What is the mechanism that prevents microevolution to become macroevolution?

This idea that empirical evidence is required here is just wrong. If you really followed the argument I would think that should be clear. When one is bringing out the implications of a known set of facts, the proof is in the reasoning, not in new evidence.If anybody needs to supply evidence, it's the evolutionists who merely assume without evidence, as crashfrog did in a recent post, that mutation explains the development of new phenotypes.I'm sure experiments could be constructed to test some facets of what I'm saying, however, but I'm not in a position to do it.

I've already told you what the evidence is. If you reject it, you certainly haven't provided a reason why.

It seems that the title is not true.Just because evolution is defined as a change in allele frequencies does not mean that all historical evolution can be accounted for simply in terms of changes in frequency without the addition of new alleles. In fact you have been presented with examples where new alleles do appear in bacterial populations. It say that a change in allele frequencies includes the case where no new alleles appear is simply not relevant. What you need is EVIDENCE that new alleles do not appear in sufficient quantity.Moreover the fact is that to explain the observed genetic diversity without accepting a significant role for mutation - which is known to occur - you have to produce a completely ad hoc explanation which to the best of my knowledge you can't even clearly explain - with no evidence at all for it.

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Thinking about mutation in this respect, however, why should that prevent interbreeding either? Mutation simply changes an allele, but if the basic gene is there in both populations why wouldn't the new allele simply combine with whatever other alleles exist in either population?

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It's an area that is being studied. However, a priori, it seems far more likely that cumulative changes could produce incompatible genomes than that there could be a huge number of genetic incompatibilities within an existing population. Moreover incompatible alleles just by being incompatible would have reduced fitness - a constraint that is only relaxed when one of the alleles is removed from the population. Thus it is hard to say that incompatibilities are likely to arise without mutation since otherwise it would require a rare allele to take over at least one of the subpopulations. Which seems less likely to me than a gradually accumulating incompatibility through mutation and drift starting after the populations split.

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Right. I lose track of what I'm trying to say sometimes. Rare alleles WOULD be more likely to be lost, that is, lost to a new population that migrated from the original.

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They are ALSO more likely to be lost through drift after the split. Because the allele is only present in small numbers it can be mmore easily lost to chance than a more established allele.

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f you would just keep mutation out of the picture for the time being and just think through the processes I'm describing, which are all standard science that evolutionists refer to all the time, you ought to be able to follow it all to the logical conclusion I keep pointing out here, which is that genetic depletion IS the overall trend in all these processes. There's nothing of opinion in this at all, it logically follows from an understanding of what these processes actually do.

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Here is the statement you were supposed to be supporting again: So you see that the questin is whether mutation can "take up the slack". You quoted this in your post do I don't see how you could have missed it. Are you really asserting that your claim that mutation cannot compensate for the loss of alleles is based on ignoring mutation ? If so you cannot call it a logical or even a rational argument.Regardless, it is true that you have not produced a valid argument or evidence to support something you are quite happy to call a "fact"

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Well, if you would just follow the argument here, you'll have to see that what presently is credited to mutation is nowhere near supplying the number of useful changes needed, that is, the number needed to rival those changes that take place in every sexual recombination, or for that matter in whole populations as allele frequencies change over time, all of which tend in the direction of decreasing genetic variability.

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Sexual recombination doesn't reduce allele frequency in itself. And without a measurement of the relative rates at which alleles are lost and gained - or at least a good estimate - there can be no valid logical argument. In short I know that I am following the argument because I have found the gaping hole in it.To get a valid answer we need to consider the actual rates at which alleles are lost and added. And you don't have any estimate of those rates. All you offer is an opinion, which you call a fact.

It is possible that new alelles can form without a mutation even occurring, so Faith's concept isn't entirely wrong. I don't think it has been shown to be a major source of new alelles, for reasons that might be apparant.From an encyclopedia article on recombination: Some of that isn't germane but the first part is. To simplify it has been said that recombination is the reshuffling of genes. Given where Faith is coming from I think a little more is needed (sorry if it has been brought up already).There is no process or marker which says 'this is a gene' in the DNA. So it is possible that during one part of meiosis (where the DNA is sliced up and recombined) that a gene will be sliced up. The shorter the gene the less likely that is. If a gene gets sliced up and paired with another sliced up gene with some other purpose, it might create an entirely novel gene.I can't see any evidence of this actually happening, but I might be wrong. Dawkins goes to great lengths to talk about genes as a unit of selection, and one selection pressure is for genes to not be too long, or they will basically be destroyed with this method.I'd be interested to hear from Faith and the biologists for comments on any studies or the like that have been done in this area. I believe that this kind of thing might technically known as a mutation, just as inversions and deletions are.

You are arguing that mutation cannot drive evolution on the basis of rarity, am I right? You are making a rational assertion about the physical world. You need empirical evidence to confirm it. But you are contradicting other known facts about mutation! You keep asking me to "just follow the argument". Are you incapable of accepting that your arguments do not equate to evidence? I'm sure Percy and others have provided several examples of mutations being seen to occur in isolated bacterial populations. In any case there's plenty of stuff out there for you to find.Here's one about the rapid mutation of a particular allele in fruit flies.
High mutation rate of a long microsatellite allele in Drosophila melanogaster provides evidence for allele-specific mutation rates. | Molecular Biology and Evolution | Oxford AcademicAlso, I am still a little puzzled by your stance on this subject. On the one hand you accept that "genetic change" and speciation occur, whilst on the other hand you deny that genes mutate.With this in mind I think you need to further clarify what you mean by "species" and "genetic change".Edited by RickJB, : No reason given.

Hi Mod,What is ultimately confusing to me is Faith's apparent acceptance of both "speciation" and "genetic change", but only as long as the they don't invove new alleles.Isn't the mutation of an allele an example of "genetic change"?Edited by RickJB, : No reason given.

From what I know, Faith is happy with genetic change and mutations. It is her opinion that mutations that cause genetic change lead to a decline in viability overall, and perhaps the loss of an allele. It is her opinion that these mutations may convey certain advantages under some conditions but at a cost of the populations being less viable overall.I could be wrong, but that's how I read it.

Even if life was in some sort of post-fall slowdown, is Faith now accepting that some form of "evolution", complete with some form of "speciation" and "genetic change", will be at work for as long as any viability remains?Edited by RickJB, : No reason given.

How many gennomes do we have? Is this 'mutation' dominant? Do we know how many ppl are so resistant?

I was not aware she ever denied that.

Yes. The mutation alters a protein product, resulting in new function; such mutations are almost always dominant as a rule. (Mutations that disable a protein or remove its function are almost always recessive as a rule.) 33, all of whom are decendants of a single individual who lived in the 18th century.Here's a whole talkorigins page on it. I linked it to Faith before. It has a pretty significant bibliography, too: Apolipoprotein AI Mutations and Information

Thank you Crash. That seems to be very convincing indeed. I'll have to go back upthread and see what Faith has to say? (la-la-la --I'm not hearing you probably)

So, OK, it's dominant, it can't be hidden etc. But the fact that all these people have it apparently from a common ancestor certainly suggests it's passed on just as any allele is, so I don't see any reason to believe it's a mutation. How do you know the ancestor didn't inherit it in the usual way?Edited by Faith, : No reason given.

The fact that all the people with the allele had a relatively recent common ancestor suggests that it was that ancestor who first had that allele - i.e. that it IS a mutation. Once a mutation occurs it IS passed on as any other allele is, so I can't see why you would think that significant.

Apparently the explanation is that it is simply extremely low frequency in the population, not unexpressed or hidden, just present in very few. The actual facts don't suggest that it was inherited in any way other than the normal, and I see no reason to assume that it originated in a mutation from anything you've said. Perhaps I'm missing the essential point you're making? I dunno. It all looks like what I've been describing. Edited by Faith, : No reason given.