Evolution Requires Reduction in Genetic Diversity

I would like to see more details than we have had so far. I am trying to construct a simple example of what might happen to produce separate species without mutations. Can others help to make this clear and sensible?Population Splitting and EvolutionLet's presume we have a population of 2,000 individuals. They have 10 genes in their genome. Label these A through J. Each gene has 5 alleles A1, A2,... D1,D2,D3... through J5. The alleles are not evenly spread:A1, B1, C1, D1...
50 %
A2, B2, ...
20 %
A3, B3, C3...
10 %
A4, B4...
10 %
A5, B5, C5...
10 %Now let's imagine that an earthquake creates a huge chasm splitting the population into exactly two equal groups. There are a number of possible scenarios:1: The group was ranging over their home area randomly and there was no special bunching of animals with a particular allele.At the end of the split the percentage of each allele in each group is exactly the same. Now each population has 400 individuals with A1 and B1 and C1 ... instead of the 800 individuals that were in the total population of 2,000 animals. The genetic diversity is exactly the same as the original population is it not?2. One the other extreme could be a split (by chance or for some other reason) where all of one allele fell on one side of the chasm. This could happen to various degrees for each allele.Now we may have a northern population that has 100 % A1 and zero of A2,A3, A4 and A5. That is the 1,000 amimals with A1 all ended up in the north. It may also by chance have 40 % of B2 that is all of the individuls with B2 ended up in the north.The souther population would now have zero % A1 and 40% A2, 20% A3, 20% A4 and 20% A5 in the 1,000 animals there.This in some mix or another could apply to each allele.3. Intermediate MixesAny intermediate mix could happen also but I don't think they matter for this discussion.I think that Faith's argument isn't based on scenario 1 at all. If that is wrong I'd like to see it corrected.So let's look at scenario 2. There are no alleles lost in the total population. The genetic diversity of the 2,000 animals is exactly as it was before the earthquake.However, the northern animals have zero diversity in gene A and the southern animals have reduced diversity in gene A.Does this make the two populations different species? It can't, mixed back together it is exactly the same 2,000 animals from before.What possible combination of allele resulting from splitting the original 2,000 animals can produce a different species? It seems to me that none can.All possible combination of the different alleles of each of the 10 genes were allowed and fertile before the split. Now that we have two separated populations each with reduced diversity what must happen to make the northen and souther populations no longer interfertile?

Was lactose tolerance already in place in those times, then?

Faith did make this claim, but perhaps it is a red herring to focus directly on the claim. After all, she does not even believe speciation occurs.Her claim is that by the time enough change occurs to cause the impossible, the loss of diversity required to make a 'breed' will have kicked in. However, there are a number of problems with this as a generalization. First, species are not homogenous collections of traits, second, speciation and isolation may not occur until new traits are dispersed through a population making it more diverse than at its time of creation, and mutations may cause a lack of interfertililty much more readily than Faith envisions with here impossible method.Again, given that there are competing processes that add and subtract diversity, nobody should accept a mere assertion without evidence or even any argument. And of course there is also the contrary evidence.

What I was hoping was that Faith might put some effort into using an example of this sort to actually explain what she is thinking.Don't laugh! It might happen.

I was considering it. Don't know if I want to get back into this thread.

I think I better start by clarifying a few things. I don't think we are in disagreement on any of this or that you don't understand it, but I may (once again) be approaching this in a highly technical way that may not be readily apparent. Reproductive isolation is any barrier that prevents or reduces gene flow between two populations. Reproductive isolation is the first step in speciation but is not synonymous with it, nor is it synonymous with genetic incompatibility. Speciation cannot be thought of as an event, but as a process. It is essentially impossible or impractical to identify the point or event at which speciation occurred. We can however, identify the key steps in the process and even determine their relative importance and the likely order in which they occurred. Genetic incompatibility is when there is a genetic basis for the inability of the hybrid offspring to contribute to the recombining of the parent populations. Or another way to put it: when there is a genetic basis for the reduction in gene flow (as opposed to a physical barrier). ABE: Genetic incompatibility could be synonymous for postzygotic isolation, although technically "isolation" is what it *does* and "incompatibility" is what it *is* (if that makes sense). /ABENow, I will admit that this is my own definition so I would be happy to debate it but I'll give some justification here for this definition.I think it is pretty obvious that if the hybrids are not viable, (ie. they don't develop into adults) that they will not themselves breed and produce offspring and so cannot contribute to recombining the parent populations. It should also be obvious that if the hybrids spread through the population and completely homogenize it, they are NOT genetically incompatible. However, in-between these two extremes is a whole gradient of possibilities.Here is an example. Let's say we have a population of plants that is adapted to higher elevations and one that is adapted to lower elevations. Where these two population meet there is a hybrid zone. However, the hybrids are not well suited to the higher elevations; but neither are they well suited for the lower elevations. So the hybrids remain confined to this narrow zone and the two populations retain their distinct character, thus gene flow is restricted to a small section of the two populations. This would be considered partial incompatibility, but it would be enough to allow each population to remain differentiated. We could even measure the amount of partial incompatibility by creating a cross and transplanting the hybrids to both habitats and measuring fitness. A reduction of fitness by say 90% in each habitat would indicate a 90% incompatibility. No, I wouldn't combine them. They are two different ways of restricting gene flow. Prezygotic isolation could occur without geological isolation and geological isolation could occur without producing prezygotic barriers. The factors that prevent most of the two northern varieties from interbreeding are probably genetic (although bird songs can be learned from the parents, so if that were the only difference then it may not be genetically based). So perhaps it could be partial genetic incompatibility but unless we know something about the hybrids, more likely simply prezygotic isolation. Yea, of course defining the line between species is always a controversial subject in taxonomy. Perhaps you are a "lumper"? I don't think that the biological species concept requires 100% incompatibility, so perhaps I'm a "splitter?" Without having done much study on this, I would guess those populations are distinct enough to consider separate species even though they hybridize at very low rates. But maybe they could all be considered sub-species of one species, but really, what's the difference? Just a longer name to write Phylloscopus trochiloides subsp. trochiloides . But I do believe that they are now considered to be subspecies by most authorities, not completely sure though. At first I was a bit uncomfortable about requiring the "function" of the gene to change, but the more I think about it, that is pretty accurate. However, it wouldn't necessarily be "protein production." I think I would leave that out and just say the function of the gene would need to be different. It seems a bit difficult to make a generalized statement regarding this. I think we would need to talk about some specific examples. However, I think by definition that if an allele is recessive then its expression is masked by the dominate allele. But could a mutation change a normally recessive allele into a co-dominate allele? Yes, certainly. Two things; First, I was unclear in my statement. I should have said that "in theory one mutation could result in prezygotic isolation." I don't expect postzygotic incompatibility to arise from a single mutation (although I would still say it's not completely inconceivable, but I am just not sure how it would). And as I explained above, I would also consider there to be incompatibilities even if they were not 100%.Second, even if one mutation resulted in pre or post-zygotic isolation, speciation would still be a process. Even in the case of polyploidy, that mutation would need to establish as a breeding population before speciation would be considered to have occurred.Here is a study on Monkeyflower where a substitution at one locus (YUP) caused a dramatic shift in pollinator preference and sympatric populations are now 99% isolated - because of this one mutation resulting in prezygotic isolation. They will hybridize in the lab, which is how they made their NILs (near isogenic lines - which is single gene from one species introgressed into the background of the other). But they are reproductively isolated in nature.Genetic incompatibility can be very simple as in the case of Mimulus

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Much evidence has shown that postzygotic reproductive isolation (hybrid inviability or sterility) evolves by
the accumulation of interlocus incompatibilities between diverging populations. Although in theory only a
single pair of incompatible loci is needed to isolate species, empirical work in Drosophila has revealed that
hybrid fertility problems often are highly polygenic and complex. In this article we investigate the genetic
basis of hybrid sterility between two closely related species of monkeyflower, Mimulus guttatus and M. nasutus.
In striking contrast to Drosophila systems, we demonstrate that nearly complete hybrid male sterility in
Mimulus results from a simple genetic incompatibility between a single pair of heterospecific loci. W

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The following chart is adapted from a lecture on DMI (Dobzhansky—Muller Incompatibilities) in my Evolutionary Biology course.

# subtitutions	# incompatibilities
1	0
2	1
3	2
4	3
5	6
6	9

It shows how one substitution causes no incompatibility but the number quickly rises as the number of substitutions increase.So in the case of this monkey flower (Mimulus) there are substitutions at 2 loci, hms1 and hms2 resulting in 1 incompatibility which causes almost complete male sterility in the hybrids.HBDEdited by herebedragons, : No reason given.

But the problem is that it is not clear any such thing exists. I linked earlier to [/url=http://genomics.princeton.edu/...files/Haddrill_etal2008.pdf]a study[/url] that tested neutrality of non-coding DNA in two species of Drosophila. Their conclusion (emphasis mine):

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In summary, we have examined patterns of evolution at several classes of noncoding DNA in D. simulans and find that all noncoding DNA is subject to the action of negative selection, indicated by low levels of polymorphism and divergence and a skew in the frequency spectrum toward rare variants.

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I lack the expertise to assess the maths behind their claims, but if they're right then we can see detectable evidence of negative selection against changes in non-coding DNA. They also claim evidence of positive selection in untranslated DNA in Drosophila simuans.

Then why don't we see evidence of selection against indels in those sections of DNA? How much energy? What portion of a the body's energy is spent on very low level transcription of junk DNA? What harm would be caused by RNA transcriptase that was too stringent and failed to transcribe important genes?IOW, there is a balance between energy and and a somewhat sloppy RNA transcriptase that can more reliably transcribe important genes. If you make RNA transcriptase so selective that it no longer transcribes junk DNA it may not reliably bind to promoters upstream of the genes that you really do want transcribed. Not really the same thing. There are still harmful mutations that can happen in cytC.Being transcribed is not the same as having function.

The tests for negative and positive selection do exist, as do results from those tests. In those results. non-coding DNA is split into categories, one of which is junk DNA.I agree that those tests are not 100% accurate, but this doesn't change the fact that junk DNA is a subcategory of non-coding DNA, and therefore adds more specificity for what you are talking about. They detected negative selection in the several classes of noncoding DNA that they looked at in the D. simulans genome. They aren't making claims about all noncoding DNA in all species. They didn't even make the claim that all noncoding DNA in D. simulans showed signs of negative selection.

For example, giant sized, Nephilim, milkmen?

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Genesis 6:4

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The Nephilim were on the earth in those daysand also afterwardwhen the sons of God went to the daughters of humans and had children by them. They were the heroes of old, men of renown.

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Et voil exactly what I mean by NOT blurring concepts and terms, see my posts Message 626 and Message 505.Let's start with what was meant by the authors of your article:

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There is now a wealth of evidence that some of the most important regions of the genome are found outside those that encode proteins, and noncoding regions of the genome have been shown to be subject to substantial levels of selective constraint, particularly in Drosophila.

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Now what exactly is non-coding DNA?
Well: much of the DNA that is non-coding, actually STILL is functional, including such things as transcriptional and translational regulation of protein-coding sequences (Hox-genes), centromeres, telomeres, scaffold attachment regions (SARs), genes for functional RNAs, and many others.But non-coding parts of the DNA ALSO include junk DNA without any function or use: old disabled genes from our evolutionary heritage, ERV's (former retrovirus virus infections that were surmounted but left remnants of the virus in the DNA), retrotransposons (chunks of DNA that randomly copy themselves selfishly and are scattered over the genome) and many others.Hence, much of the non-coding is non-functional but other parts DON'T.One SHOULD NOT use "non-coding DNA" as a synonym for "non-functional DNA". They are different. Non-functional DNA is at most a subset of non-coding DNA. Junk DNA may be used as an alternative wording for non-functional DNA but NEVER for non-coding DNA.The part of non-coding DNA that is functional is prone to selection.Your article was referring to that part, the "some of the most important regions of the genome" that are "found outside those that encode proteins" and, thus, [those] "non-coding regions of the genome have been shown to be subject to substantial levels of selective constraint". OF COURSE they are. They happen to be the functional parts of non-coding DNA. Junk DNA is referring to the rest of non-coding DNA, the parts that are non-functional.Hence it was not the mathematics here that bring better understanding, but a precise definition of terms used.

<.>Edited by Denisova, : Changed my mind.

Why should we?
And what made you conclude that we don't see evidence of selection against indels?
An indel that impairs the spacer would be detected by the adjacent genes not being transcribed properly. In eukaryotes, spacer DNA can be extensive and include repetitive DNA, comprising the majority of the DNA of the genome. So, its function does not depend on its base-pair sequence as such but on its position. I don't know how much exactly. But every cell has its own transcriptome spectrum of mRNA molecules present within it, adding up to literally thousands of different mRNA molecules present in the cell at any given time. Some of these are rare but others are quite abundant. Moreover, transcripts for structural proteins may remain intact for over ten hours, but transcripts for signalling proteins may be degraded in less than ten minutes. Hence, both of them have to be produced at a constant rate.I think that accounts for notable amounts of energy consumption. And notable it is when a reduction of this consumption, without any functional consequences, would retain energy for other purposes. When this were the case, that would certainly happen because it leads to energy efficacy. fitness is sometimes measured in a few %.Why do you call it "low level" transcription? If you meant transcription with a low biological signal, OK with me, but transcription of junk DNA costs as much energy as transcription of functional DNA, how "low level" it might be. That of course would be one reason why transcription of junk DNA turns out to be persistent.
But, even still then, energy is lost by transcribing junk DNA. Of course, in the one-third part of it that specifies its function.
Still leaving two-third of it completely redundant and only copied for the cat's violin.Edited by Admin, : Fix quote.

You should realize that leaving the thread does not solve your inability to answer the questions.

If the spaces between genes are important then mutations that change those spaces should be harmful part of the time and be selected against. We do see evidence of negative selection against indels, but only in 10% of the genome. If that were the case throughout the genome, shouldn't we see selection against indels in 100% of the genome? Both of those are empty assertions. In this context, low level transcription refers to the number of copies of any given RNA transcript. For the junk DNA that ENCODE found mRNA copies for, the number of copies were several orders of magnitude lower than commonly transcribed genes such as B-actin. In fact, these areas had so few copies that they had to use special techniques to detect them.If you want to make the argument that the observed rate of junk DNA transcription is energetically expensive then you need to have a handle on the number of RNA copies and bases per copy since the energy is spent making the nucleotides and linking them with phosphates. What matters is the amount of energy that is expended transcribing junk DNA. If it is just 1% of the energy compared to transcribing functional genes then it isn't a problem. When comparing orhtologous cytC genes between species these would show up as regions of conservation. When those are found within an open reading frame, it indicates function. Junk DNA has none of these features. It doesn't have regions that are highly conserved between species. It doesn't have open reading frames that have upstream ribosome binding sites, for example.