That’s what you wrote just 4 comments above at #320.
But I’m gearing off the paper, which proposes a change of 1% at each step–which steps involve many trials, certainly.
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But in the scenario I am envisioning, there are two trials, each with 2000 steps. And I am trying to compute the probability, not the expected value.
Many steps (successes), many trials, that not at all like rolling two dice.
Two mutations for a 1 in 10^20 organism rate is reasonable, though, given that 1 mutation produces atovaquone resistance in about 1 in 10^12 organisms.
But the 1 in 10^20 number includes all the listed factors.
If two mutations are indeed required for resistance, and the rate is about the square of atovaquone resistance, then it would seem appropriate to focus on mutation and selection, leaving other considerations to the side.
I’m also basing my comments on Behe having read the paper.
No, he implied he had read recent research.
I’m sure you know these areas better than I do.
No one has counted up 10^20 organisms, if that’s what you mean. But he has documented his points extensively with references to papers, and described many of the papers in his books, implying he has read them.
That’s the beauty of Behe’s approach, where he bases his deductions on what evolution actually did.
That’s correct, he goes on to generalize the argument to two new protein-protein binding sites, as the edge of evolution.
That would be nice to have, but I think we can still deduce that a flagellum is improbable to evolve:
“With the criterion of two protein-protein binding sites, we can quickly see why stupendously complex structures such as the cilium, the flagellum, and the machinery that builds them are beyond Darwinian evolution. The flagellum has dozens of protein parts that specifically bind to each other; the cilium has hundreds.” (The Edge of Evolution, p. 146)
Just what it says. The vast majority of mutations are not limited to two specific mutations. There are many, many combinations of mutations that can produce the same adaptation.
That’s false. Behe’s approach ignores the the vast majority of variation because it singles in on the solutions that were found instead of all the solutions that existed but were not found.
The problem is that he uses the same math which is incorrect. Millions of new protein-protein binding sites are created just with antibody recombination. Behe’s math doesn’t even start to approach reality.
In other words, you can’t point to a single demonstrable adaptation that goes beyond Behe’s edge of evolution…
I’m afraid I can’t do that. I’m willing to agree that you’re wrong about almost everything you have said, and in fact you’re wrong about everything you have said about Nilsson & Pelger 1994. “Agree to disagree” implies some kind of epistemic equality that just does not exist.
That appears to be the only part of my post that you actually read. This seems to be selective, highly convenient blindness.
I agree that this is not like rolling two dice. And each step must succeed, or the eye does not evolve. I’m proposing that each step corresponds to a single trial, where you succeed or you don’t, say, over the life of a species.
If you inflate a beach ball by having twenty people each blow into it once, they don’t need to act in any particular sequence, and if the beach ball has two valves they don’t even have to act at separate times.
Explain why the same cannot apply to mutations that increase the size of an optic orb.
I’m proposing that each step corresponds to a single trial, where you succeed or you don’t, say, over the life of a species.
I understand that is your assumption, but I don’t think it can be justified. Biologically it makes no sense (leaving that for others). Mathematically it’s a geometric distribution (# trials to first failure). Evolution very clearly generates a lot of failures, it doesn’t stop because one step fails.
Do you understand that not every trial needs to succeed for a step to succeed.
So you do not use the total number of lineages. What you wrote was not true.
So you did miss the point.
You still haven’t shown that you’re capable of calculating the probability of drawing a full house in poker (or even anything simpler). Nothing you say about probabilities has any weight.
The steps are not mutations. The steps are not a series of mutations. The steps are not trials. They do not “succeed” or fail. You have not read Nilsson & Pelger 1994, though I suppose it’s possible that you stared at a few of its pages for some period of time.
Though in fact I’m not sure how many of the people arguing with you about all this have read Nilsson & Pelger either.
Behe attributes the number entirely to the factors of mutation and natural selection. That’s where he’s wrong.
No, I don’t see that you have any evidence to support that claim.
You don’t know whether he did or not. What you do know is that nothing in the abstract suggests that it would have supported Behe’s claim, which he has publicly admitted is false. Behe has been called out on this but did not respond.
That’s objectively false, Lee. Please stop.
I am too. So why do you keep pretending that you know better? Why do you keep quoting Behe as though I should view him as authoritative in these areas?
No, I mean that Behe has made zero observations himself. It is deceptive to portray him as having made any.
But as you’ve learned, the papers he cites don’t necessarily document his points.
What exactly was his description of Yang’s review, which he used to support a claim he now admits is false? How does describing a paper imply that one has actually read it? After all, you’re here pretending to know what is or isn’t in a paper without reading it.
You should refresh your memory, because @lee_merrill hasn’t read it at all, and at least one of you should know what it says. For one thing, it doesn’t talk about mutations.