Can Genetic Loss Increase Diversity?

In the previous A barrier to macroevolution & objections to it there was a lot of discussion going on about how mutation might make up for the loss of alleles due to speciation. Both myself and Parasomnium brought up some objections: Faith's most recent reply was the following. Emphasis mine.I feel the response given by Faith was wholly unsatisfactory as the underlined section needs to be established. If it is not a "given" that allelic loss does cause speciation then why is it necessary to show that mutation MUST make up for allelic loss?Faith and MJ identified a potential "barrier" to macroevolution by saying that mutation was insufficient to account for the increase in alleles necessary for significant novelty during series of speciation events that REDUCE the frequency of alleles in the population. This is FOUNDED on the idea that speciation is accomplished by allelic loss. That this CAN EVEN HAPPEN must be established before one can even examine that mutation needs to make up for anything.It is my understanding that mutation in and of itself is NECESSARY for speciation even of the "microevolution" type that creationists identify as "change within a kind".I don't want this to be too much of a continuation of the last topic. I want this thread to focus on if speciation CAN occur in the normal sense without the presence of mutation. Also, are there any documented instances of speciation that have occurred without mutation?I would ask Faith and MJ, without this verification, how can you continue to hold such a requirement to overcome your "barrier" without this concept as a base mechanism of speciation?

---

Of course, biblical creationists are committed to belief in God's written Word, the Bible, which forbids bearing false witness; --AIG (lest they forget)

Thread moved here from the Proposed New Topics forum.

anyone else willing to take up the torch or any knowledgable bio folk who can speak to the concepts and questions outlined in the OP.

---

Of course, biblical creationists are committed to belief in God's written Word, the Bible, which forbids bearing false witness; --AIG (lest they forget)

At the demise of that thread, I was afraid my question to Faith would remain unanswered, so I am happy to see it mentioned here in your topic, Jazzns. Thanks for that.I think your topic cuts right to the heart of one of the most stubborn misunderstandings of genetics among creationists: the idea that mutations only lead to the degradation of an originally perfect genome.Apart from answering the question of your topic, I think it should also - and maybe even first - be established whether this idea of genetic loss is valid at all.

---

"Ignorance more frequently begets confidence than does knowledge: it is those who know little, not those who know much, who so positively assert that this or that problem will never be solved by science." - Charles Darwin.

The only example of reproductive isolation that is not dependent, fundamentally, upon differences between alleles present in divergent subpopulations of a single species, is the case of wolbachia infection in arthropods.Wolbachia is a bacterium that infects arthropods such as insects, spiders, isopods, etc. The infection has a variety of interesting effects on its carriers (including such things as biasing the sex ratio of offspring, transforming individuals into hermaphrodites, and other strange things varying from species to species) but as far as speciation is concerned there are two common effects of wolbachia infection that are of interest.First, an infected male is unable to fertilize an uninfected female. Second, if both male and female are infected, they must be infected with the same strain of the bacterium if fertilization is to be successful. Imagine a single species of insect, with two neighboring population A and B. If A gets infected and B does not, the result will be severely diminished gene flow between the two populations, because while males of population B can mate with members of either population, males of population A can only mate with members of their own population. The exact amount of gene flow reduction will depend upon patterns of migration between the two populations. Now if population B gets infected with a different strain of wolbachia, reproductive isolation will be complete, and in the long term speciation could follow.The exact mechanism whereby wolbachia effects these changes to mating success are currently unknown. We know that the bacterium does not cause direct changes to the DNA of its host because the effects can be removed by treatment with antibiotics. An overview of some possible mechanisms can be found at this articleThe bacterium has been demonstrated to be the sole source of reproductive isolation between two species of parasitic wasp, Nasonia giraulti and Nasonia longicornis (see this article). So it does really happen in nature.As far as I know, cytoplasmic incompatibility caused by wolbachia is the only known source of reproductive isolation that does not depend on mutations to the species' genome itself. Whether it qualifies as "speciation without mutation" is a different matter. Obviously the phenomenon requires different strains of wolbachia to exist if it is to generate complete reproductive isolation, and these different strains could only arise through mutation of wolbachia. So you might get speciation in an insect, driven by mutation of its wolbachia parasite rather than by mutation of the insect itself. Mutation is still at the bottom of it all.Hope this is of interestMick

I can't take much time here because of the condition of my computer. It will freeze up if I read too much or write too much.The point was that I've been ARGUING for the reduction in genetic diversity as the reason it's not "taken for granted." But it gets to a point where everybody tries to prove that mutation makes up for it, and during THAT part of the discussion it's AS IF it's taken for granted because everybody is trying to answer it.I've shown in thread after thread that all the selecting processes, which include natural selection, migration, bottleneck, random selection, gene drift etc. do over time tend to bring about a reduction in genetic diversity. ALL OF THEM. I also gave links to breeder and conservationist discussions that confirm this. Mutation is the only thing that works in teh opposite idrection. That is in fact what evolutionists do assume and it's good to get it stated. That is why we are always encountering this AS AN ASSUMPTION, with apparently no need felt to provide evidence for it. You get for instance a discussion of novel alleles appearing in a ring species and this all by itself is taken to be caused by mutation -- it is simply assumed. It is assumed because the ToE requires it. The problem is that mutation is so taken for granted that nobody is studying this in a way that could demonstrate it one way or the other.I'm not going to write more for fear of my computer freezing up.Edited by Faith, : No reason given.

Already had a freeze up trying to answer this. Could happen again. Can't make Word work with it either for some reason. Anyway. You aren't getting the picture here. Reduced genetic diversity refers to reduced numbers of alleles in a new usually smaller population, whether it's gene drift that selects a few and leaves others within a population, or a geographic split in which some lose contact with the original population and so on.Sometimes there is no actual loss, merely a change in frequency of the number of various alleles. Either way you get new combinations of alleles and new traits will eventually emerge from these. Over time, many splits, especially bottleneck, a very severe reduction, you can get to the point of speciation, as happens in ring species. Quetzal's example of the Ensatina is a good one. It assumes mutation brings about the new traits, but the existing alleles in the original population are explanation enough.You do NOT get uniformity, you get change at the phenotype or population level.Think dog breeding. The more you reduce the population, even down to a few founder dogs, the more alleles you eliminate, which allows the alleles you favor to be expressed in the breed. Over time you select for the traits you want, and in this process you are eliminating the genetic material for the traits you don't want. This is how you get new breeds, and ultimately species. I hope my explanation above is clear. It does not produce uniformity, it reshuffles the alleles, changes the frequencies, which is the definition of evolution after all. "Evolution is a change in the frequency of alleles in a population" isn't that how it goes? There may not be loss every time, although a severe split may very wwell cause loss, but over time, many splits, etc. there will certainly be a trend to loss of alleles and therefore a reduction in genetic diversity. I've explained it at endless endless length on many threads by now and have just explained it again above. I hope it gets across.Edited by Faith, : No reason given.Edited by Faith, : No reason given.

Start a thread on it and let some of the whizz's here sort you out. It might be fairly simple.

That sounds like a testable hypothesis to me!Here is some data on the level of microsatellite heterozygosity in 20 dog breeds. First comes the name of the dog breed, followed by the heterozygosity. The data is from an analysis of 100 microsatellites in this article. Now, according to your theory, these breeds have undergone strong selection and multiple severe bottlenecks, therefore should exhibit considerably lower heterozygosity than wild canids such as wolves or foxes which have never been domesticated and have never been subject to human breeding programs in order to generate novel breeds.Studies of wild canids do NOT find higher levels of heterozygosity. Here is a summary of a few different articles (each species has a number of measured heterozygosity values, each one from a different location in the world):Gray Wolf: 0.421, 0.536, 0.605, 0.532, 0.593, 0.533, 0.547
Coyote: 0.540, 0.554, 0.653, 0.649, 0.596, 0.502
Red Wolf (captive): 0.507
Golden jackal: 0.412
Red fox: 0.7, 0.68, 0.72, 0.63, 0.56 reference 1reference 2So, your prediction fails. Your understanding of the population genetic consequences of bottlenecks and selective breeding is incorrect.Mickin edit: In order to preempt the complaint that these are microsatellite heterozygosity measures rather than allele counts, I would like to point out that allele diversity is correlated with heterozygosity, populations with high allele diversity tending to be more heterozygous.Edited by mick, : No reason given.

This is exactly what I am claiming has not been established. There has been no connection or valid argument to suggest that NEW TRAITS can arise from recombination alone.WHat you are doing in your "assume no mutation" scenario is restricting the traits for a specific loci to fewer and fewer options. This has not been established as being possible by recombination alone. Even in the case of selective breeding, you cannot uncatagorically state that the resulting allele frequencies and list of traits are brought about by recombination and loss alone.The evidence we have for mutations is that many of them can happen repeatidly in a population at the same location in the DNA. The is no guarantee that a particular trait is a byproduct of a new combination. It could very well be a common mutation. Selection then, even artificial selection, if selecting against that trait would then be selecting against a mutation and not a pre-existing allelic combination.For your barrier to work, you need to demonstrate that speciation can occur with recombination alone. This so far has been only assumed with "NO EVIDENCE" as you like to put it.

---

Of course, biblical creationists are committed to belief in God's written Word, the Bible, which forbids bearing false witness; --AIG (lest they forget)

I have a number of years of tech support experience. I am also a computer hardware enthusiast. If you would like to describe your problems I may be able to suggest a course of corrective action.Despite our disagreements, I would hate to have your participation limited to to technical problems.

---

Of course, biblical creationists are committed to belief in God's written Word, the Bible, which forbids bearing false witness; --AIG (lest they forget)

That is absolutly facinating. I am curious to how the bacteria creates the compatability/incompatability.Unfortunatly for faith though this is also not a case where allele recombination caused a speciation event.Edited by Jazzns, : No reason given.

---

Of course, biblical creationists are committed to belief in God's written Word, the Bible, which forbids bearing false witness; --AIG (lest they forget)

Oh my! That Brittany Spaniel is goin' to hell for sure!Yet more evidence that Brittany Spears is of the devil.(but all joking aside - thank's Mick for some actual data, and quite relevant too.)Edited by Equinox, : added thank you for Mick

Great OP, Jazz.However, I have been mulling over Faith's (and to a much lesser extent MJ's) arguments in the previous two threads, and would like to start out with an observation.I'm not sure you've captured Faith's entire argument. Admittedly, she occasionally has some difficulty in getting across what she means. However, although it appears superficially that she and MJ are reading from the same sheet of music - and in fact she mentioned something along those lines herself at one point - there are quite substantial (albeit subtle) differences between their formulations.Faith has not argued consistently that loss of alleles leads to speciation - i.e., is a causal factor. I think she may have stumbled across that line once or twice, but the overall trend has been her claim that loss of alleles is an inevitable result of speciation. Leaving aside for the moment the mutation argument (which you have said doesn't really apply in this thread), her formulation is only wrong in her insistance on the "inevitable" part. In other words, there IS a mode of speciation that automatically results in could be considered "loss" of alleles, but in most other cases this is not the "inevitable", immediate result.Another subtle point on which she is partially correct, and partially incorrect, is her insistence on the time required for "beneficial" genetic sequences to appear in diverging populations. She seems to be saying that "beneficial" sequences are required for speciation to take place as the ToE suggests, and that there is insufficient time for such "beneficial" sequences to appear to off-set the "loss of diversity" caused by speciation. Both points are interwoven in her formula. Since she insists that only recombination of existing sequences can account for speciation, the ToE is wrong. So, restating her concept:Speciation = loss of alleles + requirement for beneficial sequences + insufficient time => an intrinsic barrier to evolution.My problem in discussing her ideas has been that I have consistently missed the subtlties. Simply dismissing her formulation out of hand as "creationist nonsense" doesn't work, because there are parts that she is actually correct on. It's taken me two whole threads to twig to my mistake. So what I'd like to do is discuss why her formulation doesn't work - and doesn't reflect the reality of speciation. Unless someone really needs them, I will avoid using the technical literature in support, and cover concepts in this thread rather than specific examples, which seem to serve only to take us off on tangents. What's right: What Faith is describing is one of the particular cases of the peak shift mode of speciation known as peripatric speciation - more specifically the subform of peripatric speciation known as the founder effect. In peripatric speciation, a portion of a source population "colonizes" a new habitat, becoming geographically isolated from the source. (Peripatric is derived from the word peripatetic - meaning wandering or traveling about; itinerant - and is very descriptive of what happens). There are any number of reasons why this might occur, from accidental dispersal to intraspecific competition, but in any case the "colony" represents a statistical sampling of the allelic diversity in the source population. If the new population is large enough, the population can contain all of the diversity present in the source. Smaller "bud" populations, on the other hand, may "miss" some rare alleles due simply to what is known as sampling error.The founder effect is an extreme, and rare, example of peripatric speciation. In this case, the “bud” is represented by at most a few organisms and often by a single individual. Obviously, this extreme example represents the ultimate bottleneck - and a statistically very small sample of the available diversity. This is the form of speciation that Faith is generalizing from.What’s wrong: Peripatric speciation doesn’t equate to "loss of alleles" as Faith insists - the alleles are still present in the source, and may be also present in the colony. Nor does the act of colonization automatically lead to speciation, and is in fact a normal dynamic of almost any population with any kind of dispersal ability (for those interested, a general discussion of source-sink dynamics can be found here). Speciation does not occur due to recombination of pre-existing alleles in the new population, especially in the founder case that Faith is insisting on (considering the dearth of alleles to begin with). Only in the specific instance of what Ernst Mayr categorized as “instantaneous speciation” can cytological changes create a new species (for example, by polyploidy or chromosome rearrangement). Even here, we’re talking at least the F1 generation - not the first, parent colony generation - and usually several generations. However, since these types of changes are mostly limited to plants and a very few animals, we can safely ignore them for the purposes of this discussion. I’m also ignoring asexual organisms, so don’t ask.What else is right? Loss of alleles CAN be the result of speciation. In small populations, the “drunkard’s walk” of genetic drift alone can cause the loss of alleles that are not under stabilizing selection. Drift can also increase the frequency of rare alleles. In fact, genetic drift has been postulated as one method for reproductive barriers to arise in a small population separated from the source (i.e., may be a cause of speciation itself). Since drift is essentially random (but see epistatic selection), it can result in loss of alleles. In addition, given enough generations, vicariant selection due to different environmental pressures, and in the absence of heterozygote incompatibility (which occurs in hybrid populations, for instance), alleles can be lost from a population even without them being different species. Ultimately the differences between isolated populations become great enough through this and the other speciation processes that we proclaim them varieties, subspecies, semi-species or true species - one or both populations has lost alleles over the generation to the point that they are incompatible.So what else is wrong? There is no requirement, however, that the “new” population lose the alleles - loss can occur in the ancestral population even if the colony retained all of the original alleles! Peripatric speciation writ large requires that the sampling error in the initial population be accompanied not just by changes in frequency (Faith’s claim), but by changes in frequency that lead to reproductive incompatibility between source and colony. In essence, then, either:1. Drift drags enough alleles over the generations to fixation that epistatic (basically, “linked”) effects at other loci cause incompatibility between the populations;2. Vicariant selection (adaptive divergence) due to the action of natural selection emphasizing or penalizing existing or new alleles does the same.Beyond the sampling error of peripatric speciation and the action of genetic drift, only over extended numbers of generations can loss of alleles be related to speciation. Hopefully this explains what is right - and what isn’t - in Faith’s formula.Making a long story short: whereas speciation may cause loss of alleles, loss of alleles cannot (to my knowledge) cause speciation. Mere changes in the frequency of alleles, except as noted, do NOT drive speciation.I'll save the "beneficial" part for another post if it really is necessary. The short critique is that "beneficial" is not a requirement - merely differences that lead to incompatibility. Indeed, rare deleterious traits can become fixed in a population through drift (as long as the pleiotropic effects are net positive - i.e., hitchhikers).Oh yeah. You may have noticed I didn't bring in MJ's formulation. Primarily because whereas Faith is right in some parts (at least as far as she goes), MJ is irrevocably wrong in just about every aspect - beginning with loss of genes (not alleles) causing speciation and passing through a complete lack of understanding of what speciation actually is. He's not in the same league as Faith, to be honest.Edited by Quetzal, : No reason given.

Expressed more eloquently, you have very directly described what my concerns are about Faiths proposition. I have a caveat that I will describe towards the end. Those quotes describe my point exactly. If I misunderstood Faith to believe that speciation is not required for her argument then I stand dumbfounded. The whole basis for diversity from the original kinds is in stark contrast to her claim that mutation is ineffectual to drive this diversity. She is obviously claiming that mutation cannot do it. She is claiming, although it seems to be incorrect, that allelic recombination can do it. If not those then what else? Correct me if I am wrong, but is not drift driven at least partially by mutation? If the only thing that is happening in drift is allele reshuffling then how can the drifting populations ever be made incompatable?

---

Of course, biblical creationists are committed to belief in God's written Word, the Bible, which forbids bearing false witness; --AIG (lest they forget)