Summations Only

And that too was covered in the example.The webbed feet were inheritable.If a Creationist does not want to accept the fact of Evolution, then evidence will seldom sway them.Those that do honestly look at the evidence though soon abandon Creationism; and that is what drives the avoidance schools, the avoidance textbooks, the avoidance radio and TV networks, the avoidance browsers ...

I agree. But the more facts we have, the harder it is to deny. And anyway, I'd love to be able to demonstrate it from direct evidence myself just for its own sake.
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But today we can identify not just individual species from a DNA sample, but often specific populations within a species.That shows that genomes do change over time.

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A key problem in evolutionary biology is to connect genotype with phenotype for fitness-related traits.

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It is apparent that the conclusion in your citation for changes in color of the studied mice (second paper) are the result of expressions of different alleles in the genome (a start codon disruption).

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The black-and-tan mutation in the laboratory mouse produces a dark dorsum with unbanded hairs and is caused by an insertion disrupting the dorsal promoter, ≈15 kb 5′ of the start codon (15). We reasoned that a similar mutation in C. intermedius might be detected through linkage to polymorphisms at neutral sites over moderate genomic distances (0—50 kb, depending on the age of the mutation). We observed 16 single-nucleotide polymorphisms and 5 insertion/deletion polymorphisms, including several at intermediate frequencies; none showed an association with coat color.

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Reference (15)

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We demonstrate that the distinct insertions in a, a(t) and Aw cause pigmentation differences by selectively inactivating the expression of different forms of agouti transcripts.

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The genetic basis of adaptive melanism in pocket mice - PMC

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Creationists never disputed any particular advantage of random insertions in gene sequences used for adaptation; but only if regulated by genomic programming. This principle is obvious in the immune defense mechanism of higher mammals to anticipate infections as well as changing the expression of preexisting gene sequences; for mice color and other phenotype characteristics. Creationists have always maintained that random mutation with out regulation is disadvantageous or antithesis to an organism. In other words, the mutations are to provide adaptation of the genome. It is contrary to the evidence that these types of mutations are capable of a speciation event in an organism. This rules out mutations as a mechanism for evolution but promotes the viewpoint of mutations for adaptation. Edited by zaius137, : No reason given.

(jar) my friendWebbed feet in a dog probably would not be from genetic drift. More than likely such an occurrence would be from a detrimental mutation in a single individual. You have not made any suggestion on how such a mutation could be fixed in a population since breeding with a normal dog would probably mask the deformity (dogs are diploids). Anyway, a dog is still a dog not another species; albeit deformed.

OK, so that wasn't me, it was Taq. That aside your point is obscure, are you claiming that these were always existing alleles rather than novel? That the only difference is in expression changes?If the first then it is largely a moot point, the paper identifies 4 amino acid substitution mutations (not start codon disruption as you claim) in Mc1r, all of which are single nucleotide substitutions. The authors don't definitively identify which one or more mutation is the actual cause of the melanic phenotype in the Pinacate mice but it is hard to see what argument you could make that would bar such an allele arising at random through known mutational mechanisms although I suppose a probability case could be raised if 3 or 4 of the substitutions are required.The paper also notes that there is an entirely different basis for melanism in the Pinacate mice than in the similarly phenotyped melanic Armendaris mice. They also note that these specific Mc1r mutations are distinct from ones that have previously been associated with melanism in other melanic mice, again a point arguing against any form of programmed adaptation.I'm still confused as to what you meant when you describe the mutation as 'a start codon disruption', the only thing I can think is that you were getting mixed up by the description of the black-and-tan mutant mouse ... But even then the mutation clearly isn't described as a start codon disruption, it is a disruption of the promoter sequence roughly 15kb away from the start codon. You don't seem to have understood this paper very well. What you seem to be saying is that creationists will admit the existence of beneficial mutations provided they are allowed to hold an unfounded belief that these mutations were the product of intelligent design. Where is the evidence for such genomic programming? I think this characterisation needs to be clearer. Are you saying that the mere existence of the immune system anticipates the existence of the phenomenon of infection in general or are you making the much more controversial claim that the immune system anticipates specific antigen challenges?If it is the second then this just highlights one isssue with the IDist creationist approach, ignoring selection and the generative power of random mutation. The generation of immune variation through VDJ recombination is well understood and it is not based on any sort of specific anticipation of a challenge but rather on building up a vast repertoire of immune variation such that almost any immune challenge will have a suitable epitope that is targeted by some antibody. The generation of this vast immune repertoire is principally driven by the recombination of of the V(D)J elements, addition of random untemplated nucleotides in complementarity determining regions and through subsequent somatic mutations in the immune cells. These mechanisms allow the generation of sufficient diversity to recognise more than 10⁷ different epitopes. The system also produces many broken recombinations, including some frame shifts which effectively destroy the MHC protein, and long stretches of untemplated nucleotide which are effectively non-functional, many of these non-functional forms are strongly selected against in the bone marrow so what is seen circulating in the body is already a population selected for a minimal level of functionality.This is not anticipation in any meaningful sense. Yes they have, they just haven't provided substantive evidence to support the claim. No one disputes the existence of deleterious mutations, but to claim that all deleterious mutations are random and all beneficial ones the result of 'programming' requires some really substantial evidence to support it because at the moment all the evidence suggests they are both generated through exactly the same molecular mechanisms. Contrary to what evidence? There is good evidence that small genetic changes in one or 2 genes can produce hybrid inviability and
sterility or postzygotic reproductive isolation, key elements of speciation under the BSC (Presgraves et al., 2003;Mallet, 2006). That isn't to say that we can identify specific causative mutations that led to speciation, because it turns out there can be hundreds of such hybrid incompatibility genes between species and it is challenging to impossible to determine which one would be the initial isolating mutation, especially since these may have arisen subsequent to reproductive isolation through some entirely different mechanism such as geographical isolation of the parent and daughter populations.The genetic evidence for small mutations giving rise to reproductive isolation is clear. Where is your evidence that such mutations can't contribute to speciation?TTFN,WKEdited by Wounded King, : spelling

Would the same random insertions, then, have no particular advantage if they were not regulated by genomic programming?Why not? They'd be the same mutations. Again, why? A mutation has the same value, for good or ill, no matter how its produced. If a mutation would be good if produced by random mutation with regulation, then it would also be good if produced by random mutation without regulation.If I win a million dollars in the lottery, the money is just as valuable to me if the lottery wasn't rigged in my favor as if it was. This barely means anything. What do you think "adaptation" means? Which evidence would that be, then? Er, what? Do white blood cells have a power of precognition now?---P.S: If you wish to be honest, do not use phrases such as "Creationists have never disputed ..." and "Creationists have always claimed..."Creationism does not constitute a homogeneous body of thought. What you personally have always asserted and never disputed is one thing, but creationists as a whole have very little in common besides a belief in a god (not always the same one) and a preference for magical explanations for things.Edited by Dr Adequate, : No reason given.Edited by Dr Adequate, : No reason given.

Actually this is incorrect, the achondroplasia (or chondrodysplasia) in dogs is caused by an additional copy of FGF4 rather than a mutation in FGFR3 (Parker et al., 2009). The authors do however speculate that the effect of this additional copy may be to indirectly cause misexpression of FGFR3.In regard to the current discussion they make this observation ... Intriguingly they looked for a particular combination of genetic characteristics, an FGF4 gene with a particular rare haplotype that the retrogene copy has and the 24Kb haplotype that characterises the site where the retrogene inserted. They didn't find that combination in any modern dog breed that they looked at but did find it in wolves from Europe and the middle east.They also raise they key issue when looking at domestic dog breeds in the context of evolutionarily novel features ... TTFN,WK

What do you think genetic drift is? You seem to be using it here in a context that makes very little sense. Genetic drift is a phenomenon like selection that acts on already existing variation, it does not generate novel variation itself. The question is what makes this a 'detrimental' mutation? If it provides a selective advantage to the organism is it still a 'detrimental' mutation? Now here the answer could be genetic drift, at least that and a fair helping of selection. Of course in the case of domestic dogs the answer is almost certainly artificial selection, humans chose to systematically breed dogs with the trait with other dogs with the trait until the trait became fixed within the breed. The basis of speciation is a separate question from the origin of novel features. If you want to talk about speciation you should probably start a thread on that topic. If we are discussing the de novo origin of a feature we are rarely going to be discussing speciation since we are interested in how the trait arises within a population.TTFN,WK

Hi again Tangle,catching up here ... You lasted 48 hours talking about biological facts? wow. As is the word "adaptation" (ie microevolution as an accepted part of evolution, due to force of evidence ... but call it a different word to hide the fact). The bugbear for creationists is macroevolution, but not biological macroevolution per se, but the reptile becoming mammal macroevolution type changes. Yes it is a mutation, just a rather frequent type that disrupts developmental processes, hence it occurs in many species.My original intent was to start with web footed dogs and short legged dogs, then segue into otters as fellow carnivores with high usage of webbed feet and short legs, then to seals.When does a new trait become undeniably novel?The problem here of course is that this uses "inference" to go from one species to the next, so maybe what we need is to look into the ancestors of these species to see where they came from (as in the use of horses on the Dogs will be Dogs will be ??? thread... which creationists shy away from ... ).Perhaps we need to look at horses (or something similarly well evidenced in the fossil record) and then show that the stages from one to the next are simple adaptive steps such as seen in living species? This is the problem - creationists are comfortable with misinformation if it suits their beliefs. We've seen many here that are like Vanessa's lady at the conference that prefers her belief over truth.You can bring a horse to water, but you can't make it drink.Enjoy.

Actually, you are wrong on all counts.It's obvious that you are clueless what a detrimental mutation is if you think that webbed feet in this case was one.And I also explained the method that led to the mutation becoming fixed in terms an eight year old could understand.Since the full explanation was in Message 51 over in the first thread I'll repeat it for you here.

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Let me give this a try.

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There is a population of doggies.

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The doggies have puppies.

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A few of the puppies are not perfect copies.

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Those puppies have webbed feet.

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The other puppies think they look funny and call them names.

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The environment changes; water levels rise.

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The puppies with webbed feet were happy; they played and swam and all hung out together while they laughed at the puppies without webbed feet that couldn't swim real fast all the way from here to there and all the way back again.

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The puppies without webbed feet moved to higher ground and they played chase and catch the tail and run around the tree and laughed at the puppies with webbed feet.

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Soon there were two different populations, the clean foot puppies and the web foot puppies.

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And that is how evolution works.

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The two populations developed through sexual selection; the clean-foot puppies laughed at the web-foot puppies and the web-foot puppies knew that clean foot puppies had cooties.It really is that simple.The process is the same regardless of the number of such events. Homo sapiens is still just a Primate.

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.

It's also pretty damn cool

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.