drift. Population growth. Selection. From this perspective, there's no "adding and subtracting," there is only genetic divergence between populations (which can be counteracted by gene flow, though not always -- e.g., when the ecological niche selects against immigrants).
Whoever or whatever gave you that idea?
Well, bacteria are actually freakin' beautiful, but by your description, it seems your proposed lab experiment can be done with diploid yeast populations. Anyhew, responding to the rest of your posts later.
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Genomicus Member (Idle past 1178 days) Posts: 852 Joined:
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At the onset of this debate, one of my stated intentions was to “show that Faith's argument is not a viable critique of the plausibility of the modern evolutionary synthesis.” Even a cursory reading of Faith’s responses will reveal that far from presenting a robust critique against the modern evolutionary synthesis, she is instead focusing on a very narrowly described anti-evolutionary fantasia that is not grounded in biological reality.
As I continue to marshall the evidence that refutes Faith’s notion, the keen reader will note a common, recurring theme: namely, that Faith’s argument is exceptionally ineffective at making accurate predictions about the living world. So while her argument is repeated over and over again, and expectations of the argument tentatively offered up, a consilience of observations, experiments, and research from a breathtaking range of biological disciplines continue to refute her notion. For the sake of making this discussion easier to follow, I have organized my rebuttal in topical fashion, rather than in chronological order: I. General Responses
That's not a personal attack in any way. It's merely highlighting the curious nature of your reality, wherein you get to decide what "evolution" means even though you don't know what electron transport chains and cytochrome c is.
This is not true. The emergence of a new species only implies a loss of genetic diversity at a few chromosomal loci, namely those loci with alleles directly involved with reproduction. For cladogenesis to occur, the only real, relevant requirement is that a population is not able to reproduce with the parent species. Indeed, for some Metazoa -- such as Spodoptera latifascia and S. descoinsi -- only a couple of genes are required to change for reproductive barriers between the two populations to arise (Monti et al., 1997). The salient point here is that you have yet to demonstrate (either via biological observation or through principles of genetics) that the emergence of a new species necessarily entails a loss of genetic diversity at most chromosomal loci. For if only a couple of genes are required to change for speciation to occur, then there are hundreds and hundreds of other loci which can continue to diversify, increasing the overall, net genetic diversity of the population even while speciation is occurring. This alone is enough to render your argument egregiously flawed, but I will press on.
You have to demonstrate the truth of this above statement on mutations and the so-called clear-cut-ness of species. So demonstrate it. It's relatively easily dismissed, anyway. We know mutations regularly occur in gametes, and we know that these mutations have a certain probability distribution of spreading throughout the population. So long as these mutations do not alter the reproductive capability of the individuals in which they are found, then these mutations will not make the species any less "clear-cut."
Except that mutations are often what create the phenotypes that lead to the "true breeds." Consider, for example, Belgian Blue cattle, which have been bred through multiple generations to get the desired muscular physique. This phenotype is the result of a 11 base pair deletion in the gene coding for myostatin (Kambadur et al., 1997). In other words, it is a mutation that originally gave rise to the double-muscle phenotype. Furthermore, mutations do not of necessity "mess up" the breed. Mutations can occur anywhere in the genome, and anywhere along a chromosome. In the case of the Belgian Blue cattle, so long as extensive mutations do not occur in the myostatin gene (and functionally related genes), then the breed's desired phenotype will remain intact. So your argument really doesn't make any sense at all.
You're right about the gene flow, but deathly wrong about the mutation part. Mutations in a new population increase the genetic distance between the parent and daughter populations, and this is really all that needs to happen for reproductive barriers between the two populations to emerge.
Only a few loci within the new population will lose diversity, as a consequence of reproductive system related phenotypes being fixed in the population. The other hundreds and thousands of loci can increase in diversity, and you have yet to counter this argument effectively.
No, mutations speed up the emergence of evolutionary adaptation. Why do you think viruses are able to evolve drug resistance so rapidly? It's because of their rapid rate of mutation, coupled to rapid generation time.
Yes, but mutations will add to the genetic diversity. You still haven't refuted this point. ***** THE EVIDENCE FROM HUMAN GENOMICS
A common thread you will soon discover being weaved throughout this discussion is your claim that we can’t really “tell if these things are an increase over time” -- only to be confuted by numerous lines of research which mesh together in elegant concordance. First, archaeological and census evidence indicates that the Sardinian population (which goes back thousands of years) never grew beyond about 300,000 individuals until around 1728, when the population began to grow rapidly (see Calò et al., 2008). Second, sequence analysis of Sardinian mitochondrial DNA also suggests that this population was initially a small “bottleneck” but has experienced growth over time (Di Rienzo and Wilson, 1991). This is further corroborated by research on allelic richness and heterozygosity, which can indicate population growth from an initial, smaller population (Cornuet and Luikart, 1996). So we have here multiple lines of independent evidence for a small founding population on Sardinia, which was followed by population growth. There is, moreover, compelling genetic evidence from nuclear DNA polymorphisms, mitochondrial DNA sequences, and other markers that the Sardinian population has been isolated with no gene flow from outside the island (Di Rienzo et al., 1994). Now, for the clincher. In a beautiful piece of genomics research, Caramelli and colleagues (2007) analyzed mtDNA D-loop sequences (which are basically the most variable regions of the human genome) from ancient Sardinians who lived between 3,430 and 2,700 years ago (the DNA was extracted from teeth using a highly rigorous laboratory approach). The diversity of these sequences was then compared to the mtDNA of present-day Sardinians. The haplotype diversity (a way to measure genetic diversity, and a form of heterozygosity) of the ancient population was 0.83, compared to a haplotype diversity of .96 for modern Sardinians (the larger the number, the greater the diversity). Revealingly, too, was the discovery that the average number of indels (a form of mutation) between sequences from the ancient population was a low 1.43, whereas the mean value for indels between modern Sardinian sequences was 4.68. This neatly demonstrates, again, that the modern Sardinian population has increased in genetic diversity, despite being isolated. The study by Caramelli and colleagues also provides evidence for clear genetic continuity between the ancient population and the modern Sardinian population, indicating a lack of gene flow from the “outside” world. So how does your notion explain the above experimental results, Faith? ***** THE EVIDENCE FROM ELEPHANT SEAL mtDNA
And yet the molecular sequence data is in direct contradiction to your above statement. Again, I must call attention to how consistently, and how often, the expectations of your argument can be immediately eviscerated by what we observe in biological reality. In the late 1800s, the northern elephant seal population hit an all-time low, with numbers dipping below a mere 100 individuals. However, the northern elephant seal’s population size has recovered, and now has over 175,000 individuals. This situation, then, allows an empirical test of the expectations of your argument. In an analysis of mtDNA sequences, Weber et al. (2000) sought to compare the genetic diversity of northern elephant seals prior to their bottleneck, during the bottleneck, and after the bottleneck when the population recovered. Like other studies referenced in this response, the control region of the mitochondrial genome was used, given the highly variable nature of this genomic region. In other words, changes in nucleotide and haplotype diversity would show up most clearly in the D-loop region of mtDNA. So what were the results (from Table 1 of Weber et al., 2000)? Haplotype Diversity, Elephant Seal Population DNA from 1892: 0.00 Nucleotide Diversity, Elephant Seal Population DNA from 1892: 0.0000 What do these results tell us? Both haplotype diversity and nucleotide diversity of modern northern elephant seals are significantly higher than that of the elephant seal population from 1892, when the population hit an all-time low. And unlike heterozygosity, which is not necessarily the result of novel mutations, nucleotide diversity is the result of mutations introducing new DNA changes throughout the population. Furthermore, in recent history, the northern elephant seal population has not been subjected to gene flow from other species, so the only way these observations can be explained is through mutations. To re-quote you, Faith: ”But I think this expectation is truly wishful and not real, which is proved by the situation of the elephant seals which have increased enormously in population size in a condition of genetic depletion that shows no signs of being mitigated by any increase in mutations.” Yet here we have direct empirical evidence that categorically refutes that comment, and further bolsters my argument that population growth, coupled with mutation, can increase the genetic diversity of a population. So how does your notion explain the above experimental results, Faith? *****
Explain why you think so-called junk DNA in the human genome is evidence for your position, so that I can more properly refute it. More later on ring species, etc. I think you've got a lot to chew on here, and some experimental results to explain -- and that's an understatement.
Edited by Genomicus, : No reason given. Edited by Genomicus, : No reason given. Edited by Genomicus, : No reason given. Edited by Genomicus, : Multiple cups of coffee to stay awake = multiple typos.
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Genomicus Member (Idle past 1178 days) Posts: 852 Joined:
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Yeah, but examining the facts in a new light in no way means you can force your own meaning on words with already established definitions. You don't get to decide what evolution is and is not. You do realize that, yes?
I mean those alleles that must change in order for reproductive barriers to emerge between two different populations. In the case of S. latifascia and S. descoinsi, only changes in 2 alleles are needed. Which means that so long as those changes to those 2 alleles are fixed in the population, all other chromosomal loci can diversify through mutation -- such that both populations experience a net increase in genomic diversity, despite the origin of a new species.
But only a fraction of the genome must change in order for reproductive barriers to emerge between two sister populations or a parent and daughter population. Do you understand that?
Yeah, and then mutations happen to those loci not relevant to the emergence of reproductive barriers, with the consequence that the net genomic diversity increases. What part of this do you not understand or do you disagree with? Because your "simple logical point" still hasn't refuted the role of mutations in generating new genetic diversity.
Literally wut?
We're talking about changes to two particular genes. And this is deeply problematic for your position because if only changes to two genes are required for speciation in this case, then all other chromosomal loci can diversify through mutation, such that there is a net increase in genomic diversity.
Yeah, I have no problem with "counting on mutation to make random changes in two genes," given the preponderance of evidence that mutation is a major diversifying force in biology.
Yes, but those changes are only relevant to speciation if they directly contribute to the rise of morphological or biochemical reproductive barriers between the two populations. A bunch of those changes can result in an increase of genetic diversity.
No, but only two chromosomal genes need to be fixed in order for the reproductive barriers to emerge. Sure, plenty of other changes will occur, but these changes will often tend towards diversity, not homozygosity.
Sometimes, sometimes not. Like...one morphological trait could result from a bunch of different possible changes = a bunch of different possible genomic changes = a bunch of diversity on a molecular level. Do you have any evidence for your argument quoted above or is it just something you're making up?
No, the cause of its genetic problems is that the cheetah has extraordinarily low diversity in all parts of its genome. As usual, you're just stating things as if they are true ("what good does it do the cheetah to have lots of diversity in other parts of the genome if all the loci for its salient characteristics are fixed") when you have no genomic evidence, from e.g. cheetah studies, for these claims.
Sometimes mutation does affect the "collection of loci that determine the species." When that happens, the result can be a new species. Sometimes mutation doesn't ultimately drive population-wide changes to these particular loci, because (a) the population size is so large that the odds of a particular neutral mutations being fixed in the population is so small, (b) selection keeps new mutations at these loci at bay, depending on the strength of selection and the rate of mutation at these loci.
Okay, time out. All parts of the genome are evolving as the population experiences changes in environment, etc. So it's not like only the parts of the genome that are homozygous are "evolved" or something like that. And what do you mean by "offsetting the loss in the selected part of the genome"?
Wut? What good does what to do the creature?
If your argument depends on not accepting the force of mutation, then your argument is sunk. Yes, mutations do happen, and yes they do diversify gene pools.
Wut? Define "evolution." And once you have defined "evolution," stick with that meaning, because you seem to be all over the place with what "evolution" means.
No, that's not the point. The point is that only a fraction of the genome is involved in the emergence of reproductive barriers between two populations. All other loci can diversify, which means there is no "net decrease" in genetic diversity as a consequence of speciation. Will other loci also tend towards homozygosity? Sure, and that'll lead to the fixation of new phenotypes. But other loci will also tend towards heterozygosity and new alleles will arise, leading to a bunch of diversity at those loci. So your challenge is demonstrating that speciation necessarily entails a net loss of genomic diversity. So demonstrate it.
No, that's not what I'm claiming. Whoever said anything about some hidden part of the genome? That's very disingenuous.
Wut? There is no "hidden diversity." There is a loss of homozygosity at some loci, and a gain of homozygosity at other loci. Yet there is no reason at all to suppose that there is a net decrease in genomic diversity as the new population/species propagates.
If a novel mutation arises in a gene that maintains the reproductive barrier between the parent and daughter population, then it will either (a) be selectively neutral, (b) be detrimental, (c) be beneficial. If it detrimental, then it won't really spread throughout the population, so the species will remain intact. If it is beneficial, then it will spread throughout the population. So what's the problem with mutations occurring in traits that have been fixed?
No, you don't get to keep doing that in this debate. Stop vaguely skirting around the issue of mutations; either your argument requires a disbelief in the diversifying power of mutation or it does not. If it does not require such a disbelief, then stop saying stuff like "I always have the doubt that mutations can be a good thing," because it's not relevant. And if it does require the disbelief, then articulate your position on mutations and bring to bear the relevant evidence that supports your position.
Umm, plenty of mutations are beneficial. Most of selectively neutral, meaning they don't have a benefit to the animal. They exist because of the chemical nature of deoxyribonucleic acid replication and polymerase.
Nature could care less about "maintaining the characteristics" of a species. The only thing that really matters is whether the population's fitness changes appropriately over the course of changes in selection pressures.
I didn't say anything like that.
I don't want it. That's just the way biology is. Plenty of mutations do not affect morphology; plenty of mutations do affect gross morphology, and this does change the appearance of the animal.
Nope, not always. Selection works to speed up the fixation of high-fitness alleles. And the fitness of the organism goes well beyond morphology. Besides, morphological change happens all the time in species (e.g., there's plenty of morphological diversity among Homo sapiens). So what?
Nope, it only requires the loss of genetic diversity at the myostatin locus (and a few other loci). There are plenty of other loci that can diversify, leading to a variety of different Belgian Blue cattle. They're not, like, all clones of each other, you know?
No, mutations wouldn't "mess up the breed" (whatever that means), because the vast majority of mutations wouldn't occur in the myostatin locus which defines the breed -- and those that do occur at this locus would be selected against through the breeding process. Edited by Genomicus, : No reason given.
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Genomicus Member (Idle past 1178 days) Posts: 852 Joined:
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You then go on to cite different examples of immigration to Sardinia over the course of relatively recent history. However, your error here is assuming that immigration implies gene flow. In reality, gene flow from the migrant population to the indigenous population will only occur if if the immigrant population is sufficiently large or has strongly beneficial alleles. In fact, migrant alleles are often of a lower fitness than alleles of the indigenous population, as the migrant alleles have not been adapted to the environmental conditions of the native population's habitat (see Lenormand, 2002). This is a point worth emphasizing because you mistakenly believe that "Where there is immigration, there is gene flow." Sometimes, but sometimes not -- which is why independent evidence is needed to ascertain if there has, in fact, been gene flow from a migrant population to the native population. Simply pointing to immigration from the European continent to Sardinia is not at all enough, as this doesn't tell us if gene flow has actually happened from the migrant population --> indigenous population. Nor do arguments from incredulity help your case ("...it is highly improbable that all that immigration since the time of the Roman Empire would not have mingled the peoples"). Have you calculated the probability of gene flow from the migrant populations to the native populations? You have not, so your argument boils down to nothing but pure incredulity -- and that, of course, is not a rigorous scientific defense of your thesis but just an emotional response. Now then, as to the molecular evidence that there has been no meaningful gene flow from migrants to the native Sardinian population over the course of history. For starters:
The above represents but a portion of the armamentarium of genomics evidence that Sardinia has indeed been genetically isolated from the European continent, despite small amounts of migration. Not only have you failed to demonstrate that Sardinian genomics diversity has been impacted by gene flow, but you also must now grapple with the ample molecular evidence for Sardinia's genetic isolation.
Your ignorance of genetic processes -- and of how gene flow works -- is not a valid argument. "A history in which there couldn't possibly have been a lack of gene flow" is something you're making up. Gene flow doesn't automatically happen when a migrant population arrives, and you should have known that. To conclude, then, I'll simply re-quote what I stated in my original Message 15: In a beautiful piece of genomics research, Caramelli and colleagues (2007) analyzed mtDNA D-loop sequences (which are basically the most variable regions of the human genome) from ancient Sardinians who lived between 3,430 and 2,700 years ago (the DNA was extracted from teeth using a highly rigorous laboratory approach). The diversity of these sequences was then compared to the mtDNA of present-day Sardinians. The haplotype diversity (a way to measure genetic diversity, and a form of heterozygosity) of the ancient population was 0.83, compared to a haplotype diversity of .96 for modern Sardinians (the larger the number, the greater the diversity). Revealingly, too, was the discovery that the average number of indels (a form of mutation) between sequences from the ancient population was a low 1.43, whereas the mean value for indels between modern Sardinian sequences was 4.68. This neatly demonstrates, again, that the modern Sardinian population has increased in genetic diversity, despite being isolated. The study by Caramelli and colleagues also provides evidence for clear genetic continuity between the ancient population and the modern Sardinian population, indicating a lack of gene flow from the “outside” world. So how does your notion explain the above experimental results, Faith?
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Genomicus Member (Idle past 1178 days) Posts: 852 Joined: |
C'mon, Faith. A Scientific American blog article is a fine citation for a high school sophomore's term paper, but in a scientific debate? That blog article isn't original research -- it's just summarizing studies that, like, you yourself can go and read. You know that, right? So where in the article is the reference that details the evidence for declining genetic diversity among the elephant seals? If you can't find that reference, then this article doesn't help you one bit, a misleading headline notwithstanding. You didn't actually even refute the evidence I presented for the increasing genetic diversity of the elephant seals, so give it a go again:
So how does your notion explain the above experimental results, Faith? Edited by Genomicus, : No reason given. Edited by Genomicus, : No reason given.
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