The Great Debate: Molecular Population Genetics and Diversity in Evolution

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.

I suppose it’s proper debate form, but it is odd to be on a two-person debate thread with someone who is addressing the audience instead of me.

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 Gen writes: 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? Faith writes: 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.

Remarkable how personal this highlighting isn’t getting.

“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. Understandably (?) the Establishment may have hurt feelings over it, but if we can’t reinterpret the facts to demonstrate our different point of view there is simply no debate. I try to be clear how I arrive at my different views so it shouldn’t be hard for you to follow the argument.

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...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.

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. Do you mean those that underlie the most salient characteristics of the breed perhaps? But ALL alleles are “directly involved with reproduction” not any select collection, that’s why I can’t be sure what you mean. The genome as a whole reproduces, not some select batch of genes/alleles.

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. I’m sorry, none of this is making sense.

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. This is a simple logical point, it shouldn’t need special evidence. The same situation should exist in the wild wherever the changes are brought about by a population split creating a smaller daughter population. Just as a matter of probability, some alleles even at the most diverse loci are going to be left behind even if the locus doesn’t become homozygous.

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).

So shall I guess that you are English-challenged to the extent that the word “moth” Is beyond your vocabulary?

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.

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.

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. Breeds and species involve changes in the whole genome, simply because it’s the whole genome that reproduces, or the entire individual animal. 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. Mutation of course can’t be counted on to make specific changes on demand, and isolating a small population can’t help but reduce the diversity of the entire genome because there are fewer individuals contributing their alleles to the new population. Besides, my argument is that it’s where the traits of the new population are different that the genetic diversity is reduced, meaning to get those changes requires the reduction (but actually there may be unselected traits where this also happens). 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?

But none of this is very clear to me, perhaps I’m missing something, so you can explain.

This alone is enough to render your argument egregiously flawed, but I will press on.

You do seem to be rather prone to wishful thinking. Nothing personal implied of course.

But although I’ve worked some on the rest of this post I think I’ll stop here for now because it’s not really making sense to me up to this point. I don’t know why you think the moth example proves anything and I don’t know how you think you could get change in only two genes, or in any portion of the genome without affecting the whole in some way.

So I’m sure I’ll come back with the rest of this eventually.

Edited by Faith, : No reason given.

Edited by Faith, : No reason given.

Edited by Faith, : No reason given.

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.

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. And at what point does that supposed increase in diversity offset the loss in the selected/evolving part of the genome? And what good does it do the creature?

In any case my basic principle seems to be confirmed by all this, in that loss is to be expected where new phenotypes are emerging. I’m just having a problem making sense of this idea that increase where the selected changes are NOT happening 1) really happens, and 2) has any effect on evolution, since the evolution is occurring where the change is occurring. And yes, if you start getting an increase THERE then you’ll lose the breed, or species.

I also have a question about the idea that there are “other” loci that aren’t involved in the breed or species anyway. Seems to me it takes the entire genome to make the entire animal. Even if some of it relates to internal systems that don’t show up in the selected traits that make for outward appearance, even that part of the genome can certainly determine the overall character of the creature. Could affect personality of an animal perhaps, which is important in breeds.

The idea that genetic diversity goes on increasing in some hidden part of the genome 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?

Any form of selection of a particular phenotype or set of phenotypes must of necessity select the whole genome. It isn’t possible for part of the genome to be selected because it’s the whole individual that is selected. And if the whole genome is selected how is any part of it going to avoid being subject to changed gene frequencies brought about by the selection? That is, just as with the particularly selected phenotypes any that are now more high frequency than they were in the original population.

Sorry I know I just keep going on and on about this because it isn’t making any sense to me.

You have to demonstrate the truth of this above statement on mutations and the so-called clear-cut-ness of species. So demonstrate it.

Again it’s hard to imagine that mutations would occur to enough of an extent where the salient characteristics of the breed or species are not involved to make any kind of difference to the animal or to evolution or to anything, especially given that most mutations are up to no good as it were.

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."

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? But in any case I always have the doubt that mutations can be a good thing anyway. If they are occurring as frequently as you claim what’s the benefit to the animal? 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. Also, there’s certainly no reason mutations should choose to occur only in other genes than the selected ones, 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? How would that benefit evolution? I mean doesn’t evolution select for the basic structure and appearance? Isn’t that the whole point? I don’t get the thinking here at all.

Sorry again. I’d edit all this if I had a better grasp of the problem but it just keeps bugging me and making no sense.

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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.

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. Why even mention this example really? It has nothing to do with this debate. (And I did read through the paper and end up thinking it might have been best for this trait not to have been selected anyway, as it doesn’t seem to be a good thing for the animal (and, apropos of nothing, lean beef was an undesirable fad anyway).

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.

Yeah but again, selecting a mutation for breeding is not what I was talking about. You are changing the subject. 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. You keep addressing an entirely different situation that doesn't affect my argument.

So your argument really doesn't make any sense at all.

Well, your version of it doesn’t make much sense.

This is just going on and on so again I’m going to stop and resume later.

Edited by Faith, : No reason given.

Edited by Faith, : No reason given.

So far you haven’t even addressed my argument, although you keep claiming to have refuted it. I thought debating with you might be a welcome relief from the usual debate here, some idea that besides being very knowledgeable about genetics, you really could follow my argument as others here don’t despite their constant declarations that they do; but you keep getting it wrong too. And it looks like you’ll be going on in the same vein for a while yet, then maybe get to something more relevant toward the end. I guess I’ll just continue where I left off.

...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.

Thanks for the gene flow acknowledgement. But mutations do the same thing, increasing genetic diversity, even where you don’t want it, just as gene flow does, where it will interfere with the formation of the new species. But are you actually saying that mutation is THE reason for reproductive barriers to arise? Is that official wisdom or your own claim? First there can be behavioral reasons for the cessation of interbreeding with former populations, but my argument has been that it’s most likely that after a chain of population splits which keep reducing genetic diversity while bringing out new phenotypes, the last population in the series is likely to be genetically depleted enough just from that situation alone, for breeding to become impossible, certainly after some generations of inbreeding within the isolated population itself, mixing the new gene frequencies, losing some alleles etc. – mutations wouldn’t be needed to bring interbreeding to an end. That they would do that is of course no doubt true.

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.

Again, how can only a few loci lose diversity when the formation of the new population itself brings about the new gene frequencies that lead to the loss of diversity, and the new numbers must of necessity affect the entire genome as they affect the entire individual? And again, what does “reproductive system related phenotypes” mean? What is a NON-reproductive system related phenotype anyway?

As I’ve been trying to deal with this idea about all those “other” loci that can gain genetic diversity from mutations without affecting the breed or species, again I don’t see why mutations would make a distinction between loci, preferring to wreak havoc upon affect only those “other” loci, but also I don’t see what good it would do the breed/species OR evolution, because selection, even random selection, works on the salient characteristics of the creature. We’ve got the cheetah because its salient traits are all homozygous/fixed in the population. If THOSE traits varied we’d start getting a different kind of cat. But if all those “other” loci vary what good does it do the cheetah, OR the ToE? Zip, nada, that I can see. Does it even happen? I don’t know, you say it does and that’s about the sum of it.

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.

Are you really going to compare viruses to mice and cattle and human beings and so on? The rapid rate of viral evolution can make mice, cattle and human beings pretty sick, but as for being a model for their adaptation or evolution, no way. I can hardly believe you said this.

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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.

I’ve discussed this to death above so I think I’ll just go on to the next subject.

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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.

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.

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).

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:’

Wikipedia writes: … during the Roman rule there was a considerable immigration into the island from the Italian peninsula; ancient sources mention several peoples of likely Italic origin living in Sardinia, like the Patulcenses Campani (from Campania), the Falisci (from southern Etruria), the Buduntini (from Apulia) and the Siculenses (from Sicily). Roman colonies were also established in Porto Torres (Turris Libisonis) and Usellus.[25] Strabo gave a brief summary about the After the fall of the Western Roman Empire, Sardinia was ruled in rapid succession by the Vandals, the Byzantines, the Ostrogoths[26] and again by the Byzantines. During the Middle Ages , the island was divided into four independent Kingdoms (Sardinian: Judicados; Italian: Giudicati); all of them, with the exception of that of Arborea, fell under the influence of the Genoese and Pisan maritime republics, as well as some noble families of the two cities, like the Doria and the Della Gherardesca. The Doria founded the cities of Alghero and Castelgenovese (today Castelsardo), while the Pisans founded Castel di Castro (today Cagliari); the famous count Ugolino della Gherardesca, quoted by Dante Alighieri in his Divine Comedy, favored the birth of the mining town of Villa di Chiesa (today Iglesias), which became an Italian medieval commune along with Sassari and Castel di Castro. 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.[27][28] A local dialect of Catalan is still spoken by a minority of people in the city of Alghero. Also groups of Gitanos, named locally Zinganos, migrated to Sardinia from Spain starting from the 15th century.[29] In the 16th and 17th centuries, the main Sardinian cities of Cagliari (the capital of the Kingdom), Alghero and Sassari appear well placed in the trades of the time. The cosmopolitan composition of its people provides evidence of it: the population was not only indigenous, but also hailing from Spain, Liguria, France and Corsica in particular.[30][31][32] Especially in Sassari and across the strip of territory that goes from Anglona to Gallura, the Corsicans became the majority of the population at least since the 15th century.[32] This migration from the neighboring island, which is likely to have led to the birth of the Tuscan-sounding Sassarese and Gallurese dialects,[32] went on continuously until the 19th century. The Spanish era ended in 1713, when the whole island was ceded to the Austrian House of Habsburg, followed with another cession in 1718 to the Dukes of Savoy, who assumed the title of "Kings of Sardinia". During this period, Ligurian colonists, escaped from Tabarka, settled on the little islands of San Pietro and Sant'Antioco (at Carloforte and Calasetta), in the south-west area of Sardinia, bringing with them a Gallo-Italic dialect called "Tabarchino", still widely spoken there. Then, the Piedmontese Kingdom of Sardinia annexed the whole Italian peninsula and Sicily in 1861 after the Risorgimento, becoming the Kingdom of Italy.

Can’t imagine why your sources would have left all this out. It’s quite a lot of gene flow for a place that supposedly had none.

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.

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. All those invasions and conquests certainly mingled many different peoples, which of course would explain any growth in genetic diversity. The various proofs you cite from that article of genetic continuity, isolation and so on, need some kind of explanation given the historical record of so much genetic mixture. I don’t have an explanation myself. I would certainly hesitate to find such a study at fault on such a crucial factual issue, but something is out of whack here that utterly destroys the point you were trying to make.

So how does your notion explain the above experimental results, Faith?

Well, I can only refer you to the above contrary information that suggests the claim of lack of gene flow is inexplicably wrong.

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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?

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:

Northern Elephant Seals: Increasing Population, Decreasing Biodiversity Scientific American, May 24, 2013

Handy, Sci Am writes: Amongst Northern elephant seals, genetic drift is a concern since each of the 127,000 individuals is descended from same 20-100 seals. The successful repopulation of the elephant seal is misleading because, although they recovered from the brink of extinction, the genetic diversity loss that occurred is detrimental to the health of the species in the future. Currently, the future of Northern elephant seals is uncertain and researchers lack the ability to determine what will happen to the population in the face of environmental stresses such as pollution, disease, or coastal development.

Yes, it’s not a breed or a species but the result of an unfortunate bottleneck, but I’d argue that a bottleneck is really just an extreme version of what happens in a breed or the formation of a new species in the wild, and in fact it really IS what breeding used to do anyway.

Have things changed in the last three years to the extent that you can now declare not only population recovery but recovery of genetic diversity?

How to explain these discrepancies? I can’t do it, can you?

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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.

It’s a lot of dead DNA, so I take it to represent a lot of dead creatures. It’s the greater part of at least the human genome and many others, So I tend to trace it back to the Flood where a huge bottleneck occurred in many species. Something like this: just as the elephant seals are genetically depleted because the large original genetic diversity of the population was wiped out, leaving the remaining individuals deprived of all those alleles, the same would have happened to all the species on the ark. All those other alleles would have died. They simply no longer existed for the remaining individuals. I think that over time after the Flood this lack started showing up here and there as gene loci without any viable alleles, or dead genes, since such a huge number would have simply died in the Flood. Mutation probably played a big part in killing off whatever alleles were present on the ark. I haven’t worked out the details. It’s an effect I figure increased over time, reflecting not only the Flood bottleneck but all death ever, eventually accounting for almost as much dead DNA as there have been dead creatures.

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.

I did think you must have scored some points this time, but weirdly it turns out not to have been the case.

Edited by Faith, : No reason given.

Edited by Faith, : No reason given.

Edited by Faith, : No reason given.

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.

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?

"Forcing???!!!" I should be able to make the clear obvious recognizable distinction between the processes that add genetic material and the processes that subtract it and call the latter "evolution" or "active evolution" because it's a real distinction, and it's not totally something new since periods of population stasis are said by YOUR team to be "NOT evolving." There can't possibly be anything wrong with using the term as I do as long as I'm clear. And it fits with the whole history of evolution too, since it's selection that is particularly associated with evolution since Darwin.

I'm sure someone could write a book using the terms as I do and get away with it.

I refuse to give it up. There are no alternatives that would convey what I want to convey. Sorry. Complain all you want. You're wrong.

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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?

It matters not one whit to me how much of the genome "MUST" change to bring about reproductive barriers and I really don't get why you are making so much of this. What I'm looking at is the changes that must occur throughout the genome due to new gene frequencies -- whatever parts are capable of change, and I'm aware there are some regions that aren't -- and I don't care if they produce reproductive barriers or not, or how many of them might be involved in that condition -- the point is that they lead to reduced genetic diversity overall.

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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.

1) And fixed alleles are somehow immune from mutation? Why is that, pray tell?

2) Certainly more than two alleles are going to be involved in the formation of any new species, in fact quite a large number I would think, taking breeds as the usual reference: not just features such as fur color and texture but color markings and facial features and personality traits and general body stature including size, bones, musculature, the works, many of which traits are governed by more than one gene. So confining the mutations to OTHER parts of the genome seems to be asking a lot of the laws of probability.

3) Not to mention that evolution is usually described as going from species to species and the traits I've mentioned above are always going to be the salient characteristics of any species, so how does it further the ToE to get so many changes in the other part of the genome that can't produce a new species anyway? Are you following me? Of course I don't think such changes occur at anything like the rate you claim, certainly not nondestructive changes, and that can only be the reason why you might expect not to get them at the loci that represent the species. But this is just a secondary point.

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.

I've given reasons galore already, in former posts and in this series of posts, why mutations in the "other" part of the genome accomplish absolutely zip for the organism or for the ToE, the main problem being that if they don't change the species characteristics, which is of course your whole argument, then they can't possibly be the foundation for further evolution. And besides, all you have done is ASSERT that all these mutations occur, you haven't proved it. You've shown that one mutation can be the trait chosen for breeding, but not that mutations add to a breed or species once established. I guess that's what you intended to do with Sardinia and the elephant seal but somehow you didn't pull it off.

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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.

OK, which particular two?

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.

1) You haven't proved this happens

2) How does mutation choose to change only some loci and not others?

3) Even if it did happen, managing not to affect the salient characteristics of the breed or species, it doesn't change the fact that to get that breed or species required the loss of genetic diversity for those evolving new traits. THAT is where the changes are occurring, the new phenotypes and the loss of diversity. Of course it MUST occur throughout the genome anyway just because reduced numbers has to bring about a change in gene frequencies wherever in the genome this can happen, and that in turn has to bring about the loss of genetic diversity I'm talking about. Etc etc etc

4) It also fails to add diversity where the ToE would need it if further evolution beyond any species really were possible -- in those traits that most clearly characterize the breed or species. That is, net diversity that leaves the new species intact doesn't help the ToE at all. Blurring the species with mutations destroys evolution, and so does leaving the species intact, with or without increased diversity. But of course overall decreased genetic diversity is what brings evolution to a natural stopping point.

5) Since apparently Sardinia had lots of gene flow over the centuries although your referenced study said it didn't, and the elephant seals are also still considered to be genetically depleted despite their great increase in population, although your study there said their genetic diversity had increased, I'm beginning to wonder how good all those supposed markers of genetic diversity in those studies really are. Microsatellite information for instance. Mitochondrial information for instance. What do you really learn from those things about the organism's overall genetic diversity?
Etc
etc
etc

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(Great Debate)

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.

I'm wondering more and more just how good this "evidence" is that mutation is a major diversifying force. I mean there is something wrong with your evidence in relation to Sardinia and the elephant seal, and there is also something wrong with the study Tangle came up with for mutation as the cause of the change from the light to the dark peppered moths. I presented my objections to that on his thread but will repeat them here because I'd really like your response to this:

Tangle writes: The peppered moth's evolution from white to black and back to white again is pure observation. That's how we know about it - it is documented. The mechanism that allows the selective survival of black moths over white moths has been observed - the darkening of the trees on which the moths rest during the day leaving them open to predation against the newly black trunks. The predation process was reversed when the trees were no longer black. Observed and documented. [Faith] That much is common knowledge, and quite easily explained in terms of a built-in allele for the black moth. Mutation is in fact harder to explain. See my post to jar above. There is something very very weird about the idea that it was a mutation instead of built-in for the reasons I give there. You either need many same or similar mutations at the same locus to counteract the constant loss to predation, which doesn't fit with the general observations of mutations as random accidents of replication, or you have to count on one mutation surviving against ridiculous odds, or showing up so exactly at the right time that only a teleological mechanism could explain it. Not what the ToE normally has in mind. There has to be something wrong with the science that supposedly "observed" this mutation.

Also seems to be the case with many other studies that find mutations to be the cause of genetic changes.

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Just so you know, I am still working on your post although also being distracted. I hope it's not a problem breaking it up into small bites; it seems to help me get my responses organized. But I'm working on a bigger bite next time. I'll post it in this box.

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?

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?

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I'm sorry to inform you that this is not exactly "A Scientific Debate" as I am not a scientist and not required to be one to debate at EvC. Scientific American ought to be an acceptable reference, and whether you accept it or not I'm considering it so for purposes of this discussion.

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.

Nobody has explained to me what either haplotype or nucleotide diversity has to do with anything, what it actually is, why I should regard it as more important than the usual measures of genetic diversity. But I think I get some idea from this post.

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.

So what I'm getting is that you get a lot of mutations at these locations. I understood that to be the case for MtDNA, which is the "haplotype" DNA, but the import of that wasn't apparent at the time. The fact that you get these mutations at this location you call an increase in genetic diversity, which technically of course it is I suppose, but I have no idea why it should be taken as any kind of measure of the genetic condition or general health of the seal population. What does this DNA do anyway? It seems to do nothing more than accumulate mutations. Does it do anything else in the organism? I can see why accumulating mutations so frequently could make cytochrome C a good marker of species since each would get its own mutations, and cytC has something to do with MtDNA, sorry I forget exactly what and I don't want to abandon my post to go find out.

Perhaps you will explain if that haplotype DNA actually DOES something. Because if it doesn't, if it does nothing but accumulate mutations, I don't see what it has to do with any kind of genetic diversity that would benefit the elephant seal.

The kind of genetic diversity that is needed is the kind that makes traits, phenotypes, changes in the animal itself that can benefit it by giving it options for variation, without which it remains in danger of extinction. THAT kind of genetic diversity is measured by heterozygosity: the more homozygosity the more endangered the animal, which is the problem for the cheetah as well as the elephant seal. Homoygosity at the loci that most characterize the animal used to be the criterion for a purebred until it became known that it put the animal at risk of genetic diseases. All this goes on in the genome where genes make phenotypes. What does MtDNA do?

I don't have a clear idea about nucleotide diversity except that it implies a change in the sequence of a gene, which would of course be the result of mutation. Mutations aren't very often a good thing so I don't see how this "increase in genetic diversity" bodes any good for the seal anyway. Since nothing is said about how it relates to the measure of heterozygosity I've always taken as the indicator of true genetic diversity, I'm going to assume that these mutations are generally bad for the seals and it's just a bit of word magic to call them an increase in genetic diversity as if they solved the poor creature's plight of genetic depletion. This of course means I'm saying some unkind things about scientists which I'm sure you'll take with your usual indignation, but really you should just take it as a reason to explain why I should regard this evidence as answering my argument that normal evolutionary processes lead to decreased genetic diversity.

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.

Yes you would have to be right about this. But nothing in these studies shows that either of these sources of increased genetic diversity is REAL increased genetic diversity that gives the genetically impoverished elephant seal any more genuine opportunities for further variation than it had before. I believe that Scientific American blog you so haughtily dismiss as unworthy of your scientific consideration is right: the elephant seal remains genetically endangered even with all this bogus increase in genetic diversity. Now, an increase in viable heterozygosity -- THAT would be SOMETHING.

Edited by Faith, : No reason given.

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?

After answering the post about the seals maybe I just got an influx of cynicism but it hit me that what's being measured in both these studies has nothing whatever to do with REAL genetic diversity. MtDNA has nothing to do with anything related to normal evolution of traits so its accumulating mutations is just the usual accumulation of garbage, which is what most mutations are, nothing that could possibly contribute to the health of any organism or human being.

It's kind of like the logic of someone needing to measure the dimensions of a whole apartment who decides just to measure the broom closet because it's easier and it also is measurable in feet and inches just like the whole apartment so it should suffice as a measure of the apartment. Of course it's absurd but that's how it hits me. MtDNA has nothing to do with the evolution of traits that I've been talking about so how can it have anything to do with increasing the diversity that is lost through that process?

So you've got increased MTDNA diversity, which is nothing but a bunch of meaningless mutations absolutely unrelated to the genetic diversity that is lost in the evolutionary scenarios I've been describing. I realize this is too absurd to be true but I have no other way of making sense of this.

So this is your next project: proving me wrong about this.

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