What is the mechanism that prevents microevolution to become macroevolution?

What kept it from being expressed? What turned it on only in this one Italian village?If we sequence the gene and find no evidence of it in anybody else - random members of other populations - is that sufficient to conclude that this is recent, rather than an ancient, mutation? Why wouldn't we notice it if it were in other populations besides the one in Italy?

Ok, well, I'm a layperson. Here I go:You say "genetic adaptation" like it's a different thing than a mutation. What is the adaptive mechanism operating on genetics if it isn't selection operating on random mutations?

How does that apply to this case? The trait is dominant. You can't hide a dominant trait, you can only lack it by being homozygous recessive.If an individual has a trait that is dominant, but neither of the parents have the trait, then either the gene came about through mutation or the parents aren't who you think they are.Genetics 101. How can your mechanism of "pre-existing alleles" possibly apply in this case?

A brief discussion of the mutation which you can read here: Apolipoprotein AI Mutations and Informationshows that this is not the case. All known carriers of the mutation are heterozygous for it - they only have one copy of the gene, and the trait is dominant. We would be able to detect evidence of that - the "pieces" of the gene, if you will, much as we detect the vitamin C pseudogene. It would take millions upon millions of generations for a gene to be rendered completely unrecognizable by mutations, and in that amount of time, it would be impossible for anyone to have the gene. The near-immunity to arteriosclerosis regardless of lifestyle? I would think that would be something fairly easy to notice in a society where people eat fatty food and smoke - like the US and Europe - and heart diseases are some of the leading causes of death.

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

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

Mutations are passed on like any allele, because mutations form new alleles. Because only his direct decendants have it (and not all of them). His indirect decendants - those people who are decended from his parents or grandparents but aren't decended from him - don't. Thus, we have ample reason to conclude he's the origin of the allele (pedantically, I guess, the origin would be a mutation in the germline cell of one of his parents, either the sperm or the egg from which he was born.)It's basic inheritance. He's the top of the pyramid, thus, it began with him.

It's present in even less than very few - 33 individuals. That's it.The trait is pretty prominent, as I said, particularly in a society where heart disease is a leading cause of death. It would be all but impossible to conceal this gene for any extended length of time, especially once we started looking for it. That seems to be a point that you've chosen to ignore; why is that?Also - could you explain how you find the evidence for mutations in the bacteria experiments I've mentioned lacking? You've dismissed that evidence without actually giving a reason why.

By tracing the ancestry of every human being who has it.That's 33 people. When you trace their ancestry, it all comes back to one guy in the 18th century.If it had been in everyone, at one point, then we would find that the most recent common ancestor of everyone who had the gene would be a lot further back. People who weren't so closely related to each other would have it.But they don't. The only people it's found in are these 33 people who are all closely related through one guy in the 18th century. Hence, it's a mutation that arose with him, not a mutation that arose with anybody before him or was "created in the beginning" (same thing.) Not this rare. Not 33/6000000000 people. And why would an allele that provides near-immunity to arteriosclerosis due to dietary cholesterol be selected against? You don't just get to assert "selection" without explaining the selective influence. This is a beneficial mutation in Western civilization. Under what circumstances do you believe it would be selected against?

It does, though. The alternatives are far, far too unlikely. It's far more likely that one man had one mutation that he passed on to some of his ancestors, than to suggest that more than six billion people all happened, coincidentally, to have the very same mutation that the decendants of that one man somehow didn't inherit. My, what a coincidence, that out of 6 billion people, the only ones that could be found to possess this dominant allele, which has profound and obvious effects on anybody with dietary risk factors, the only people who could be found all happen to be the direct decendants of one man who lived in the 18th century. The mind reels!Faith. Finding people with this gene would be as simple as sending an email out to cardiologists and geriatricians asking them if they've ever encountered any individuals who, despite eating cholesterol-heavy foods and smoking, stubbornly refuses to develop any arteriosclerosis. The effects of this gene are profound and obvious. It should be very easy indeed to find other people with the very same gene, but they don't seem to exist. The only people on Earth known to have this gene are the 33 people decended from that one guy.That's entirely consistent with a mutation emerging in a single individual. It's completely inconsistent with your model, where a beneficial mutation somehow, inexplicably, is outcompeted by detrimental mutations in every individual on Earth except for the direct decendants of one man.Your explanation doesn't make any sense. But how did the grandparent get the trait? And why didn't any of the grandparent's siblings have it? If they did, why didn't any of their children get it?Beneficial mutations increase in frequency over time. In this case, the gene has gone from one individual to 33. Beneficial mutations, almost as a rule, don't decrease. If a mutation goes from lots of people, to one person or less, by definition, that's not a beneficial mutation. Selection doesn't select like that. The way you say "it's possible" indicates to me that you understand how highly unlikely this would be to happen, even just in one generation.You're asking us to believe that, before Patient Zero back in the 18th century, that arrangement of offspring is exactly what happened every single time, in every single generation.How can you expect anyone to take you seriously with that? You're asking us to believe that an extraordinarily unlikely arrangment of alleles occured not just once, but thousands upon thousands of times, going all the way back to Adam. And what evidence to you provide to convince us that this extraordinarily unlikely sequence of genetic events actually occured? Why, none whatsoever. Faith doesn't need evidence, after all. It's sufficient for her to simply assert that a thing happened, and we're all completely unreasonable for simply taking her word on it. And his aunts/uncles? Greataunts/greatuncles? Greatgreataunts/greatgreatuncles? Why didn't any of them get it? We know they didn't, or else they would have passed it on and then we'd know of people that had it beyond this guy's direct ancestors. How many do you suppose there would be, if we're talking about the line of this guy's ancestors stretching back to the beginning of time?

Maybe, but remember it's not about how many children you have, it's about how many grandchildren you have. Having babies that don't themselves survive to reproductive age is as much an evolutionary failure as never having babies at all.To the extent that this mutation extends the life of a person who can help in the raising of their offspring's offspring, it could easily have a beneficial effect.Faith has yet to specify a mechanism of negative selection, so her model that somehow this is the original and we all have the broken mutation is nonsense. The probabilities don't work out. Further she states that it's more likely that a protein will be broken than improved, and while this is true, it's irrelevant to this specific case.The mutation substituted one amino residue in the polypeptide, correct? So there's no difference in probability between a substitution occuring on Apo-AI that results in Apo-AIM, and a substitution occuring on Apo-AIM that results in Apo-AI. They're probably equally likely.So the only relevant probability is whether it's more probable that one person gains one mutation and passes it along, or that six billion people all coincidentally gain the exact same mutation and pass it along to everybody but 33 people.Imagine this. I walk out of a room and tell you that there's 50 quarters inside, laying on the floor. Before I entered they all were showing the same face up, but I don't tell you which. I also tell you that I flipped some number of them, but I don't tell you how many. And by "flip" I mean I picked some number of them up, one at a time, flipped them through the air, and set them back down with their new face up.You walk into the room and see 47 coins heads-up and 3 tails-up. Is it really so hard to reconstruct what side all the coins originally showed, and therefore which coins were changed because I flipped them? Certainly there's the possibility that I flipped all 50 coins. But the chances that 47 of them would be heads if I had done that are less than one in one trillion. You would have to have the mind of a child to emerge from that room and accuse me of flipping every single coin, or even most of them. You'd have to be pretty ignorant indeed to accuse me of flipping any more than 4-5 of the coins, max.Edited by crashfrog, : No reason given.

Selection, Faith. Why wouldn't those people be outcompeted by the people with the Apo-AIM, who live long enough to support several generations of children?You're proposing that a deterious allele overtakes a beneficial one. Why would I accept such a counterintuitive outcome absent any evidence? Here and where? Where else is it?

When a big fat smoker dies, and during his autopsy they see tar in his lungs, and his 300 lbs of fat, but they can't find any evidence of arterial plaque - which is pretty obvious in a chest exam - the coroner is going to notice.And he's going to think back to that email he saw, looking for candidates for genetic analysis to detect Apo-AIM. Just about. How hard do you think it is to do a DNA test?

Lemme tell you what. Any time you've heard about someone living to advanced age, on the news, somebody's collecting a blood sample for use in research on the genetic properties of aging.Like that guy who lived to be 127 or whatever eating nothing but eggs and sausage. Read it on Pharyngula the other day.I'm not saying that they get everybody. But everybody who lives long enough to attract any kind of attention, yes, they're getting a blood sample to do genetics research. It's not that hard to do, after all. Running genetic tests is fairly cheap.

In fact, autopsies are performed in more than 20% of American deaths.