Summations Only

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:

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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strong support for the role of Mc1r in the observed phenotypic differences (H.E.H., H. Fujino, J. Regan, and M.W.N., unpublished data).

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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. The authors describe it as a function gain through mutation:

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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.

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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.

I'm not aware of the work, but it does make sense. The traits that we introduce are often beneficial to us, not the plant. For example, the "Golden Rice" that produces beta-carotenes, important for preventing vitamin A defeciencies (which can lead to blindness) in third world Asian countries. What does beta carotene offer the rice? Probably nothing.A very popular gene here in the states is the gene for Roundup resistance. Unless a plant population is under constant selective pressure from Roundup the gene will probably not stick around.

If memory serves, there are wild populations that do not have the frameshift mutation in the nylC gene. I think it is more than fair to state that we can not be 100% certain that one descended from the other. However, a simple one base frameshift mutation is easilyt produced by the known mechanisms of mutation, so the point is moot. Whether that mutation occurred in Flavobacterium or Pseudomonas has little to do with the fact that mutations can produce novel enzymes.ABE: The Ohno paper can be found here:
http://www.ncbi.nlm.nih.gov/...345072/pdf/pnas00609-0153.pdfA quick snippet from the abstract:

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Analysis of the published base sequence residing in the
pOAD2 plasmid of Flavobacterium Sp. K172 indicated that the
392-amino acid-residue-long bacterial enzyme 6-aminohexanoic
acid linear oligomer hydrolase involved in degradation of
nylon oligomers is specified by an alternative open reading
frame of the preexisted coding sequence that originally specified
a 472-residue-long arginine-rich protein.

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Edited by Taq, : No reason given.

That is very true. The abstract led me astray on that one. The original sequence is completely hypothetical, but well argued by Ohno.Overall, I would say that the nylon bug is a much weaker argument than the pocket mice. I think it would be more productive to search for something other than the nylon bug as an example of a novel enzyme produced by mutation.

We ignore it because the evidence doesn't support it.

That evidence still stands. The author arived at an estimate for a mutation rate by measuring the appearance of genetic diseases such as achondroplasia. These are dominant genetic diseases meaning that you only need one copy of the disease allele in order to express the disease phenotype. So when a child is born with one of these diseases while the parents do not have the disease this indicates that the change is due to a mutation.So why would cells guide the process of mutation to produce these diseases? Or are mutations random, producing a wide range of effects?I can also cite the Luria-Delbruck fluctuation experiment, the Lederberg plate replica experiment, as well as direct studies of polymerases all of which demonstrate random mutation. I have gone through these experiments with you in the past, and you still ignore them. The evidence hasn't gone away. The evidence clearly demonstrates random mutation with respect to fitness.

What it means is that you have an ad hoc explanation for guided mutations. The same process produces beneficial, neutral, and detrimental mutations and there is no way to predict which type of mutation it will produce next. They are OBSERVED to be random with respect to fitness. I see a lot of vague claims but zero evidence.

Yes, and those mutations are random with respect to fitness. We are all aware that chemical mutagens and radiation cause mutations. We are also aware of things like the SOS response in E. coli. In each case, the mutations that are produced are random with respect to fitness. DNA repair mechanisms are not specific to any sequence. These repair mechanisms can not tell if the repair will result in a decrease or increase in fitness, nor are they gene specific.Going back to my lottery analogy, a poor person buying more lottery tickets than a rich person does not make the lottery non-random. In the same way, a bacteria producing more random mutations while under stress does not make those mutations non-random. They are still random. Increasing the random mutation rate does not make mutations non-random, it just produces more random mutations.Edited by Taq, : No reason given.

Excellent question. In the case of the SOS response in E. coli it is triggered by DNA damage. The presence of ssDNA and halted replication forks activates RecA. RecA interacts with the repressor LexA which removes LexA from the upstream promoters of certain genes allowing them to be expressed. Amongst those proteins that are upregulated are error prone polymerases and DNA repair mechanisms that can result in gene duplications and other recombination events. Wiki has a decent page on it:SOS response - WikipediaThere is also evidence for increased transposon activity in stressed cells and just plain ol' DNA damage due to starvation conditions. Precisely. It is an increase in the random mutation rate. It is analogous to a gambler playing 10 slot machines at the same time instead of just one. This doesn't change the random nature of each result, but it does increase the chances that the gambler will hit the big jackpot.

I did more than say. I demonstrated with evidence. We have known since the 1950's that mutations are random with respect to fitness because that is what the evidence DEMONSTRATES. We do have the proper technology. We have the technology to determine how mutations occur, when mutations occur, and how they affect fitness. The evidence clearly indicates that mutations are random with respect to fitness.

We don't need to know where the first life came from in order to determine that mutations are random with respect to fitness. As an analogy, we don't need to know where matter came from in order to determine that the roll of the dice in Craps is random with respect to the bets on the table. All we need to do is compare the results when money is on a certain bet and when it isn't, and then compare the results. As it turns out, the odds of rolling craps is not affected by whether your bet is on the Pass line or the Don't Pass line. The result is random with respect to your bet. In the same way, mutations are random with respect to fitness.

This reminds me of a brilliant piece written by Ernst Mayr:"By the end of the 1940s the work of the evolutionists was considered to be largely completed, as indicated by the robustness of the Evolutionary Synthesis. But in the ensuing decades, all sorts of things happened that might have had a major impact on the Darwinian paradigm. First came Avery's demonstration that nucleic acids and not proteins are the genetic material. Then in 1953, the discovery of the double helix by Watson and Crick increased the analytical capacity of the geneticists by at least an order of magnitude. Unexpectedly, however, none of these molecular findings necessitated a revision of the Darwinian paradigmnor did the even more drastic genomic revolution that has permitted the analysis of genes down to the last base pair."
--"80 Years of Watching the Evolutionary Scenery", Ernst Mayr, 2004The essay is quite short and well worth a read, for evolutionists and creationists alike.Edited by Taq, : No reason given.

Each and every time you bring up the randomness of mutations I cite EXPERIMENTAL RESULTS. In this thread I have referenced two experiments which demonstrate random mutations. I even started a thread where I discussed a paper written by Wright who is much more friendly to your ideas of guided mutations than most scientists (thread found here).Now you are once again claiming that we are ignoring some phantom evidence that you fail to supply each time, all the while ignoring the experimental results we post.To help steer this somewhere else, I would be happy to start a new thread on a peer reviewed primary research paper of your choosing (no secondary reviews please). Are you up to the task?

Understanding the relationship between fitness and mutation is vitally important for understanding how novel features evolve.Going back to the pocket mouse example, the authors found that the mutations in the MC1R (which is thought to be responsible for dark fur) only occurred in one of the populations found on dark lava. However, the other populations still had dark fur. This is a very important observation.First, we observe that the lava fields are separated by hundreds of miles. We also observe that the dark allele is strongly selected against in the range between the dark lava fields. Therefore, there is no expectation that the mutations conferring dark fur will be able to move from one lava field to the other given that the dark allele is dominant.This offers a way of testing whether mutations are guided or random with respect to fitness. Given the multitude of possible mutations in different genes that can give rise to dark fur we would not expect random mutations to result in the same mutation in independent populations. If mutations are guided then we would expect the same mutations to occur in each population. What do we observe? Different mutations in each populaton. This is extremely strong evidence for random mutations.We can apply this same knowledge to evolution in general. Given the random nature of mutations and the contigencies within the genomes that they occur in we would expect different solutions to the same problem in different lineages. This is why we see feathers and fur as two separate solutions for thermoregulation in mammals and birds. This is why we see different solutions for eyes, wings, and fins amongst different lineages.So I would say that the random nature of mutations is strongly on topic. However, an extended discussion of why we think that mutations are random probably deserves a focused topic of its own.

Very much so, at least in the opinion of this non-moderator.What is needed is evidence of these guided mutations and how they lead to novel features. I think the pocket mouse example found earlier in this thread may be useful in such a discussion, but I think it should be up to zi ko to choose the examples to be used.