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Author Topic:   Introduction to Genetics
Taq
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Posts: 8519
Joined: 03-06-2009


Message 184 of 236 (719996)
02-19-2014 3:00 PM
Reply to: Message 183 by Faith
02-19-2014 2:58 PM


Re: Factual versus interpretive tendentious terminology
But the question does remain: what do those mutations actually DO and if they don't do anything of benefit at all what is the point of even counting them as an increase in genetic variability?

These mutations will improve fitness, reduce fitness, or not change fitness at all, just as they always have.

What is the point of talking about genetic variability if you ignore genetic variability?


This message is a reply to:
 Message 183 by Faith, posted 02-19-2014 2:58 PM Faith has replied

Replies to this message:
 Message 186 by Faith, posted 02-19-2014 3:07 PM Taq has replied

  
Taq
Member
Posts: 8519
Joined: 03-06-2009


Message 187 of 236 (720003)
02-19-2014 3:25 PM
Reply to: Message 180 by Faith
02-19-2014 2:43 PM


Re: QUESTION ABOUT PSEUDOGENES
Anyway, I have a question about pseudogenes or "junk DNA" again. I understand these occur here and there throughout the genome.

Junk DNA makes up 80 to 90% of the genome.

1) if there's anything about them that meets the eye, just in their sequences or how they appear as you are sequencing the genome, to tell you they are not normal genes? Or do you have to do some kind of testing to see if they actually make proteins to find out that they aren't true genes?

Junk DNA accumulates mutations at a rate consistent with neutral selection. That is how it is identified. This can be done by comparing genetic variability among humans, or comparing the human genome to the genome of other species.

Open reading frames (ORF's) are much easier to identify since they will be intact and not interrupted by frameshift mutations. You will also be able to find transcription factors and other intact promoters upstream of the open reading frames. However, RNA genes and other non-coding functional DNA can not be identified by looking for ORF's, but they can be identified by finding sequence that is under selection.

what it is that has led geneticists to determine that some of them have a "regulatory function," and what that function actually is and how you tell? And how many of them can be described this way?

The classic examples is the lac operon found in E. coli, and it is still the example that students become familiar with in introductory classes in genetics. The operon has the B-galactosidase and other genes which which are responsible for breaking down lactose for energy. Upstream of the B-gal gene are two DNA binding sites. First, you have the cAMP protein binding site. As glucose gets low the levels of cAMP increase in the bacterium causing the protein to bind and increase production of the lac operon genes. Next is the lac repressor site. This is there the lac repressor protein binds and blocks RNA transcriptase from binding to the DNA. When lactose metabolites are present it binds to the repressor and releases the repressor from the DNA. This allows RNA polymerase to bind and transcribe the genes. If the cAMP protein is also bound to the upstream DNA binding site, it increases RNA polymerase binding and also increases transcription.


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Taq
Member
Posts: 8519
Joined: 03-06-2009


Message 188 of 236 (720005)
02-19-2014 3:28 PM
Reply to: Message 186 by Faith
02-19-2014 3:07 PM


Re: Factual versus interpretive tendentious terminology
But that too sounds like an article of faith . . .

It's not, as I have shown in previous posts.

And again, where's your EVIDENCE that your mutations affect fitness

Compare the fitness of humans and chimps in an arboreal or savanna environment. The mutations that have given humans their species specific morphology is beneficial in an open savanna. The mutations that chimps have give them increased fitness in an forest setting. That is the evidence, the observed and beneficial differences in the two genomes caused by mutations.


This message is a reply to:
 Message 186 by Faith, posted 02-19-2014 3:07 PM Faith has replied

Replies to this message:
 Message 190 by Faith, posted 02-19-2014 4:30 PM Taq has replied

  
Taq
Member
Posts: 8519
Joined: 03-06-2009


(1)
Message 191 of 236 (720015)
02-19-2014 4:37 PM
Reply to: Message 190 by Faith
02-19-2014 4:30 PM


Re: Factual versus interpretive tendentious terminology
You don't even seem to know all you are doing is reciting your theory.

Yes, theories backed by evidence. What is wrong with that?

You're assuming that mutations are alleles as I've said.

No such assumption is being made. The evidence demonstrates that these are mutations that have occurred in each lineage since sharing common ancestry. This is a conclusion drawn from evidence, not an assumption.

You have no proof of this,

I have 150 years of gathered scientific evidence, from transitional fossils to genetic evidence.


This message is a reply to:
 Message 190 by Faith, posted 02-19-2014 4:30 PM Faith has replied

Replies to this message:
 Message 192 by Faith, posted 02-19-2014 4:41 PM Taq has replied

  
Taq
Member
Posts: 8519
Joined: 03-06-2009


(2)
Message 193 of 236 (720019)
02-19-2014 5:06 PM
Reply to: Message 192 by Faith
02-19-2014 4:41 PM


Re: Factual versus interpretive tendentious terminology
You've never presented any evidence that supports your claim that all the alleles were originally mutations.

It is found throughout the other threads and throughout the scientific literature. As a start, you can check out this paper on ERV's shared by humans and chimps as smoking gun evidence of common ancestry and the evolution of sequence through mutation and selection.

http://www.pnas.org/content/96/18/10254.full

However, I have this haunting suspicion that you don't give a lick about the facts, so why bother showing you evidence that you will ignore?


This message is a reply to:
 Message 192 by Faith, posted 02-19-2014 4:41 PM Faith has replied

Replies to this message:
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Taq
Member
Posts: 8519
Joined: 03-06-2009


Message 194 of 236 (720020)
02-19-2014 5:06 PM
Reply to: Message 185 by Faith
02-19-2014 3:01 PM


Re: Factual versus interpretive tendentious terminology
Well I'd put it "DNA that actually affects the organism for good versus not so good or doesn't do anything at all."

That is still an artificial separation of DNA sequences.


This message is a reply to:
 Message 185 by Faith, posted 02-19-2014 3:01 PM Faith has replied

Replies to this message:
 Message 195 by Faith, posted 02-19-2014 8:51 PM Taq has replied

  
Taq
Member
Posts: 8519
Joined: 03-06-2009


Message 211 of 236 (720094)
02-20-2014 10:41 AM
Reply to: Message 195 by Faith
02-19-2014 8:51 PM


Re: Factual versus interpretive tendentious terminology
It isn't artificial if it's true.

It is a human construct, so it is artificial.

But it IS an artificial position to take to pronounce it all normal alleles if it isn't -- again, an assumption, an article of faith.

You have a habit of ignoring evidence.


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Taq
Member
Posts: 8519
Joined: 03-06-2009


(1)
Message 212 of 236 (720095)
02-20-2014 10:44 AM
Reply to: Message 202 by Faith
02-19-2014 11:40 PM


Re: Just some examples of assumptive mystification versus genuine science
THIS on the other hand is science mixed with pseudoscience:
http://en.wikipedia.org/wiki/Endogenous_viral_element
Most of it is science. The paragraph about paleovirology is where the pseudoscience comes in, where the data is crammed into the ToE's Old Earth assumption of millions of years for this or that. It purports to give the actual history of "germline integration events" as if it were possible to know anything about events in the genome millions of years ago.

It is possible because we find retroviruses in genomes. That is the evidence. No faith or pseudoscience needed. It is no different than finding a fingerprint at a crime scene.

This next one is the one Taq linked. Since it's about finding phylogenetic markers it's bound to get into the pseudoscience territory, and reading stuff like this is a horrific struggle for me, being a combo of unsupportable assumptions with genuine scientific facts, and of course some terminological struggles as well, but that part I'm not faulting:

And yet you can't point to any unsupported assumptions or pseudoscience. All you have is hot air.


This message is a reply to:
 Message 202 by Faith, posted 02-19-2014 11:40 PM Faith has taken no action

  
Taq
Member
Posts: 8519
Joined: 03-06-2009


(2)
Message 213 of 236 (720096)
02-20-2014 10:46 AM
Reply to: Message 208 by Faith
02-20-2014 4:28 AM


Re: Paradigm clash
We can both repeat our complaints about our opponents' point of view, plus you've added the usual Science Creed and the Evo Creed, and it's all simply a statement of belief.

Hot air, again. We have shown you that it is a scientific theory backed by scientific evidence. Ignoring the evidence doesn't make it go away.

All you are doing here is a tit for tat, echoing exactly what I've been saying about evolutionism. Of course I suppose it can be said on both sides, but it IS true of evolutionism as I've been pointing out, that the interpretive sciences that support the ToE are wrapped around bald assumptions without any verification whatever.

And yet you can't show us a single bald assertion that is not backed up by evidence. Again, hot air.

•The ToE says All life was descended from earlier life. This is an article of faith, of belief, based on commitment to the ToE. It hasn't been shown to be true and it can't be shown to be true (is this a better way of saying it than "proved?) The particular Creationist model I've been pursuing says all life was created as separate Species in the same time frame as human beings. This IS a different model, wouldn't you say?

I just showed you the evidence demonstrating that humans and chimps share a common ancestor. ERV's are that evidence. All you did was run away from the evidence without ever engaging it.

•THe ToE says DNA evolved just as everything else did; YEC as I've been pursuing it says DNA was built in to the original Species or Kinds and the genome of each governs only that Species, and again, surely this must be considered to be an alternative model.
--- My particular defense of this idea is that the processes of evolution that isolate populations from each other, which is the general way races are formed, lead to reduced genetic diversity. This also appears to be the main route to "speciation" but if the supposed "new species" in fact has reduced genetic variability this is clearly a wishful fantasy. The YEC model as I understand it says that life was created to vary, to evolve over time, into myriads of fascinating new races, but that a calamity known as the Fall brought death into the world and now all life is threatened by disease and death whereas if the Fall had never happened we'd just have beautiful subspecies of every known Species. And again, this IS a model and it does have explanatory power. It's obvious that species are threatened by extinction. That's why we have conservationist programs.

That evidence is also found in ERV's. We can see ERV's diverge over time, both between species and between LTR's of the same ERV. It is all in the paper I gave you.

•The ToE says that mutations are the means by which DNA was/is created, while also admitting that most mutations are neutral and many are deleterious, claiming the latter are selected out. My YEC view says this is a complete misunderstanding, that mutations are not a normal occurrence, or let's say most of them aren't, they are mistakes, and their overall effect is destructive, even though this may not show up for quite some time. There ARE, however, thousands of known genetic diseases, and only a tiny number of mutations that are even claimed to confer any known benefit, and in most cases the benefit is a trade-off with another disease, such as malaria protection by sickle cell anemia. This looks like a thoroughly inadequate method for producing viable genetic material. And again, this is a plank in a creationist model. The facts fit the model of life's actually deteriorating rather than improving in any way.

Your view is meaningless. What matters is the evidence, and you ignore it.

•The ToE also proposes of course that mutations make up for any reduction in genetic diversity. My YEC model says 1) mutations hardly ever IF ever make DNA that acts like normal functioning DNA. The best it can do is manage not to change things, but then what do you have? Nothing really. And 2) if mutations did add genetic diversity of a valid kind to a new population, all they could add is an allele to replace another allele and one or the other is going to get selected to make up the overall "look" of the population and in the end since one gets selected out there is nothing that can really be called an increase in genetic diversity.

Your model is meaningless. What matters is the evidence, and the evidence demonstrates that mutations cause species to diverge and increase their genetic variability.

•The ToE says evolution has created everything that now lives and that this has been going on for many millions of years.

The ToE says that biological reproduction has created everything that now lives. You have been taught about the birds and the bees, have you not?

•The ToE's evidence includes the fossil record which is remarkably sorted from bottom to top according to what seems to be a hierarchy of development from more primitive to more advanced or modern (certainly complexity is not the criterion since the "lower" creatures are often amazingly complex). Of course one could wonder why evolution would operate in any particular identifiable direction onwards and upwards since one of its cardinal "tenets" is "fitness" which shouldn't imply any particular direction of adaptive traits, but it does have to be admitted that it LOOKS plausible if you allow for that idea and it seems to defeat the YEC idea that the worldwide Flood of Noah explains all the strata and their fossil contents. Nevertheless the Flood does remain the YEC alternative model to the Geologic Column, and it does have explanatory power.

Fossils fall into a nested hierarchy, just as the theory predicts. You have never been able to explain this away.

Edited by Taq, : No reason given.

Edited by Taq, : No reason given.


This message is a reply to:
 Message 208 by Faith, posted 02-20-2014 4:28 AM Faith has taken no action

  
Taq
Member
Posts: 8519
Joined: 03-06-2009


(1)
Message 216 of 236 (720149)
02-20-2014 12:46 PM
Reply to: Message 215 by Faith
02-20-2014 12:15 PM


Re: Just some examples of assumptive mystification versus genuine science
I've answered you about the word "proof," that I think it's just a way to rationalize pretending that evolution is scientific in the same sense that the hard sciences are. If you disallow the idea of "proof" you also disallow that distinction. You apparently haven't read anything I said in answer to you about that. But if you are going to insist, I can use other terms like "verification," or "validation" or "confirmation."

Evolution is no different than any theory in any of the hard sciences. All theories rely on testing of hypotheses and induction, just like evolution.


This message is a reply to:
 Message 215 by Faith, posted 02-20-2014 12:15 PM Faith has replied

Replies to this message:
 Message 218 by Faith, posted 02-20-2014 3:15 PM Taq has replied

  
Taq
Member
Posts: 8519
Joined: 03-06-2009


(2)
Message 219 of 236 (720168)
02-20-2014 3:48 PM
Reply to: Message 218 by Faith
02-20-2014 3:15 PM


Re: Just some examples of assumptive mystification versus genuine science
Against the evidence, however.

What evidence? It would be a refreshing change if you actually presented some.

What evidence did you present with respect to ERV's? From what I could see, all you had was hot air with no references to any scientific papers or evidence. None. I present real scientific studies and you present . . . nothing.


This message is a reply to:
 Message 218 by Faith, posted 02-20-2014 3:15 PM Faith has replied

Replies to this message:
 Message 220 by Faith, posted 02-20-2014 7:52 PM Taq has replied

  
Taq
Member
Posts: 8519
Joined: 03-06-2009


Message 221 of 236 (720283)
02-21-2014 11:00 AM
Reply to: Message 220 by Faith
02-20-2014 7:52 PM


Re: Just some examples of assumptive mystification versus genuine science
The evidence of the ERVs was undecipherable, so I asked if you'd please put it into your own words.

Actually, this might serve as a good introduction to some other concepts in genetics and molecular biology. We will take this step by step so that you can ask questions if you need any clarification.

First, let's take a look at the genome of a generic retrovirus.

As you can see, the retroviral genome is pretty simple. You have two genes, gag and env, that produce proteins that are found on the outside of the viral particle. You also have pol which is responsible for producing a series of proteins that copy and insert the retroviral genome into the host genome. Then we have the LTR's on either side (LTR stands for long terminal repeat), kind of like bookends. They are made up of a repeating sequence of DNA.

Here is an important concept to understand as it becomes important later. When a retrovirus inserts into the host genome it copies one of the LTR's to produce the LTR on the other side. This means that when the retrovirus inserts the LTR's are identical in sequence.

Once the retrovirus inserts into the genome, the LTR's act as promoters for the retroviral genes which in turn results in the production of new viral particles. Here is a diagram describing the life cycle of a retrovirus.

As you can see, the retroviral genome becomes a permanent part of the host genome, and new retrovirus particles are produced from that endogenized retrovirus. This is where we get the acronym ERV which stands for endogenous retrovirus. These are retrovirus that have become endogenous to the host genome due to integration.

Any questions so far?

Edited by Taq, : No reason given.

Edited by Taq, : No reason given.


This message is a reply to:
 Message 220 by Faith, posted 02-20-2014 7:52 PM Faith has replied

Replies to this message:
 Message 223 by Faith, posted 02-25-2014 11:37 PM Taq has taken no action

  
Taq
Member
Posts: 8519
Joined: 03-06-2009


(1)
Message 224 of 236 (720685)
02-26-2014 11:30 AM
Reply to: Message 222 by Faith
02-25-2014 11:08 PM


Re: Mouse Genetics
Funny then that all you've done is declare it rhater than show such observations.

The genetic basis of adaptive melanism in pocket mice

It is demonstrated in the paper above.

Well, this topic has come up before and I vaguely remember that fact anyway. But this fact doesn't necessarily end the discussion. Fur color is one of those traits that is often governed by more than one gene and when that is the case the pattern of dominant-recessive at one gene may not be the dominating influence. I'm not sure how this works, but maybe we could discuss it here.

In the study, the mutant allele correlated 100% with the dark fur color, even in mice that were carrying a single copy (i.e. heterozygotes). The mutations are also found in the same gene that governs melanism in humans.

The fact that there are many genes that can mutate to change fur color only strengthens my case.

It isn't said but the very existence of the agouti suggests that more than one gene is involved.

This is for black and white not "light" and "dark" and I'm not sure whether we're talking about two different genetic pictures or if the same principles apply, but if it's the same situation the hard thing to explain would be the light mice rather than the dark, because they would be recessive and if only one gene governs the color it would have to be paired to produce it. But if the statement from the first link is correct that both dominant and recessive alleles remain in the population then we can assume that the alleles for dark are in the light population. The D for dark would be rare in the population but you could still get a combination of Dl with ll which would most often always produce the light type, and also even the occasional Dl with Dl which would produce the light type half the time.

Then what happened when the dark were selected for the lava area would have been the favoring of the DD type and the loss of the ll type. If other genes are involved, however, there could be other factors that produce the light (or dark) even more often. I may not have the clearest grasp of how all this works but that's one reason I brought it to this thread.

This goes back to what I was saying before. The black fur color is deleterious in the light colored desert because they stick out as much as the light colored mice do on the black lava. It is selected against. This is why you don't find the DL or DD individuals in the light colored desert.

This is also why this trait could not have been present in the population before the recent production of the black lava fields. As soon as the mutation occurred (or within very few generations), it would have been selected against and would have disappeared from the population. The lava fields are very recent relative to the brown desert. On top of that, the different genetic mutations in two different populations that both produced black fur also supports this conclusion.

How do you know this? It could be rare rather than nonexistent.

The selection is strong enough that it overcomes the dominance of the allele.

That being the case, this really isn't a strong argument for mutation at all, but for the rare occurrence of a normally occurring D in the population from time to time. When the selection pressure occurs it would be when some of the light population have ventured onto the lava with a few darks among them.

Then explain why the two separate populations have different mutations that each produce dark fur.

"Interestingly, another melanic population of these mice on a different lava flow shows no association with Mc1r mutations, indicating that adaptive dark color has evolved independently in this species through changes at different genes. "
http://www.pnas.org/content/100/9/5268.long

These two lava fields are separated by hundreds of miles of light colored desert. The facts support de novo mutations appearing in the two different poplations, not a single pre-existing trait that was then selected for at two points.

ABE: There is also the fact that the dark allele has less sequence variation than the light allele.

"Finally, the pattern of nucleotide variation observed among Mc1r alleles from the Pinacate site suggests the recent action of positive selection. Thirteen polymorphic sites are variable among the light haplotypes, whereas only one site is variable among the dark haplotypes (Table 1). The ratio of variant to invariant sites is significantly different between dark and light alleles (1/953 and 13/941, Fisher's exact test, P < 0.01). "
http://www.pnas.org/content/100/9/5268.long

If the dark allele had been around as long as the light allele then we would expect to see the same sequence variation, but we don't. There is much less variation in the dark allele which is consistent with the recent emergence of the allele.

Well, the observed mechanisms of mutation are usually described as mistakes, and the various ways they occur certainly look to me like mistakes and nothing I'd expect to happen *normally* to the amazingly complex and incredibly well organized DNA system.

Plus the fact that you all acknowledge that mutations are the cause of an amazing number of genetic diseases, not ALL of which are "selected out" by the way although that is the accepted wisdom. I just saw an article about a very rare genetic disease that two brothers didn't know they had until adulthood when now their lives are threatened by something they didn't even know they had, this Alport syndrome.

PLUS all those "neutral" mutations which are observed, which as far as you know do nothing, which is rather odd, again, in such an incredibly complex and amazingly organized genetic system.

PLUS the fact that you really don't KNOW of many clearcut beneifts of mutations, and even those you can point to are rather iffy.

PLUS the fact that the mutation would have to occur specifically at the gene for fur color in time to produce the favored dark mouse and occur in mice that have ventured onto the lava field rather than in the light mice where it would only be selected against. What are the odds?

Plus the fact that it would have to produce the right sequence so as not to mess up the fur color gene completely. Maybe that's not too hard since a "neutral" mutation wouldn't change much anyway, but then wouldn't we expect just another "light" to show up? How is it going to produce enough of a change to produce a dark over a light? Odds again seem to be a problem here.

There are a few reasons for you.

That doesn't even come close to answering the question.

Just because they are mistakes does not prevent them from producing beneficial changes. Just because some changes are neutral or detrimental does not prevent other changes from being beneficial.

There are 40 million mutations that separate humans and chimps. Do you really think that none of those differences are beneficial to humans or chimps?

Edited by Taq, : No reason given.

Edited by Taq, : No reason given.


This message is a reply to:
 Message 222 by Faith, posted 02-25-2014 11:08 PM Faith has replied

Replies to this message:
 Message 225 by Faith, posted 02-26-2014 1:49 PM Taq has replied

  
Taq
Member
Posts: 8519
Joined: 03-06-2009


(1)
Message 228 of 236 (720698)
02-26-2014 4:17 PM
Reply to: Message 225 by Faith
02-26-2014 1:49 PM


Re: Mouse Genetics
How did the mutant allele occur just in time to form a dark population of mice?

The mutation would have been popping up now and again throughout the history of the pocket mice population. The same thing happens with antibiotic resistance in bacteria. The mutation is occuring at a set probabilistic rate. It isn't until you add selection that antibiotic resistance comes to dominate the population.

Experiments like the Luria-Delbruck fluctuation experiment and the Lederberg plate replica experiment demonstrate why it only appears that the mutation shows up in time. The truth of the matter is that the mutation is occuring at the same rate through history, irrespective of if it is beneficial or not.

http://en.wikipedia.org/...%E2%80%93Delbr%C3%BCck_experiment

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC169282/

Those are the two classic experiments that still define what biologists mean by random mutation. They might be worth going over if you would be willing to discuss it.

Because it gets passed on. Just when the light mice are getting to the lava field apparently.

I, nor anyone, ever made that claim. It only had to happen in a population near the lava fields sometime after the eruptions. Could have been 10,000 years after the eruption, or 100,000. Could have happened 500,000 years after the eruption, and just a few thousand years before humans moved into the area.

It's a Dl, it will have to pair with an ll.

Ever use a Punnet square?

http://en.wikipedia.org/wiki/Punnett_square

In this case, offspring from Dl ll parents will have a 50% chance of being dark because D is dominant over l.

And what's to stop this predator that has kept the population light forever from just picking off those two little dark babies as soon as they are born?

Nothing. The gene could have appeared and disappeared multiple times. Doesn't change the fact that it did survive and was passed on at some point, and in two lava fields to boot.

As you say there is apparently more than one gene that can mutate to make dark fur color. The problem is that the odds are against this happening for starters, just in time for the lava field, then they are against the offspring surviving assuming they get produced, then they are against them growing up to make more dark mice.

Yes, there are at least two gene loci where mutations can produce dark fur, and probably more than two.

I will also look forward to seeing your probability calculations that show why this is improbable. You will be showing us those calculations, won't you? You wouldn't just claim that it is improbable without anything to back it up, would you?

The odds aren't a LOT better for built in alleles . . .

What built in alleles? Evidence please.

Edited by Taq, : No reason given.


This message is a reply to:
 Message 225 by Faith, posted 02-26-2014 1:49 PM Faith has taken no action

  
Taq
Member
Posts: 8519
Joined: 03-06-2009


(1)
Message 231 of 236 (720702)
02-26-2014 4:57 PM
Reply to: Message 230 by Faith
02-26-2014 4:50 PM


Re: Mouse Genetics
The problem with that argument is that it justifies my claim that it wasn't a mutation but a regularly occurring allele.

It would have been removed from the population by negative selection, so that explanation is out.

But Taq insisted that it had to be a mutation because it's dominant, meaning that there had been NO allele for black fur in the population earlier, so it had to have occurred just in time for the selection.

Where did I say that it had to happen "just in time for the selection"? I never said any such thing.

An earlier mutation would have put it in circulation just as a regularly occurring allele would have.

It couldn't circulate because of negative selection.

That particular argument by Taq that it's a mutation from its dominance therefore no longer applies.

It most certainly applies, as does the lack of sequence variance in the dark allele compared to the light allele. On top of that, the regional differences for dark color adaptations is the cherry on the Sundae.


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