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Author Topic:   How novel features evolve #2
Dr Adequate
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Message 91 of 402 (664409)
05-31-2012 5:11 PM
Reply to: Message 89 by Taq
05-31-2012 4:17 PM


Re: Getting off topic here
Quite so. They keep jumping up and down shouting: "All the evidence may show that it's true, but it's impossible in principle!"

They don't grasp that if this is so, then this falsifies their principles.


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Taq
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Member Rating: 2.6


(2)
Message 92 of 402 (664416)
05-31-2012 6:12 PM
Reply to: Message 90 by Wounded King
05-31-2012 4:29 PM


Honestly, I'd quibble with this argument. The synonymous/nonsynonymous ratio tells us more about selection and the timing of the selective pressure rather than the relative temporal origin of the alleles' necessarily. So while it is consistent with a recent origin I'd suggest it is equally consistent with a strong selective pressure bringing an already existent low frequency allele up to near fixation levels. I'd be careful of treating this as some sort of slam dunk for the timing of when the allele first arose.

My population genetics is a bit rusty, so feel free to correct me where needed . . .

They didn't even point to the synonymous/nonsynonymous ratio, but just overall sequence diversity. There was just one polymorphism in the dark allele while there were 13 in the light allele. I could see a possibility where the dark allele could lose function with fewer mutations than the light allele, but given the already strong identity between the two I just don't see how that could be supported.

But again, I could be completely mistaken on this.

I'd say that the fact that there is a different basis for melanism in the other dark population of the same species is better evidence for the dark alleles being a derived trait than the variation levels. If there was an already existing melanic trait in the species it would be reasonable to expect that it would be the selected melanic form in both populations.

Extremely good point. It also demonstrates that there is strong selection against the dark allele in the range spanning the two lava fields, otherwise the MC1R allele could move between lava fields through gene flow.

Edited by Taq, : No reason given.


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Tangle
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Posts: 6676
From: UK
Joined: 10-07-2011
Member Rating: 2.7


(2)
Message 93 of 402 (664418)
05-31-2012 7:01 PM
Reply to: Message 90 by Wounded King
05-31-2012 4:29 PM


WK writes:


I'd say that the fact that there is a different basis for melanism in the other dark population of the same species is better evidence for the dark alleles being a derived trait than the variation levels. If there was an already existing melanic trait in the species it would be reasonable to expect that it would be the selected melanic form in both populations.

Presumably that means that there's a different mutation in another location in the other dark mice that does the same job. Bugger, we now need to find two smoking guns not just one.

(Or God is an even bigger tease than we first thought; those fossils were only the start of the big wind up.)


Life, don't talk to me about life - Marvin the Paranoid Android

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Wounded King
Member (Idle past 2172 days)
Posts: 4149
From: Edinburgh, Scotland
Joined: 04-09-2003


(1)
Message 94 of 402 (664419)
05-31-2012 7:09 PM
Reply to: Message 92 by Taq
05-31-2012 6:12 PM


They didn't even point to the synonymous/nonsynonymous ratio, but just overall sequence diversity.

Sorry for the confusion, I assumed you were talking about synonymous mutations since you specified that the mutations were neutral.

I could see a possibility where the dark allele could lose function with fewer mutations than the light allele, but given the already strong identity between the two I just don't see how that could be supported.

I'm not sure what you mean, I'm not suggesting purifying selection is the reason for the lack of variation. The point is that a sudden switch in selective pressure can vastly inflate the proportion of a low frequency allele beneficial in a new environmental context, this expansion will be accompanied by a similar expansion in the representation of the SNPs/haplotype associated with that allele. So the lack of variation can represent a recent expansion rather than a recent origin, for exactly the same pop. gen. reasons.

TTFN,

WK


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Wounded King
Member (Idle past 2172 days)
Posts: 4149
From: Edinburgh, Scotland
Joined: 04-09-2003


Message 95 of 402 (664421)
05-31-2012 7:22 PM
Reply to: Message 93 by Tangle
05-31-2012 7:01 PM


Bugger, we now need to find two smoking guns not just one.

Which is almost exactly what Zaius was saying in Message 48.

TTFN,

WK


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RAZD
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Posts: 19756
From: the other end of the sidewalk
Joined: 03-14-2004
Member Rating: 5.6


(1)
Message 96 of 402 (664426)
05-31-2012 9:49 PM
Reply to: Message 74 by zaius137
05-30-2012 11:08 PM


Re: Getting off topic here
Hi zaius137

The problem is it has never been observed…

Corrected.

Do you know who Haldane is? Major evolution calculations are based on Haldane’s work.

Yes, do you?

Do you understand that math cannot alter or affect reality in any way? That if there is a conflict between math and reality that reality wins every time?

Math is a model, a hypothetical representation, and when falsified needs to be altered, fixed, or forgotten.

Curiously, I note that ...

http://en.wikipedia.org/...ixation_%28population_genetics%29

... does not mention Haldane nor any problem with fixation occurring. In fact there is an equation there ...

Enjoy.

Edited by RAZD, : < & > instead of [ & ]


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Tangle
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From: UK
Joined: 10-07-2011
Member Rating: 2.7


(1)
Message 97 of 402 (664447)
06-01-2012 3:25 AM
Reply to: Message 95 by Wounded King
05-31-2012 7:22 PM


WK writes:

Which is almost exactly what Zaius was saying in Message 48.

That's fair.

However, at that point it was irrelevant that there were (at least) two genes responsible for coat colouration in different populations of these mice as I thought we had found a definite mutation in the population we were looking at and had shown that it alone was dictating colour.

There's still a huge amount of evidence pointing to the fact that it's a recent mutation causing the dark colour change, but we can't yet totally rule out other possibilities.

Do you feel that we've got to the legal test of beyond reasonable doubt?


Life, don't talk to me about life - Marvin the Paranoid Android

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Taq
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Posts: 7673
Joined: 03-06-2009
Member Rating: 2.6


(1)
Message 98 of 402 (664487)
06-01-2012 11:30 AM
Reply to: Message 97 by Tangle
06-01-2012 3:25 AM


Do you feel that we've got to the legal test of beyond reasonable doubt?

The icing on the cake is the strong negative selection on the dominant dark allele in the light colored ranges. According to their findings, you could only find dark mice in light colored environments that are near a lava field. I think it selection is strong enough that this allele should not survive for many generations without the right niche to fill.


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Tangle
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Posts: 6676
From: UK
Joined: 10-07-2011
Member Rating: 2.7


(2)
Message 99 of 402 (664516)
06-01-2012 3:08 PM
Reply to: Message 98 by Taq
06-01-2012 11:30 AM


Yup, I'll go with that.

But it's not what I was hoping to get out out of this which was direct proof that a new mutation caused a physical change to an obvious characteric which was then selected for.

Very, very close though.


Life, don't talk to me about life - Marvin the Paranoid Android

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zaius137
Member (Idle past 1487 days)
Posts: 407
Joined: 05-08-2012


Message 100 of 402 (664611)
06-02-2012 9:39 PM
Reply to: Message 82 by Wounded King
05-31-2012 5:58 AM


Re: Which came first?
Wounded King my friend…

I honestly enjoy your understanding of genetics (it is far better than mine is).

So within these various papers we have the initial example of the light to dark mutation set in the pocket mice. The function of the melanocortin receptor is to mediate the signalling from certain hormones which bind to the receptors, this mediation is done via the generation of cyclic-AMP (cAMP), the level of cAMP then determines whether the target cell produces eumelanin (Darker) or phaeomelanin (Lighter). So in terms of the genetic concepts of loss- or gain-of-function the melanic pocket mouse mutations in Mc1r are gain-of-function mutations giving rise to a more sensitive receptor balanced more towards eumelanin production (Nachman, 2005).

I completely follow your explanation here (thanks) but the further connection between the mutations in Mc1r giving rise to a “more sensitive receptor balance” seems to me as a vague connection (although cited in the paper). What do these mutations actually accomplish in the mechanism for coloration changes; are they the sole control of the balance of cyclic-AMP and do these “various papers” make that proper connection? So is the “loss or gain-of-function” in the melanic pocket mouse still a case of allele mixing or is it because of mutations on Mc1r (a polymorphism in that species)? Overall, I am leaning to the former.

However when we look at the other papers we see a light phenotype arising both from gain-of-function mutations increasing the expression of the Agouti gene, which inhibits the binding of melanocortin to its receptor, and through loss-of-function mutations where the binding specificity of the receptor for melanocortin is reduced and so is the level of cAMP, tipping the balance towards phaeomelanin production.

I maintain that coloration in this mouse is reversible in all populations. If indeed these mutations are the mechanism for tipping the balance of (cAMP) then genetic recombination reverses the process (by gene flow). Very interesting but if anything, this only points to a very fluid adaptation mechanism (very Mendelian and not “unique new traits” as some participants would suggest).

…Taken to an extreme the alternative approach rapidly takes us to a position where our imperfect knowledge of the genetic makeup of previous generations makes it impossible to definitively consider any mutation novel as we can't confidently state that it never occurred transiently in any ancestral population.

The dilemma you pose might be rectified to a certain degree by examining other genomes, maybe those of a fruit fly or E. Coli. Regulated populations of fruit flies combined with long-term studies provide a better-defined ancestral population.

So we have a very heterogeneous mixture of mutations, albeit all centered on one or two genes, some are gain-of-function mutations, some are loss-of-function, In some populations the derived mutations are those producing the light colouration, in others the dark and in some there are a mixture of derived alleles in both genes giving rise to a spectrum of melanic phenotypes.

Here is some interesting finding in fruit flies indicating a very complex interaction between genes (not just one or two as the paradigm exists) and a overall tendency to retain Heterozygosity.

http://www.arn.org/.../experimental_evolution_in_fruit_flies

I suggest that the adaptive mechanism is the sole “novel new trait” source. The mechanism in question defies the Darwinian explanation via gradualism. It is a mechanism that cannot arise by processes of chance and it transcends the idea of point mutations in its origin; it is like asserting that a machine can produce itself before there were any other machines present. It is God created.


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Tangle
Member
Posts: 6676
From: UK
Joined: 10-07-2011
Member Rating: 2.7


(3)
Message 101 of 402 (664618)
06-03-2012 5:21 AM
Reply to: Message 100 by zaius137
06-02-2012 9:39 PM


Re: Which came first?
Zaius writes:


Here is some interesting finding in fruit flies indicating a very complex interaction between genes (not just one or two as the paradigm exists) and a overall tendency to retain Heterozygosity.

It's interesting work but doesn't tell us very much except that everything is far more complicated than I for one would like it to be. They conclude:

We conclude that, at least for life history characters such as development time, unconditionally advantageous alleles rarely arise, are associated with small net fitness gains or cannot fix because selection coefficients change over time

You have to ask what actual selection pressure exists in these populations that would be strong enough to fix a new allele? Not much and then if there is anything it changes, it seems.

The beauty of the mice example was that the selection pressure was strong and obvious, but even there, the complexity of the mechanisms involed put an irrefutable case maddeningly just out of reach. But it looks like it's getting close.

ABE - as an irrelevant aside, the sheer messiness and complexity of these systems are evidence against design.

Edited by Tangle, : Afterthought.


Life, don't talk to me about life - Marvin the Paranoid Android

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zaius137
Member (Idle past 1487 days)
Posts: 407
Joined: 05-08-2012


Message 102 of 402 (664704)
06-04-2012 12:22 PM
Reply to: Message 101 by Tangle
06-03-2012 5:21 AM


Re: Which came first?
Tangle my friend…

You have to ask what actual selection pressure exists in these populations that would be strong enough to fix a new allele? Not much and then if there is anything it changes, it seems.

Actually very strong artificial selective pressure was applied.

quote:
Drosophila melanogaster is a model organism for the study of genetics and some laboratory populations have been bred for different life-history traits over the course of 30 years. Professor Michael Rose, of UC Irvine, began breeding flies with accelerated development in 1991 (600 generations ago). Doctoral student Molly Burke compared the experimental flies with a control group on a genome-wide basis.
http://www.arn.org/.../experimental_evolution_in_fruit_flies

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Tangle
Member
Posts: 6676
From: UK
Joined: 10-07-2011
Member Rating: 2.7


(1)
Message 103 of 402 (664708)
06-04-2012 12:51 PM
Reply to: Message 102 by zaius137
06-04-2012 12:22 PM


Re: Which came first?
Zaius writes:

Actually very strong artificial selective pressure was applied.

It may be that there were high selective pressures but there's nothing in your article that tells me that. Sadly, the paper itself is not freely available and I'm not relying on an ID site to tell me what's in it.

However, as I pointed out, the paper's conclusion suggest a rather different emphasis to your own.

We conclude that, at least for life history characters such as development time, unconditionally advantageous alleles rarely arise, are associated with small net fitness gains or cannot fix because selection coefficients change over time

Life, don't talk to me about life - Marvin the Paranoid Android

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Taq
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Posts: 7673
Joined: 03-06-2009
Member Rating: 2.6


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Message 104 of 402 (664709)
06-04-2012 12:58 PM
Reply to: Message 100 by zaius137
06-02-2012 9:39 PM


Re: Which came first?
I completely follow your explanation here (thanks) but the further connection between the mutations in Mc1r giving rise to a “more sensitive receptor balance” seems to me as a vague connection (although cited in the paper). What do these mutations actually accomplish in the mechanism for coloration changes; are they the sole control of the balance of cyclic-AMP and do these “various papers” make that proper connection? So is the “loss or gain-of-function” in the melanic pocket mouse still a case of allele mixing or is it because of mutations on Mc1r (a polymorphism in that species)? Overall, I am leaning to the former.

There are several proteins involved in the timing and amplitude of eumelanin. MC1R is just one of the proteins in that chain. A mutation in any link in that chain could result in change in eumelanin expression, both the timing and amplitude. They did do some in vivo work, and they were able to demonstrate hyperactivity for the MC1R allele:

quote:
Functional studies using Mc1r constructs in an in vitro expression system can be used to measure the relative effect of the four mutations on the activation of the receptor. Preliminary results from cAMP assays indicate that the dark allele encodes a hyperactive receptor relative to the light allele, providing strong support for the role of Mc1r in the observed phenotypic differences (H.E.H., H. Fujino, J. Regan, and M.W.N., unpublished data).

From the work done so far, the mutations in MC1R result in a receptor that is more sensitive than the MC1R in light mice causing overexpression of eumelanin which is responsible for the dark pelage.

So is the “loss or gain-of-function” in the melanic pocket mouse still a case of allele mixing or is it because of mutations on Mc1r (a polymorphism in that species)? Overall, I am leaning to the former.

The authors describe it as a function gain through mutation:

quote:
Third, the dark allele is dominant over the light allele, consistent with observations of Mc1r mutations in the mouse (11, 16) and other organisms (21–25). In the laboratory mouse, loss-of-function mutations at Mc1r are recessive and result in light color, whereas gain-of-function alleles are dominant and result in dark color (16). All heterozygous mice observed at the Pinacate site are dark with unbanded hairs and are phenotypically similar to the homozygous dark mice.

This is not due to allele mixing since Dd mice are dark as are DD mice. The dark allele is dominant. The dark allele was produced by mutation, and was then selected for in areas with dark lava. So we have a novel feature that was produced by mutation and then filtered through selection in two different environments. Sounds like evolution to me.


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Dr Adequate
Member
Posts: 16085
Joined: 07-20-2006
Member Rating: 10.0


(2)
Message 105 of 402 (664713)
06-04-2012 1:16 PM
Reply to: Message 102 by zaius137
06-04-2012 12:22 PM


Re: Which came first?
That's not artificial selection. Artificial selection is where the experimenter decides which organisms should reproduce. The unguided adaptation of an organism to an artificially created environment is natural selection. The "selective pressure" was not artificial, the environment was.

As to whether it was "very strong", no probably not. The fruit flies were coddled. They were given everything they wanted, the experimenters did everything they could to ensure the survival of every mutant strain they managed to come up with. The artificial environment relaxed selective pressure on the flies, thus insuring the survival of strains which we know do not exist in the natural environment.


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