A test for claimed knowledge of how macroevolution occurs

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Well, I don't think those are mutations, you see

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Why not ? It’s explicitly about changes to the DNA sequence.

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I think they are normally occurring variations based on the sexual recombination of built-in alleles.

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You don’t actually know what the graphs are showing, do you ?
They are showing the frequency of particular changes in the gene sequences. Eg “A <> G” represents the replacement of adenine with guanine or vice versa.

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But this is all interesting because of the fact that evos do interpret everything in terms of mutations and I don't

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Given that you are interpreting mutations as “normally occurring variations based on the sexual recombination of built-in alleles” I think the problem is yours. Especially in the light of Message 116

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Well, but aren't you just talking about observed differences, and how do you know those differences are the result of mutations rather than the result of sexual recombination producing a new set of alleles?

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What makes you think that sexual recombination would produce new alleles. If it did why wouldn’t they count as mutations ? And why do you think that actually comparing the sequences doesn’t give all the information you need ?

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Yes, I'm more or less winging it, so I expect to have a better understanding if the discussion progresses

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Spouting nonsense because you don’t know what you are talking about is not a good way to gain understanding.

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but those differences in the placement of chemicals must also be the case when one allele replaces another

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And that is showing no sign of gaining understanding. Yes, alleles differ in sequence. But if the sequence found in the child does not match the sequence for the gene in either parent, it has to be a mutation.

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Besides, this presentation of supposed mutations is just too organized for how mutations are normally described as random

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At the level of the chemicals some substitutions are more probable than others. That is what the graphs show. (Besides the fact that we are talking about probabilities because these changes are random). If you roll two dice some totals are more likely than others. It’s still random. And that isn’t even the randomness we’re really talking about when we call mutations random.

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I said before, this is revolutionary information, isn't it? It simply does not fit the definitions we usually encounter.

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No, it’s just a detail that you won’t know about if you just skim the surface - and you haven’t even got that far.

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So in fact the pattern more reasonably reflects built in variation than mutations.

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Are you literally suggesting that differences from the parent’s genes are most likely not differences from the parent’s genes ? Because differences from the parent’s genes are mutations.Or perhaps what you are saying is better expressed as “mutations are built into the reproductive process”.

The B and the b show up as sequences of DNA and there will be a range of DNA sequences that correspond to each. Alleles are largely identified by effect, but if different mutations cause the same effect the resulting alleles would usually be considered distinct (assuming we know).I should point out, again, that the relationship between genes and morphology is complicated so the “effect” is not a guaranteed - or simple - thing once you get beyond protein sequences.

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Not only do I think this idea of millions of years is nutz, I think the idea that mutations create healthy alleles is also nutz.

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Millions of years is a fact. And if mutations are random the only thing stopping them from creating “healthy alleles” is probability. Thus it is at least possible in principle - unless you assume a non-random mechanism that prevents it - and even to say it is too unlikely requires evidence.

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Thank you. I'm sure there are things I'm misunderstanding but I also have the impression that the definitions of things change every time there's a new episode of this kind of discussion.

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I think you will find that that is almost all your misunderstanding.

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I get the idea for instance that there are many genes for a particular trait, and the next time the subject comes up, no, it's that a single gene can make a protein or proteins that make many different traits, and so on and so forth

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And in this case it certainly is your misunderstanding. Aside from the fact that there is no change of definition at all, this is just the reality being more complicated than you assumed. A gene can contribute to many traits and many genes can contribute to a trait - there is no contradiction there. And when you remember what real genes actually do it shouldn’t even be a surprise.

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The main thing seems to be that you all see mutations where I see normal built in variation and this has never been satisfactorily sorted out

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As we have seen you can see “normal built in variation” even when we are talking about mutations - where there is no doubt at all. That shows where the main problem is.

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I've argued this over and over and over again and I think it still holds but you are always throwing new things at me and haven't REALLY addressed my arguments. My main argument is that to get new phenotypes all that has to happen is reproductive isolation of a portion of a species population

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Now that may be true, but what has to be explained is not just “new phenotypes” but new species. And variations that go beyond the limits observed in breeding. Even in breeding mutations occur and are used in shaping new phenotypes - so regardless of what is “needed” mutations are going to play a part.And let us not forget that you insisted that bottlenecks would produce new phenotypes - even claiming the elephant seal and the cheetah as examples. Yet you never pointed to even one phenotypic change in either species.

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This is why I point a lot to "ring species" where phenotypic changes occur from population to population around some kind of geographic obstacle.

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But you have never shown that “ring species” support your ideas. They are entirely consistent with standard evolutionary theory which you reject.

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You all believe this is due to mutations. I don't. I think the only thing necessary is the isolation of a small number of individuals from the previous species/population.

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I suggest that all breeding can do is to create a motley collection of phenotypes while additional mutations are needed to explain new species - at least in the general case.

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Then there were the Jutland cattle, or was it sheep, whatever. This herd of whatever it was had spontaneously split into four smaller herds that somehow got reproductively isolated, by preference perhaps as in genetic drift, or some geographic isolation, I'm not sure. It's been a long time. But the point of the story that was posted here was that striking changes developed in each of the four different groups in a very short period of time. Microevolution again, no need for mutations, completely new phenotypic presentation in short period of time.

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And yet none of them is a new species.

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I also bring up the wildebeests, the African gnus that form a huge herd, millions I think. They all look alike, but there is a smaller population some distance away that has a different look to it. The big population is called I think the black wildebeests, the smaller population is called the blue wildebeests because there is a bluish tone to their hide.

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And how do you know that mutations weren’t involved in the separation of the two species ? You keep giving us what you claim are examples but you never show that they support your claims.

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Dogs and domesticated cattle are also examples I've used, and I've even suggested a laboratory experiment with mice. I think all that ever happens is that I get ignored or insulted, told I just don't understand evolution etc., or evos come along and insist it's all due to mutations and that's the end of the discussion.

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I think you have got it the wrong way round. You are the one who usually ignores or insults people and accuses them of not understanding - and you insist that your ideas are right and that’s the end of discussion. Consider this whole long post - you don’t produce any real evidence at all. You don’t get to win by just insisting you are right - even if we didn’t have evidence.

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I am not going to go through this same argument with you again for the umpteenth time. Sorry. Time to let caffeine or AZPaul argue it. If they want to rephrase what you are saying that's up to them. I'd prefer something new myself.

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In other words you have had genuine answers - and know it - and you are the one who simply insists on their opinions “end of discussion”.Thanks for admitting to that, even if it was only implicitly

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No, the argument is about what it takes to get from one species to another and all the examples of new "species" that aren't species at all but merely new populations of a species with a new look to it brought about merely by breeding together a new set of gene frequencies in reproductive isolation.

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You mean that you say that. But can you produce a single example where we know that is all there is to it ? Indeed, given that mutation plays a role even in the case of domestic breeding - with far shorter timescales - shouldn’t we expect mutations to play a part in speciation ?Can you offer an explanation of how reproductive isolation develops that is more than speculation - at least for the case where it is impossible to produce fertile offspring ? Wasting reproductive effort - mating with no chance of success - would be a definite selective disadvantage.Because so far you haven’t addressed either point with any real evidence.

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Since the usual predictable (and I dare say mindless) debunkery has been the only response to my posts

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I suppose getting serious answers gets in the way of your pretence.
But if you don’t like getting debunked don’t write bunk.

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Yes, but for the moment taking the chimp as the ancestor we descended from, the task is getting ALL the keratin differences in the chimp body to become human keratin.

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That isn’t really a problem though. If we are just talking about minor variations in the structure of a protein then it’s pretty much expected. There will be minor variations, and unless there is something very special about them then they’re just the ones that happened to turn up.

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Is this going to happen bit by bit, fingernail by fingernail or is there a place in the DNA that governs the whole thing?

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It’s complicated by the fact that there is more than one keratin in the body. But a keratin is just a protein, and changes to the gene which codes that protein will change every instance that gene is responsible for. So the finger and toenails would all change together (as well as anywhere else that got keratin from that particular gene)

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And since you note that there are recognizable differences between chimp and human organs and bones although we have the same organs and bones, evolution has the task of making all those "small" changes in all those parts of the body. Seems to me that's a case of the usual wishful thinking that fuels all the assumptions of the ToE. The smallness of the differences doesn't really make a difference since the overall changes that have to happen are really enormous.

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We’re talking about small changes to a few genes and you think it is a big problem ?

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You are of course assuming that the differences you are talking about were brought about by mutations. You all keep talking about how we all have many mutations but aren't most of them in the body where they won't be passed on anyway? This doesn't get spelled out every time someone makes such a statement. The mutations, to matter, have to be in the germ cells, but not saying so leaves the discussion in a suspended state.

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Of course it’s the mutations in the germ cells we are talking about because those are the only ones that can accumulate from generation to generation. This is another mistaken objection.

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This is really what I wanted to answer, but I got into the rest anyway. To my mind the differences are enormous despite the similarities. And I see enormous structural changes too. The whole posture of the body has to change, the legs have to lengthen and straighten out, the feet have to become feet, the arms have to shorten, the spine has to straighten, the skull has to make some pretty dramatic changes and get repositioned on the neck, the nose has to change dramatically, the mouth and teeth have to become much smaller and repositioned in the skull, and of course the brain has to undergo some enormous changes, etc etc etc

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But are any of those really massive changes from the perspective of developmental biology. Similar - or larger - differences seemed pretty small to you when you were talking about trilobites. You should probably consider the variations shown in earlier hominids, too.Anyway when this came up before I advised you to look into neoteny
- which is a big part of the picture.

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I don't see how mutations could do any of this no matter how much time you give them

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Yet you can see similar differences as just normal within-species variation. When it is convenient for your position.

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You all cannot change my mind by asserting your own beliefs and your expertise to determine their truth. You are so sure of yourselves you aren't interested in entertaining anything I say or how I arrived at it, I'm just wrong and that's the end of it. I don't find that at all convincing, you're just being arrogant know-it-alls, and yes, of course, I'm going to continue with my own beliefs, you've affected nothing, you're just being offensive and arrogant. So the conversation is over, you think you won and that's where it always goes.

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And what is the point of falsely accusing us of acting like you ?You claim your tactics wouldn’t work on you, so why do you get upset when they don’t work on us ?At least this shows that you know you have no case.

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Even though it seems unlikely that a random mutation would just show up to turn a moth or a mouse a different color under the pressure of need

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So do we. That is why none of us believe it.But let us get to the real point.It doesn’t matter if, in principle, speciation - or at least the appearance of speciation - could occur without mutations. That makes no real difference to either of our positions.The question is the degree of involvement of mutation.Now we have evidence. We have proof that mutations occur. We do have examples of useful phenotypic changes caused by mutation. We know of genes with large numbers of alleles - notably in the immune system where variety is an advantage.We also have plenty of evidence that evolution has occurred on a scale that would be completely impossible without mutations playing a significant role. Even Darwin had enough for a string case. And that is what you are arguing against.It follows then that if you want to claim that mutations do not play a significant role, you need an equally strong case. And the theoretical possibility that speciation might occasionally occur without mutation playing a significant role is nowhere near that. Especially when it is backed up by ”examples” - like “ring species” or the wildebeests- which are only assumed to be examples.Denying that mutations are mutations does not help. Nor does asserting the the small differences between human and chimp keratin is somehow a problem for evolution. Neither does your refusal to even admit that you have been given serious answers - better than anything you have contributed to the discussion.This discussion is going nowhere because you have no worthwhile case. Blaming us for not believing you anyway only escalates the hostility without helping anyone (especially you).

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The subject is the peppered moth

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In the context of the wider issue.I’ll take your refusal to discuss it as an admission that you have no real case.

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Seems to me if the mutation came along in time to save the population from extinction and start a new population to replace it, that's "showing up when needed"

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The species was not in danger of extinction, although it would have had it’s range curtailed quite significantly. As I understand it there were always areas where the light colouration dominated.The fact that this is a single mutation, that the moth population seems to have been large, that there was plenty of time for it to occur - and the fact that many species have not been saved - makes this a plausible coincidence. These things will happen on occasion - probability says so.

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I'm always being told I've "been told" this or that in the past, and here's another case where I'm "being told" something, but why should I take it seriously?

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Why should we take your assertion that the species was in real danger of extinction seriously ?And you certainly refer to things you’ve heard and expect us to take it seriously.Feel free to check any claim I make. I check your claims often enough. But then we have to because you have a record is misrepresenting your sources.

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Why should you have the definitive word?

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If I wanted to have the definitive word I wouldn’t let people know I was relying on memory. I would check the facts and provide evidence.

I think it’s more to the point to consider the question of how many mutations might have provided the dark colouration. I would be surprised if it were only one. Melanism is not that uncommon.