Not sure what the disconnect is here, but from my end it appears that you are misunderstanding binomial trials.
If we have 2000 binomial trials with p=0.99, the probability of 2000 successes is as you say, BUT the probability of at least 1980 successes is better than 0.50.
If we have 2022 binomial trials at p=0.99, the probability of at least 2000 successes is about 0.50. The probability of at least 2000 successes increases toward 1.0 rapidly as we add more trials.
No one suggests that evolution is a “one failure and your out” progression. There are many trials, most fail, but if at least one trial succeeds then it can progress to the next (in the oversimplified binomial example).
He expects the two mutations for chloroquine resistance would be deleterious, they disappear in the wild after chloroquine is discontinued. And then we have this, in his description of new protein-protein binding sites:
“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.” (Edge of Evolution, p. 134)
So existing variation is included, here.
And Behe mentions that in his discussion.
Because of the rate at which chloroquine resistance arises, about 1 in 10^20, about the square of atovaquone resistance (1 in 10^12 and one mutation). This implies two mutations (which could be on multiple paths) for chloroquine resistance. So I would conclude that Summers et al. did a thorough job of looking at variants.
Why do the variants disappear then, in the absence of chloroquine?
But I gather that chloroquine was used extensively, not intermittently, until resistance arose.
[quote=“Mercer, post:291, topic:15043”]
But evolution could take that path, if two different mutations are on different alleles. Again, Behe observes what evolution accomplished, without restricting modes of operation.
[quote=“Mercer, post:291, topic:15043”]
Because it appears that the mechanism for resistance is two point mutations. No need to expound on other mechanisms, then.
But I’m saying HIV would be mentioned in the paper if they were examples of new protein-protein interactions. The absence of mention there, then, is significant.
That’s fine, I’m just saying that if the ancestral proteins already had function, then it’s not surprising if single, selectable mutations improve that function.
But for evolution of the eye, I’m assuming a success is the next step mutating and being selected (if not fixed) in the population, and we wait until we get each step. So there are no repeated trials.
Are you suggesting there is only one chance for a particular mutation to happen, ever, and that no other mutation(s) could be able to provide an equivalent function? That is a very strange assumption. That’s like rolling a six-sided die a few times, observing that you didn’t roll any 6’s, then declaring that you will never be able to roll sixes again. That makes no sense mathematically (or biologically).
So there are no repeated trials.
OK, I’ve been working within your assumption of binomial trials, which is based on repeated trials, so that doesn’t fit your own math.
I haven’t been following this part of the discussion, but have you considered how very simple it is to make a pinhole camera? You make one by accident. I’ve even seen them occur naturally with light filtering through the leaves of a tree. I have photos.
No, you are treating functions as digital. They are much more overlapping and vague than that. We’re talking about multiple functions, not one function.
But I’m saying that to have a shred of credibility on the subject, you’d first have to know that the paper is about NEW protein-protein interactions. You don’t know that. Moreover, not mentioning something is absurd as evidence that something never happened. Even you know that!
How could chloroquine selection EVER be constant? Do you think that people transmit malaria to other people?
How does one treat mosquitoes and rats with chloroquine, exactly?
Emphasis mine. Truth simply doesn’t matter, then.
Read one sentence in a review, misinterpret it, and quit there. Why isn’t Behe working on malaria to save lives, Lee, if he understands it better than the experts do?
It only appears that way because two numbers matched. It doesn’t appear that way to me at all, but unlike you and Behe, I’m a geneticist.
Again, Behe misattributes what evolution accomplished, while ignoring most of the data, complexity, and many other known mechanisms. All of these make his generalization ridiculous.
So, is there a mechanism for getting two changes together in the same allele without them having to have occurred in the same allele?
Well, fine, I think I can still make my point, that if the ancestral proteins had functions already, then it’s not surprising if single, selectable mutations improve those functions.
“Viruses might take advantage of this low affinity to invade a host cell by evolving a stronger binding affinity to the surface receptors than that associated with physiological ligands.” (Wang, J) So “evolving” means new protein-protein interactions.
Presumably the author would be aware of new HIV protein-protein interactions, these would deserve mention in his paper.
No, but chloroquine selection in people could be constant. I’m not sure what this has to do with epistasis, though: " Genes rarely operate in isolation from other genes. Epistasis is the term that refers to the action of one gene upon another." (Nature)
Behe mentions using clusters of medications to get beyond the edge of evolution.
[quote=“Mercer, post:305, topic:15043”]
I don’t know, you brought this up as a possibility.
But we have good evidence that two point mutations are required for resistance. Thus all the other mechanisms need not be brought up.
My point is that we are talking about new functions, not just improving existing ones
No, it does not. The paper is about existing interactions. Why are you defending Behe when you know that his claim was false and you haven’t even read the paper he pseudocited?
Also, there’s an even more obvious deception here. In the footnote, Behe refers only to binding to host surface receptors, not general interactions. It gets even worse–the interaction that both Behe and you have admitted evolved is not with a host receptor, or even a host protein. You and Behe are just fabricating.
You have no knowledge of whether the paper addresses any new functions at all.
So what? From the parasite’s point of view (the organism that is evolving in response to it), it is anything but constant. Behe makes no mention of that important reason and doesn’t include it in his “calculation.”
Postulating that only one gene is involved is absurd for that reason.
Has no one in the field thought of that? And my question is about what he is DOING, not just mentioning.
[quote=“lee_merrill, post:308, topic:15043”]
It’s covered in high-school biology. Recombination.
You don’t have good evidence, because you’re ignoring all of the other relevant mechanisms, the most obvious of which is that selection can never be constant.
Yes, let’s not bother with any real science to prevent millions of deaths, most of which are children. You and Behe will just pretend to have it all figured out because two numbers match:
But once you are talking about ancestral proteins, you are talking about improving existing functionality.
It’s behind a paywall, so all I can read is the abstract, but it sounds to me like he is considering evolution of stronger interactions.
I’ve lost the thread here, are you talking about evolution of chloroquine resistance?
But Behe isn’t modeling evolution, and making a calculation based on a model, he observes what evolution actually accomplished. And having a constant medicine at one stage of the parasite’s life-cycle would certainly affect the whole life-cycle.
But mutations in genes can occur in isolation.
I’m sure it’s being thought of, but it would be more prominent if Behe’s edge of evolution was taken more seriously. So I think it is reasonable to argue for intelligent design.
I’m not sure what numbers you’re referring to, but I expect Behe (and you?) would invest time in malaria research, or in antibiotic research (the edge of evolution would be pertinent there, too), if he thought it would be productive.
No, we’re talking about changing binding specificity, the thing Behe claims can’t happen. Try to stay on track.
[quote=“lee_merrill, post:310, topic:15043”]
Then you don’t know and should stop speculating.
I’m a virologist, and it doesn’t sound that way at all. Behe cited an irrelevant reference to support an objectively false claim.
I didn’t mention modeling. I mentioned that the calculation doesn’t take intermittent selection into account.
You seem to be contradicting yourself again. Behe’s model assumes constant selection. It’s ridiculously wrong.
Not nearly as much as having it present throughout the life cycle.
[quote=“lee_merrill, post:310, topic:15043”]
Are they doing so in this case?
I’m sure that it has already been thought of. Behe adds nothing of value.
Why? If Behe himself took it more seriously, he wouldn’t have dropped this subject in his subsequent books and he would have done hands-on work in his lab at Lehigh. He has funding from the DI.
The probability of an event of probability p occurring twice is p^2 if there are only two opportunities for it to occur. If there are more opportunities - and in your scenario there are many many more opportunities than just two - the probability can be much much higher.
What you are actually looking at is not the probability that something occurs, but the expected number of such occurrences over a number of trials. This is Np, were N is the number of trials and p is the probability for each trial.
For a simple example, the probability of rolling a ‘6’ on a standard die is 1/6, and if you roll it 6 times you will get, on average, one ‘6’.[1]N = 6, p = 1/6, Np = 1. If you instead roll the dice 12 times, the expected number of '6’s is 12*1/6 = 2. So doubling the number of attempts does indeed double the number of expected successes.
This is not the same as the expected number of double-‘6’ rolls when rolling a pair of dice six times, which would be 6*(1/6^2) = 1/6. You would indeed expect to have to roll a pair of dice 36 times for one double-‘6’.[2]
Your original comment:
makes it clear that you are looking at the probability of two types of eye evolving at the same time rather than the probability of a type of eye evolving twice - equivalent to the difference between rolling two dice six times rather than rolling one dice twelve times.
If there is a “1 in 6.5 x 10^27 chance for the eye to evolve” then the expectation is that it would evolve once in 6.5e27 organisms - and hence would evolve twice in 13.0e37 organisms. This is much less than 1e40, so the number of organisms that have existed is not a barrier for eyes evolving twice, thrice or even fifty times.
While in theory this would mean eyes would evolve 1.5 trillion times in 1e40 organisms, but that wouldn’t happen for several reasons based on deficiencies in your model of evolution (such as that there is no selection pressure for eyes in organisms that already have them) which are independent of the deficiencies in your probability calculation. I won’t address those here, because it’s not necessary - your conclusion has already been overturned by highlighting your maths errors.
P.S. I have very little expectation that you will understand this, and equally little expectation that you will concede the point if you do understand it. But those who do understand it will know that you have been refuted, even if you don’t.
P.P.S. If you apply your technique for calculating the expected number of times eyes evolve to the expected number of times chloroquine resistance would evolve, you’d see that your approach would lead to chloroquine resistance having evolved twice, when it has actually evolved IIRC at least five times. Your calculation even fails for the case you base it on.
I know this is simplified, that you can calculate the exact probabilities for getting zero, one or more '6’s in six rolls, and that the probability of getting exactly one six is higher than for getting any other number of sixes, but less than for not getting exactly one six. But it suffices here. ↩︎
