Can you explain what exactly the probability of drawing a full house has to do with evolution? One is a card game, the other is biology. What do they have in common? Is an organism a hand of cards? A biochemical structure, is that a hand of cards? Are biochemical molecules shuffled like a pack of cards before being dealt by a dealer? I don’t think there is any relation at all between evolution and card games.
And while you’re on it, what is the probability of special creation by God? Because for your argument to make sense this has to be bigger than the probability of evolution however you claim to compute that.
That was based on Larry Moran’s proposal, that 4 mutations are required for chloroquine resistance. So then Behe’s CCC (chloroquine complexity cluster) would be 4 mutations, instead of 2, and a double-CCC (where Behe places the edge) might be 8 mutations, instead of 4.
I would construe it that way, yes.
Yes, “A minimum of two mutations sufficed for (low) CQ transport activity…”
I don’t think he does, the number of generations would depend on the mutation rate, for instance.
“So let’s suppose that of the five or six changes that have to happen to a protein to make a new binding site, a third of them are neutral. They could occur before the other key mutations, as a separate step, without harm. Although finding the right neutral changes would itself be an improbable step, we’ll again err on the conservative side and discount the average number of neutral mutations from the average number of total necessary changes. That leaves three or four amino acid changes that might cause trouble if they occur singly. For the Darwinian step in question, they must occur together.” (The Edge of Evolution, p. 134)
I only mention card games to show that you can compute the probability of an event before the fact, in either evolution or in other areas, without committing the Sharpshooter fallacy.
It’s 1 - “the probability of creation by nature”, if “nature” and God cover all possible causes.
Hmm. Probably not an important point, so let’s set that aside
That confirms my suspicion that people sympathetic to creationism are likely to misconstrue it that way. But can you now see that this is not what he is saying?
Not simultaneous mutations, though. Correct? So that would mean this paper did not support what Behe had written in his book.
Another question arises. I actually don’t understand why Behe has to talk about malaria at all. The odds of any specific point mutation occurring during a reproduction is 10-10 (Behe actually uses figure that is more likely but is inaccurate according to Moran). Which means the odds of any two specific mutations happening simultaneousy is 10-20. This doesn’t take into account the time to fixation, however, so if anything Behe underestimates the time to fixation of such a mutation. But the question is what does malaria have to do with any of this? What does chloroquine resistance tell us about the odds of simultaneous mutations occurring and being fixed? Can you figure that out for me?
How is that included in his calculation of the odds of a CCC occurring?
That does not answer the question. Why must they occur together?
This comes back to how you describe the ‘event’. If you describe the outcome of a dealt hand as ‘a Full House’ the probability will be different and lower than if you describe it as ‘any hand that will beat a Flush and all lower ranking hands’. In evolutionary terms, you have to describe the event as ‘any structure that provides a competitive edge for survival’. If you do that you’re going to find that the probabilities of this being achieved in some way or another are vastly higher than the one of just the specific structure you are looking at.
You are just estimating a single specific probability that is irrelevant to evolution.
So why don’t you give us the actual number then? Could it be that you can’t actually calculate it because this entire probability schtick is bogus?
In all, none of the papers he cites support his conclusions.
And for chloroquine resistance, that is incredibly complex, because only a subset of the human hosts are enforcing any selection for resistance. None of the mosquitoes and rats are being treated with chloroquine. Behe conveniently omits these complicating factors, and @lee_merrill doesn’t notice.
Well, I do understand Behe’s position on common descent, and I disagree with him, because surely multiple new groups of protein-protein interactions would be required to get from chimps to humans.
But I think the probability of a structure evolving is part and parcel of evolution. This is also important to the intelligent design argument, thus it gets emphasis.
1 in 10^40 being Behe’s edge, then we would have 1 - 1 / (10^40).
But surely two new protein-protein interactions are required repeatedly, if we go from chimps to humans.
Yes, simultaneous, or nearly so, since the mutations disappear in the wild in the absence of chloroquine–implying they are somewhat deleterious.
Because Behe looks at what evolution actually did, so chloroquine resistance appearing and becoming widespread includes all these factors.
Because the probability is deduced from the rate at which evolution actually brought it about, with the mutation rate being the actual rate of malaria.
Could you give some examples of these protein-protein interactions that are present in humans but not chimps (or vice versa)?
No, that is not a valid inference at all. They likely disappear, if they do, as a result of genetic drift.
BTW, how long does it take them to disappear? Is the time so short that simultaneous mutations are needed?
Another non-sequitur of a response. At the time Behe wrote his book, what reason did he have for assuming that the evolution of chloroquine resistance required multiple mutations?
That only applies to this one trait in this one organism. How does Behe generalize this to all traits in all organisms?
They are deleterious in that example because it is a made up example and Behe imposed the condition that four of the mutations are highly deleterious on their own.
If there was a trait that required eight mutations, all of which were neutral on their own (and in every combination) until all eight are present (at which point it is positively selected), Behe’s calculations will not apply at all. Do you understand that?
How about here? “Exon-1-encoded Sia-recognizing domains of human and ape Siglec-9 share only approximately 93-95% amino acid identity.”
“As discussed in Chapter 3, none of the changes seem to be improvements in an absolute sense. They disappear once drug therapy is discontinued.” (The Edge of Evolution, p. 136)
I gather from this that they disappear relatively quickly, i.e. not through drift, and such that simultaneous mutations are needed again.
Because the rate of chloroquine resistance (1 in 10^20) is about the square of atovaquone resistance (1 in 10^12), which requires one mutation.
He then turns to protein-protein interactions, and discusses how a new protein-protein binding site would be expected in about 1 in 10^20 organisms. He then places the edge of evolution at two new protein-protein binding sites.
But the mutations are independent events, and must occur together, so the probability of the 8 mutations is just the probability of each mutation, multiplied together. So I think Behe’s estimate does apply, in that sense.
OK, let’s take that as an example. Can you now demonstrate that this required four simultaneous mutations?
Is this just a guess on your part? Has it actually been demonstrated that every single mutation on its own is subject to negative selection? The Summers et al paper shows this is not the case.
Sorry, I misspoke there. I meant to say "multiple simultaneous mutations. In any event, we now know this is not the case because of the Summers paper.
I know he says that. How does he support that claim?
No, they don’t. They can occur separately, one at a time. Why not? You still have not answered this question, and I have asked it several time. I know Behe wants you to believe this. That is not good enough reason. He needs to provide a sound argument based on sound evidence. You still have not presented that.
You can. But before the fact, you don’t know which event to compute the probability for. Computing the probability of drawing a full house is futile if you then draw a flush instead.
All this talk of before-the-fact vs after-the-fact with poker is a smokescreen to hide that whenever you talk about biological systems instead of card games, you’re computing the probability of something that has already happened - because if it hadn’t happened you wouldn’t know what probability to compute - hence it’s after-the-fact.
Feel free to counter this by computing the before-the-fact probability of evolving something that did not actually evolve. Until then, you’re just bait-and-switching.
Well, how about here, then? “Hominoid-Specific De Novo Protein-Coding Genes Originating from Long Non-Coding RNAs”
Well, the de novo proteins were on average about 150 amino-acids long. It would be surprising if there was an all-selectable pathway to proteins of this length.
“We analyzed the characteristics of these de novo protein-coding genes. Consistent with previous reports [4], we found that the gene products were smaller, with a median length of 150.5 amino-acids, compared with 416 amino-acids in the human genome, suggesting the difficulty in de novo origination of long ORFs…”
“When chloroquine is no longer used to treat malaria patients in a region, the mutant strain of P. falciparum declines and the original strain makes a comeback, indicating that the mutant is weaker than the original strain in the absence of the toxic chloroquine. [9]” (The Edge of Evolution, pp. 50-51)
“9.Kublin, J. G., Cortese, J. F., Njunju, E. M., Mukadam, R. A., Wirima, J. J., Kazembe, P. N., Djimde, A. A., Kouriba, B., Taylor, T. E., and Plowe, C. V.2003. Reemergence of chloroquine-sensitive Plasmodium falciparum malaria after cessation of chloroquine use in Malawi. J. Infect. Dis. 187:1870–75; Cooper, R. A., Hartwig, C. L., Ferdig, M. T. 2005. Pfcrt is more than the Plasmodium falciparum chloroquine resistance gene: a functional and evolutionary perspective. Acta. Trop. 94:170–80. Drug resistance mutation in pfmdr, the other protein involved in chloroquine resistance, also incurs a fitness cost (Hayward, R., Saliba, K. J.,Kirk, K. 2005. pfmdr1 mutations associated with chloroquine resistance incur a fitness cost in Plasmodium falciparum. Mol. Microbiol. 55:1285–95).”
“In 1993, Malawi became the first African country to replace chloroquine with sulfadoxine-pyrimethamine nationwide in response to high rates of chloroquine-resistant falciparum malaria. To determine whether withdrawal of chloroquine can lead to the reemergence of chloroquine sensitivity, the prevalence of the pfcrt 76T molecular marker for chloroquine-resistant Plasmodium falciparum malaria was retrospectively measured in Blantyre, Malawi. The prevalence of the chloroquine-resistant pfcrt genotype decreased from 85% in 1992 to 13% in 2000. In 2001, chloroquine cleared 100% of 63 asymptomatic P. falciparum infections, no isolates were resistant to chloroquine in vitro, and no infections with the chloroquine-resistant pfcrt genotype were detected.” (from here)
I think this implies both mutations are subject to negative selection.
The rate of chloroquine resistance is about the square of the rate of atovaquone resistance, which requires one mutation. This is what we would expect, if chloroquine resistance requires two independent, singly-non-selectable mutations.
How so? As far as I have read, they say there are two known paths, with two mutations required in each path, for basic resistance.
I’ve posted his argument in these threads, it has to do with considerations of protein shape space. I refer you to Behe’s book, if you want the full argument.
But they won’t last long, if they are singly somewhat deleterious.
My point is that viewed before the fact, the probability of an event can be less than 1, whereas after the fact, it is 1 or 0. So we have to pick one perspective, and stick with it. I choose “before the fact”, because that’s really the probability of interest, in card games, and in biological systems.