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Author Topic:   The Great Debate: Molecular Population Genetics and Diversity in Evolution
Genomicus
Member (Idle past 1941 days)
Posts: 852
Joined: 02-15-2012


Message 1 of 30 (785012)
05-26-2016 4:48 PM


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.

  
Genomicus
Member (Idle past 1941 days)
Posts: 852
Joined: 02-15-2012


(1)
Message 3 of 30 (785114)
05-28-2016 2:06 AM


The Biological Evidence
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.
***
I will begin my responding to Message 39 of Faith, in the "Molecular Population Genetics and Diversity Through Mutation" thread.
No, an increase in allelic heterozygosity is an increase in genetic diversity. Heterozygosity at a locus under consideration is a pretty standard way to measure genetic diversity in a population. See here (warning: it's a PDF; it's a "primer" on population genetics which you might find easier to understand than standard pop gen textbooks).
Funny, I've known that and yet forgot it in this exchange: I've even said that the way to measure genetic diversity to test my argument is by looking for increases in homozygosity. I’ve saved the link and skimmed through it. There may be too much math there for me, however.
You said heterozygosity can increase from parent to daughter and I accepted that possibility but I would still expect that 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.
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. hyperboreus: 45.6
L. schistisagus: 59.5
L. glaucescens: 50.77
L. glaucoides: 47.0
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?
But yes, increased homozygosity is THE sign of reduced genetic diversity. The question now is whether the fact that heterozygosity can increase in some cases is enough to overcome the predicted trend to increased homozygosity.
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.
If a given locus exhibits a high degree of heterozygosity within a population, it means that there's whole range of different, diverse allelic combinations at that locus. Ipso facto, there's an increase in genetic diversity when there's an increase in heterozygosity (and here, when I say "increase," I do not mean an increase in frequency of a particular allelic combination; I mean an increase in diverse allelic combinations throughout the population).
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.
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.
You are describing a situation that starts out with high genetic diversity in general, which I suppose to generally increase the farther back you go along any evolving line, and where that is the case there should still be a trend to increased homozygosity all down the evolving chain of daughter populations, but it wouldn’t be particularly dramatic until you have less genetically diverse populations splitting into daughter populations, especially into significantly smaller populations.
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).
In any case I think you’d be very hard-pressed to demonstrate that I’m wrong about the TREND to decreased genetic diversity, or to make a case for an actual increase. Population splits do very much what natural selection does as far as changing gene frequencies goes, and you’ve agreed that natural selection reduces genetic diversity. A daughter population is a sort of selected population, randomly selected in this case, and even if some increase can occur over that of the parent at some loci there’s no way that could be the trend of change, because of the principle you have also already agreed with, that developing new phenotypes requires the loss of competing alleles. (Even in the case of our new high frequency B’s there is a reduction of the b’s after all.)
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.
OK, I see, and this is so as a TREND and with respect to the salient characteristics of the subspecies that is developing. There could still be great diversity for other characteristics of the creature that don’t show up in the new phenotype.
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?
The estimate of heterozygosity for human beings now is something like 7% IIRC, but taking a wild guess back a few thousand years it could have been as much as 50% or 70% or higher, and some loci could have retained a higher percentage than others even now.
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?
For if allelic sites, or chromosomal loci, do not become increasingly homozygous while a novel trait is evolving, then the population has plenty of genetic diversity -- even if novel traits are evolving. And if the population has this genetic diversity, your argument falls apart.
No it doesn’t, it just means, as I say above, that the loss is a trend over time.
Nope, because the trend can become reversed by mutation and population growth.
There was a lot more genetic diversity in the past, that has been decreasing over time...
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.
None of this changes my argument that homozygosity will be the trend down any line of evolving subpopulations, slow or fast, dramatic or hardly discernible, but always the trend.
Do you have any evidence that this "trend" cannot be reversed or counterbalanced by sufficient mutation or population growth?
The idea that a mammal evolved from a reptile assumes enormous continuing or growing genetic diversity (over hundreds of millions of years yet)...
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.
But if selection reduces genetic diversity then it’s going to treat any source of genetic diversity the same way...
No, because plenty of loci won't be under any significant selection pressure.
Wut? A single mutation won't add significant genetic diversity to the cheetah population. What's needed is an elevated rate of mutation in the cheetah population if they are ever to get out of their "genetic purgatory." The equations in the OP demonstrate very nicely why there's extremely low genetic diversity among cheetahs; the small population size, coupled with a not-very-high mutation rate, means that genetic drift and inbreeding (which is basically just an extension of the sampling error that genetic drift is) will continue to decrease the diversity of the cheetah gene pool. So I have no idea where this "waiting around for a mutation to get them out of their 'genetic purgatory'" comes from, since it's not like a single mutation will do that.
OK, so any genetically compromised species will face the same kind of problem, and if that’s what speciation amounts to, we’ve got a deteriorating system that isn’t going to be able to reverse itself.
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.

Replies to this message:
 Message 4 by Faith, posted 05-28-2016 3:44 AM Genomicus has replied
 Message 5 by Faith, posted 05-28-2016 4:11 AM Genomicus has not replied
 Message 10 by Faith, posted 05-29-2016 2:56 AM Genomicus has not replied
 Message 11 by Faith, posted 05-29-2016 10:30 AM Genomicus has not replied

  
Genomicus
Member (Idle past 1941 days)
Posts: 852
Joined: 02-15-2012


(3)
Message 7 of 30 (785125)
05-28-2016 5:40 AM
Reply to: Message 4 by Faith
05-28-2016 3:44 AM


Re: The Biological Evidence
So I've got to read that paper?
Well, yes, if you want to verify that what I'm saying is accurate.
You've agreed that selection reduces genetic diversity. So what else is going on here genetically to account for this supposed contrary information?
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.
Well I see I didn't read far enough, but I'd expect to have to spend a fair amount of time on this since your intent is obviously to swamp me.
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.
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.
Um, "gene flow" is of course specifically the main reason one would NOT get the trend I'm talking about, as I believe I've said many many times. That right there makes this study utterly irrelevant.
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?
If there's actual evidence of mutation AFTER the new species has developed that's something else to consider as an interference with the expected loss.
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. hyperboreus: .00383
L. schistisagus: .00300
L. glaucescens: .00329
L. glaucoides: .00500
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.
The REAL history of these gulls is obviously not accurately expressed in these numbers.
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.

This message is a reply to:
 Message 4 by Faith, posted 05-28-2016 3:44 AM Faith has replied

Replies to this message:
 Message 9 by Faith, posted 05-28-2016 9:08 AM Genomicus has replied

  
Genomicus
Member (Idle past 1941 days)
Posts: 852
Joined: 02-15-2012


Message 8 of 30 (785126)
05-28-2016 6:03 AM
Reply to: Message 6 by Faith
05-28-2016 4:34 AM


Gulls Troll Faith's Specs but Evolve Anyway
ABE: Why do you think I insist on REPRODUCTIVE ISOLATION? It's because that's where we see the processes of evolution most clearly.
No, we see particular processes of evolution more clearly with reproductively isolated populations. Other evolutionary processes are better captured by, e.g., ring species.
If you have gene flow that has to interfere.
So basically gene flow refutes your whole notion that evolution is necessarily limited under all biological circumstances.
Same with mutation, although I really don't think mutation occurs as is so often claimed.
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.
But again, I'm only talking about the situation of selection and reproductive isolation, the processes that bring about evolution itself, that make the changes we call evolution, bring out new phenotypes from new gene frequencies, etc etc etc.
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.
Adding genetic diversity will of course interfere with these processes. Reality is usually a lot messier than my idealized argument, of course, in reality there is often continued gene flow or resumed gene flow or hybrid zones and whatnot, but they are the opposite of the processes that bring about evolutionary change.
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.
It's because of this sort of confusion...
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.

This message is a reply to:
 Message 6 by Faith, posted 05-28-2016 4:34 AM Faith has not replied

  
Genomicus
Member (Idle past 1941 days)
Posts: 852
Joined: 02-15-2012


Message 12 of 30 (785207)
05-29-2016 5:12 PM
Reply to: Message 9 by Faith
05-28-2016 9:08 AM


Re: The Biological Evidence
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.
Yes of course, "if genetic diversity is determined by a combination of mutation rate, population size, genetic drift, and selection" you'll get increased heterozygosity. But that isn't evolution...
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?
...that isn't how new species come about.
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.
That's a see-saw between adding and subtracting that overall gets called evolution but it's only the subtractive processes that form 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).
...but it's only the subtractive processes that form the new species.
Whoever or whatever gave you that idea?
ABE: Why not bacteria? Because they're weird, they're ugly and they don't sexually reproduce. And I don't think they behave in exactly the same way as diploid animals at all. That's why it's got to be mice or something I can talk to and pet.
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.

This message is a reply to:
 Message 9 by Faith, posted 05-28-2016 9:08 AM Faith has replied

Replies to this message:
 Message 13 by Faith, posted 05-30-2016 1:20 AM Genomicus has not replied

  
Genomicus
Member (Idle past 1941 days)
Posts: 852
Joined: 02-15-2012


(4)
Message 15 of 30 (785234)
05-31-2016 5:28 AM


A Consilience of Genomics Evidence
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
II. The Evidence from Human Genomics
III. The Evidence from Elephant Seal mtDNA
GENERAL RESPONSES
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?
Interesting how predictable it is that eventually the debate will devolve into personal attack. I wonder what I said that got to you.
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.
...you cannot keep a breed or a new species if new genetic diversity keeps being added to it, because getting a new species REQUIRES a loss of genetic diversity.
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.
So what? There's still plenty of other chromosomal loci which will be increasing in diversity due to mutation...
Again if you are relying on mutations to keep occurring in the population you are not getting a clear-cut species, which is the whole point of evolution.
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."
Same as if you are developing a breed of cattle and that population keeps getting mutations, you’re never going to get the true breed breeders are always looking for.
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’ll get the clearest new species where you have ZERO gene flow or mutations.
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.
But if the way evolution works is by reducing genetic diversity to get the new species...
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.
And if you keep adding mutations all you’ll do is slow down the evolution...
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.
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?
Well, with each new daughter population you are losing genetic diversity throughout the genome just because you are starting with fewer individuals each time.
Yes, but mutations will add to the genetic diversity. You still haven't refuted this point.
*****
THE EVIDENCE FROM HUMAN GENOMICS
This would be more convincing if you knew the original state of allelic richness in the population. As it is, there’s no real way of telling if these things are an increase over time, such as by mutation, or reflect the original situation as it played out over the generations. In fact how much is known about the original settlers anyway? How far back does the history go?
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 Cal 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
Nope, because the trend can become reversed by mutation and population growth.
And of course population growth itself accomplishes nothing, except supposedly this wishful opportunity for mutations to increase genetic diversity. 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.
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
Haplotype Diversity, Elephant Seal Population DNA from 1980: 0.53
Nucleotide Diversity, Elephant Seal Population DNA from 1892: 0.0000
Nucleotide Diversity, Elephant Seal Population DNA from 1980: 0.0086
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?
*****
My evidence that human genetic diversity has been decreasing is more a necessary deduction from my argument than direct evidence. However, I'd include the huge amount of junk DNA in the genome as evidence myself, which isn't likely to convince you of the point because you could only believe it's explained sufficiently by Evo Theory.
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.

Replies to this message:
 Message 16 by Faith, posted 06-01-2016 8:04 AM Genomicus has replied
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 Message 18 by Faith, posted 06-01-2016 3:56 PM Genomicus has replied

  
Genomicus
Member (Idle past 1941 days)
Posts: 852
Joined: 02-15-2012


(1)
Message 19 of 30 (785385)
06-03-2016 10:44 PM
Reply to: Message 16 by Faith
06-01-2016 8:04 AM


Re: 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.
Get to decide? I don’t think you grasp the situation here. Creationists have to rethink the standard categories because we have a completely different idea about all these things, a different paradigm if you will.
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?
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.
I’ve read this over I don’t know how many times and have no idea what alleles directly involved with reproduction could possibly mean.
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.
Also, yes I know the definition of speciation is cessation of reproduction with the parent population, but this isn’t about any particular alleles since the whole genome is what is involved in reproduction.
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?
To continue with my example of domestic breeds, there is no way NOT to get reduced genetic diversity when so few animals are selected for the breed. Even those loci that don’t severely lose genetic diversity have to lose SOME just because there are relatively few individuals contributing to the breed.
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.
So shall I guess that you are English-challenged to the extent that the word moth Is beyond your vocabulary?
Literally wut?
It is interesting that some species may become genetically incompatible with so little change. This is, however, a very odd piece of logic, in that such a low requirement for a reproductive barrier to arise doesn’t imply anything about changes in other genes, whether required or not. Are we talking two particular genes or any two genes? In any case I fail to see how this is a problem for my argument.
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.
The problem is that unless you are counting on mutation to make random changes in two genes there is no explanation for how this comes about.
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.
Breeds and species involve changes in the whole genome, simply because it’s the whole genome that reproduces, or the entire individual animal.
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.
Even where specific traits are selected, you don't get only those traits, you get an animal with those traits but also unselected changes as well. So if such changes come about by selection or population splits it can’t be only two genes that change.
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.
Besides, my argument is that it’s where the traits of the new population are different that the genetic diversity is reduced...
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?
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, which is the cause of its genetic problems?
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.
I do have this nagging question how it is that you can count on mutations at other chromosomal loci to keep up the genetic diversity while not affecting the collection of loci that determine the breed or species.
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.
And at what point does that supposed increase in diversity offset the loss in the selected/evolving part of the genome?
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"?
And what good does it do the creature?
Wut? What good does what to do the creature?
I’m just having a problem making sense of this idea that increase where the selected changes are NOT happening 1) really happens...
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.
2) has any effect on evolution, since the evolution is occurring where the change is occurring
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.
I also have a question about the idea that there are other loci that aren’t involved in the breed or species anyway.
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.
The idea that genetic diversity goes on increasing in some hidden part of the genome...
No, that's not what I'm claiming. Whoever said anything about some hidden part of the genome? That's very disingenuous.
...is intended of course to offset my claim that breeding or speciation has to involve loss of genetic diversity. What are you imagining then? That after you get your breed or species that hidden diversity will now come into play toward toward what?
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.
What does altering the reproductive capability of the animal have to do with mutations arising in genes for the selected characteristics of the breed? I don’t get exactly what you think is relatively easily dismissed by this information but it doesn’t relate to anything in my argument. If these mutations are occurring as regularly as you say (I note that you vaguely give them a certain probability of spreading in the population, which would of course be the important thing to know), what’s to keep them from affecting those selected genes?
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?
But in any case I always have the doubt that mutations can be a good thing anyway.
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.
If they are occurring as frequently as you claim what’s the benefit to the animal?
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.
al? In any case none of this addresses what I said about their undesirability from the point of view of maintaining the characteristics of a breed after it’s been established.
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.
Also, there’s certainly no reason mutations should choose to occur only in other genes than the selected ones...
I didn't say anything like that.
...but also why do you want all that diversity in areas that have nothing to do with the basic structure and appearance of the animal anyway?
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.
How would that benefit evolution? I mean doesn’t evolution select for the basic structure and appearance?
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?
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.
First, this is not an answer to my statement about the effect of continuing to get mutations after a breed is established. Breeding for a trait that originated in a mutation doesn’t change my claim that the processes of breeding, based in this case on selection of this trait, require the loss of genetic diversity.
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?
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.
Once you have your trait selected then breeding follows the processes I’ve been outlining, that lead to reduced genetic diversity. It's AFTER all this that mutations would mess up the breed.
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.

This message is a reply to:
 Message 16 by Faith, posted 06-01-2016 8:04 AM Faith has replied

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Genomicus
Member (Idle past 1941 days)
Posts: 852
Joined: 02-15-2012


(1)
Message 27 of 30 (785558)
06-07-2016 6:44 AM
Reply to: Message 18 by Faith
06-01-2016 3:56 PM


On the Evidence from Human Genomics: The Case of Sardinia
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.
Sometimes simple historical facts make all that research questionable, as in the following discussion. In this case my suspicions were vindicated beyond even my own hopes.
You’ve said this about no gene flow more than once but all I had to do was look up Sardinia in Wikipedia and found lots of opportunities for gene flow:
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:

  1. First, there is the aforementioned evidence from nuclear DNA polymorphisms and mtDNA sequence data (Di Rienzo, 1993), which indicates no gene flow to these genomic regions.
  2. From "The inter-regional distribution of HLA class II haplotypes indicates the suitability of the Sardinian population for case—control association studies in complex diseases," Lampis et al., 2000:
    "We analysed the distribution of HLA DRB1-DQA1-DQB1 haplotypes in seven different regions of Sardinia and found that the most frequent haplotypes are uniformly distributed in the island but at frequencies unique to this population.
    The lack of significant large-scale genetic heterogeneity between the coastal regions, repeatedly invaded by outside populations, and the most internal and isolated part of the island, which was unaffected by these occupations, suggests that there has been little genetic flow from the invading populations over the last 3000 years. The high demographic ratio between the native people and the invaders may explain these findings. Sardinia was indeed densely populated (at least 300 000 inhabitants, 3500 years ago) before the arrival of any conquerors in the island."
  3. Moral et al. (1994) analyzed the genetic distance between inhabitants of Alghero and other Sardinians, and the distance between the Alghero population and Catalonians. Recall that:
    "Following the Aragonese conquest of the Sardinian territories belonging to Pisa, which took place between 1323 and 1326, and then the long conflict between the Aragonese Kingdom and the Giudicato of Arborea (1353—1420), the newborn Kingdom of Sardinia became one of the states of the Crown of Aragon. The Aragonese repopulated the cities of Castel di Castro and Alghero with Iberian colonists, mainly Catalans."
    Yet the genetic distance between Alghero inhabitants and other Sardinians is "much closer genetically to Sardinians than to Catalonians," based on Moral et al.'s analysis of 61 alleles. This, again, demonstrates that -- if anything -- there has been gene flow from the native Sardinian population to the migrant population, and certainly not vice versa.
  4. Contu et al. (2008) investigated Y-chromosome sequences from coastal and interior regions of Sardinia. Importantly, the researchers discovered that "sub-populations from the Sardinian coastal regions (the Campidano and Gallura areas), which suffered cultural and political dominations over many years do not significantly differ from the most internal and isolated part of the island (Barbagia area), which was never under foreign control. This is in agreement with other studies that analysed different chromosomes and independent samples."
    Based on the above results, as well as a Bayesian analysis of a unique Sardinian haplogroup, the authors state that: "These results suggest a largely pre-Neolithic settlement of the island with little subsequent gene flow from outside populations."

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.
But how very very odd that the Wikipedia article would give a history in which there couldn’t possibly have been a lack of gene flow.
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?

This message is a reply to:
 Message 18 by Faith, posted 06-01-2016 3:56 PM Faith has replied

Replies to this message:
 Message 30 by Faith, posted 06-07-2016 8:20 AM Genomicus has not replied

  
Genomicus
Member (Idle past 1941 days)
Posts: 852
Joined: 02-15-2012


Message 28 of 30 (785559)
06-07-2016 7:00 AM
Reply to: Message 18 by Faith
06-01-2016 3:56 PM


On the Evidence from Elephant Seal mtDNA
When you start quoting from the scientific literature about these things I do expect to be swamped and unable to answer, but oddly enough in the case of Sardinia and the elephant seals it didn’t take much research on my part to bolster my own argument. I don’t know why this is so, how the Sardinian study could have been so wrong on such a basic point; and as for the elephant seals, well, all I know is that a fairly recent Scientific American article doesn’t know about any recovery of genetic diversity:
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 what were the results (from Table 1 of Weber et al., 2000)?
Haplotype Diversity, Elephant Seal Population DNA from 1892: 0.00
Haplotype Diversity, Elephant Seal Population DNA from 1980: 0.53
Nucleotide Diversity, Elephant Seal Population DNA from 1892: 0.0000
Nucleotide Diversity, Elephant Seal Population DNA from 1980: 0.0086
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?
Edited by Genomicus, : No reason given.
Edited by Genomicus, : No reason given.

This message is a reply to:
 Message 18 by Faith, posted 06-01-2016 3:56 PM Faith has replied

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