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Author | Topic: How novel features evolve #2 | ||||||||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10042 Joined: Member Rating: 5.3
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Found an article that may be of value:
quote: Full paper can be found here: The genetic basis of adaptive melanism in pocket mice - PMC Another interesting quote from the paper:
quote:
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Taq Member Posts: 10042 Joined: Member Rating: 5.3 |
Yes, but we know that the genes for webbed feet are already in the genome - they pop up regularly even in people. No-one is suggesting - I think - that a mutation causes the webbed feet?
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.
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Taq Member Posts: 10042 Joined: Member Rating: 5.3
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How do we know that the genes for webbed feet were in the parent doggie population? 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.
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Taq Member Posts: 10042 Joined: Member Rating: 5.3
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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). The paper also shows how the dark allele was produced through mutation and then selected for through natural selection, otherwise known as evolution.
Creationists never disputed any particular advantage of random insertions in gene sequences used for adaptation; but only if regulated by genomic programming. What genomic programming? Evidence please.
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. 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.
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Taq Member Posts: 10042 Joined: Member Rating: 5.3 |
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.
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.
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Taq Member Posts: 10042 Joined: Member Rating: 5.3
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Webbed feet in a dog probably would not be from genetic drift. 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.
More than likely such an occurrence would be from a detrimental mutation in a single individual. There are many otters that would disagree.
You have not made any suggestion on how such a mutation could be fixed in a population since breeding . . . Have you never heard of selection? Really?
Anyway, a dog is still a dog not another species It is a dog with a feature not found in its ancestors that came about through mutation. Most people call that a novel feature.
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Taq Member Posts: 10042 Joined: Member Rating: 5.3
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What are these citations intended to prove about new unique functionality? That they come about through random mutations, as shown in the paper.
Clearly, these alleles preexist in the genome and are not receiving new novel coding sequences (long additional strings of base pair coding) but only experiencing shifts in ORF’s. 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.
What known mutational mechanisms are you referring to would cause an allele arising with only 3 or 4-point mutations? Replication errors by polymerases during meiosis, chemical mutagens, radiation, etc. Are you not familiar with how mutations occur?
I would say that this is only modification of existing alleles. What would you say this is?
No shit Sherlock. That's how evolution works. Evolution is descent with modification.
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Taq Member Posts: 10042 Joined: Member Rating: 5.3 |
I thought it was just me that was missing something - it turns out that finding direct evidence for mutation leading to new features is tough (but not impossible). I suppose it does mean that finding the audit trail in genes for speciation is orders of magnitude more difficult and may never be seen. 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:
quote: 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.
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Taq Member Posts: 10042 Joined: Member Rating: 5.3
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You see there must be certain coloration of mice first before there is any kind of selection to take place. 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:
You see mouse coloration is pre —existing so you cannot say it has arisen because of natural selection. 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.
Was the development of beneficial coloration a new and novel trait? No because it had to show up before selection could even work on it. 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.
Again the crux of your argument must consider fixation of these mutations in a population before you can actually say these Novel Traits arose and are not just deformed individuals. Novel traits do not need to be fixed in a population in order to be novel.
Environmental stresses and stimuli cannot exercise the creative causation of highly complex pre-coded genetic information that underlies irreducibly complex systems of adaptation. Evidence please.
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Taq Member Posts: 10042 Joined: Member Rating: 5.3
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Your scenario is right in line with most evolutionists’ beliefs (that is the good news) but those suppositions do not hold up under scientific investigation (that is the bad news).
The paper we are discussing is the scientific investigation, and it does hold up. You can lead a horse to water . . .
The problem is it has never been observed
It is observed in the paper we are discussing.
Do you know who Haldane is? Major evolution calculations are based on Haldane’s work. 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?
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Taq Member Posts: 10042 Joined: Member Rating: 5.3
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How do we know that the genes involved in the dark mice colouration arose from a mutation of the genes coding for light mice? ie how can we distinguish which came first and/or that both haven't always been there? You do this by comparing the synonymous and nonsynonymous mutations. From the paper:
quote: 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).
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Taq Member Posts: 10042 Joined: Member Rating: 5.3
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Thanks Taq, so we can now say with a very high level of certainty, backed up with real hard evidence, that the gene for light colouration preceded those for dark and that the dark mice genes are a mutation of the light mice genes. Yep. The invariance of the dark allele is consistent with a single, recent founder for the gene lineage, at least from my understanding.
But of course, they're still mice.... As they should be, if evolution is true.
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Taq Member Posts: 10042 Joined: Member Rating: 5.3
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But the major problem with creationist gibberish about Haldane is, in my opinion, more fundamental than that. They take Haldane's original calculations as gospel. Then they say that based on these calculations there can't be more than (IIRC) ~1600 adaptive mutations between more basal apes and modern humans. Then they maintain without any evidence that this would not be enough adaptive mutations to make the difference, and that therefore this couldn't have happened. 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.
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Taq Member Posts: 10042 Joined: Member Rating: 5.3
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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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Taq Member Posts: 10042 Joined: Member Rating: 5.3
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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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