Summations Only

Found an article that may be of value:

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Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5268-73. Epub 2003 Apr 18.
The genetic basis of adaptive melanism in pocket mice.
Nachman MW, Hoekstra HE, D'Agostino SL.
SourceDepartment of Ecology and Evolutionary Biology, Biosciences West Building, University of Arizona, Tucson, AZ 85721, USA. nachman@u.arizona.edu

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Abstract
Identifying the genes underlying adaptation is a major challenge in evolutionary biology. Here, we describe the molecular changes underlying adaptive coat color variation in a natural population of rock pocket mice, Chaetodipus intermedius. Rock pocket mice are generally light-colored and live on light-colored rocks. However, populations of dark (melanic) mice are found on dark lava, and this concealing coloration provides protection from avian and mammalian predators. We conducted association studies by using markers in candidate pigmentation genes and discovered four mutations in the melanocortin-1-receptor gene, Mc1r, that seem to be responsible for adaptive melanism in one population of lava-dwelling pocket mice. 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.

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Full paper can be found here:The genetic basis of adaptive melanism in pocket mice - PMCAnother interesting quote from the paper:

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In most places, these mice have a sandy dorsal pelage and white underbelly, and they inhabit light-colored rocks. In several different regions, however, these mice are found on lava flows. The mice from these lava sites are typically melanic, with dark-colored dorsal hairs and white underbellies. Most of the lava flows are surrounded by light-colored substrate and are isolated from one another by hundreds of kilometers, raising the possibility that melanic mice have evolved independently on different lava flows.
emphasis mine

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Dachsunds were possibly mentioned in the previous iteration of this thread, and they are worth mentioning here again. Dachsunds have achondroplasia, otherwise known as dwarfism. It is caused by a mutation in the FGFR3 gene, just as it is in humans. Presumably, the wild ancestors of dachsunds did not carry this mutation. As far as I know, there is not a wild population of wolves with stunted legs.

The question is whether webbed feet are heritable or not. It could be argued that some webbed feet are due to poor development and not genetics (e.g. Thalidomide). However, webbed feet breed true in many dog breeds so I think it is safe to assume that it is heritable in that case.

The paper also shows how the dark allele was produced through mutation and then selected for through natural selection, otherwise known as evolution. What genomic programming? Evidence please. I guess you missed the fact that different populations of dark mice had different random mutations leading to similar phenotypes? This directly contradicts your claims. Also, the dark allele is product of MUTATIONS.As WK points out above, the immune system is entirely reactionary. It produces a massive B-cell library that express randomly constructed antibodies. If a B-cell binds to an antigen then it is told to make more of that antibody and replicate. This is not anticipation. This is reaction.Edited by Taq, : No reason given.

Could have swore I read that it was in FGFR3. Thanks for the correction. Actually, this makes a lot of sense because FGFR3- homozygotes are usually not viable.Edited by Taq, : No reason given.

The point being that webbed feet are caused by a mutation in one of the many genes that are involved in digit development. Whether that mutation is selected for, selected against, or neutral (i.e. genetic drift) has more to do with the environment than the source of variation, which is random mutations. There are many otters that would disagree. Have you never heard of selection? Really? It is a dog with a feature not found in its ancestors that came about through mutation. Most people call that a novel feature.

That they come about through random mutations, as shown in the paper. The dark phenotype is a novel sequence that was produced by mutations. The mutations changed the ancestral sequence into a sequence that had never existed before in that population. That is the whole point. A novel phenotype came about through mutation, and was then fixed in a population through selective pressures, otherwise known as evolution. Replication errors by polymerases during meiosis, chemical mutagens, radiation, etc.Are you not familiar with how mutations occur? No shit Sherlock. That's how evolution works. Evolution is descent with modification.

In prokaryotes it is a lot easier due to a genome that is 1/1000th the size of eukaryotes and much simpler regulatory networks. In eukaryotes it can be very difficult to ferret out the mutations that cause a change in morphology. The paper under discussion is a great example of this:

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This difference is controlled in large part by the interaction of two proteins, the melanocortin-1-receptor (MC1R) and the agouti-signaling protein (12—14). MC1R is a G protein-coupled receptor that is highly expressed in melanocytes, the specialized cells that are the site of pigment production. A peptide hormone, -melanocyte-stimulating hormone, typically activates MC1R, resulting in elevated levels of cAMP and increased production of eumelanin. Agouti is an antagonist of MC1R; local expression of agouti results in decreased synthesis of eumelanin and increased production of pheomelanin.

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A change in melanin and pheomelanin can come about through changes in more than one gene. Changes in MC1R or Agouti can change expression patterns. A chaperone protein involved with either of those two genes can once again change expression patterns. A regulatory protein upstream of either gene can change expression patterns. Changes in the expression of the peptide hormone that binds to MC1R can change expression patterns. And this is just for coat color. For morphological features the number of genes involved is an order of magnitude higher.Edited by Taq, : No reason given.

And that is exactly what happened. The mutations in MC1R produced novel coloration that was then selected for. Here is the picture of the two different colorations on the two substrates. It is not that hard to figure out why there is selective pressure through predation: We are saying that it came about through mutation. That is the whole point. Mutations produce novel phenotypes which are then selected for, otherwise known as evolution. Have you not been listening? This is like the 3rd time I have said this in this thread. That is a howler, and a symptom of some very serious denial. A novel trait is a trait that was not in the population prior to that point. Once the mutation/s occurred, it was a novel trait. Whether it was selected for has nothing to do with whether it is novel or not. Once more with feeling . . . selection has NOTHING to do with whether a trait is novel or not. Novel traits do not need to be fixed in a population in order to be novel. Evidence please.

The paper we are discussing is the scientific investigation, and it does hold up.You can lead a horse to water . . . It is observed in the paper we are discussing. Do you know the problems with Haldane's work? Such as his calculations did not correctly model the fixation of two alleles, nor did it take into account selective sweeps?

You do this by comparing the synonymous and nonsynonymous mutations. From the paper:

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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). The average level of nucleotide diversity among light alleles ( = 0.21%) is >10 times greater than nucleotide diversity among dark alleles ( = 0.01%). The reduced variability seen among the dark Mc1r alleles is the expected pattern if selection has recently fixed an adaptive substitution (26—28).

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There has been more time for sequence variation (aka neutral mutations) to build up in the light variant than in the dark variant demonstrating that the dark variant is more recent. This also jives with the recent appearance of the dark lava (<1 years).

Yep. The invariance of the dark allele is consistent with a single, recent founder for the gene lineage, at least from my understanding. As they should be, if evolution is true.

It's like the story of the engineers and the bumblebee. The engineers wrote a computer program that attempted to model the aerodynamics of the bumblebee. What did their model show them? That the bumblebee should not be able to fly.At this point we have two choices. On one hand, this could indicate that the bumblebee uses supernatural powers to stay aloft. On the other hand, the model is wrong since obviously, bumblebees can fly. Science opts for the latter, and creatoinists the former. They just can not understand the simple concept that the map is not the territory.

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. 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.

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.