Not even close. For large, electrostatic binding surfaces, for example, changing a single residue to one with a different charge is sufficient to disrupt binding.
Why are you and Behe pretending that binding is binary?
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I’d like to see your wager, because you quote Behe as though you fervently believe all of his claims.
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If they were not ignored, you would be able to show where Behe included them.
Does the name Nigel Tufnel ring a bell?
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You did. Here it is again:
But I also notice you completely ignored the numerous references I gave earlier that shows how easy it is to select for a new protein binding site if such a site should happen to be beneficial, and that a considerable fraction of natural proteins are something like one mutation away from developing a binding site.
If Behe was right and new protein-protein binding sites were prohibitively unlikely to evolve in the history of life on Earth, the adaptive immune system would be impossible, and so would the entire biotech industry that relies on immunoassays, be they for things like ELISA, western blots, immunehisto or cytochemistry, or what have you.
But what we find instead supports what I’ve already said. Most proteins have some weak background affinity for each other, so much so that if improvement in this binding ability is selectively beneficial, it is trivial to select for it, which makes both the immune system and the entire industry that relies on it possible.
That’s literally what they do. They undergo both V(D)J-recombination, somatic hypermutation, and clonal selection (which is just another form of natural selection).
This is a textbook example of a blind Darwinian process that relies on the generation of a diversity of cell and antibody variants (by various forms of “mutation-by-mistake”), and subsequent selection both for the most successful variants, and selection against/elimination of the least successful one.
If the process wasn’t blind and somehow knew which changes would be most productive, it wouldn’t have to rely on the generation of a large diversity of different variants to increase the odds that a productive variant would be found among them.
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It starts with an unfounded assumption:
"Let’s assume each step in the evolution of the eye is 99% probable, "
Why not 100% probable?
For example, there are 3 billion bases in the human haploid genome. For each base there are 3 possible point mutations, so we have 9 billion possible point mutations in the haploid genome. Each human is born with 50 to 100 point mutations, so let’s go with 50. In just 180 million births we will have 9 billion point mutations. With a population of 7 billion people it is almost guaranteed that every non-lethal point mutation currently exists in the human population.
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It does.
The variation in the ~10^8 initial population comes from recombination, which you and Behe pretend does not exist.
After reactive antibodies are selected, the cells that produce them undergo somatic hyperMUTATION, so you’re wrong there, too.
It does. Cells that make antibodies with higher affinities are selected.
Utterly, objectively false. You’re just making things up. If we immunize human identical twins (or inbred mice of the same strain), they make different, new antibodies. Each individual makes hundreds to thousands of different, NEW antibodies, so your use of the singular “a” makes no sense.
All this evolution, producing high-affinity and high-specificity binding, happens in real time. Why do you ignore and/or completely misrepresent it?
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Nigel Tufnel, perhaps?
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I’m referring to organisms, about 10^20 organisms are needed in the wild for chloroquine resistance to appear.
Thank you, then “to appear” would be to fixate. But you can see the challenges in generalizing from those numbers to unrelated contexts? A mutation for, say lactose tolerance just for example, is unlikely to be dead ended in a bug zapper.
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But I think 99% is generous, your argument here proves too much, that any given structure is 100% probable to evolve.
But I don’t think the negative binomial distribution applies here, what is the number of failures you are using, for instance? With your calculation you would require only a dozen or so generations, if I’m understanding you correctly, but they estimate 363,992 generations for the eye to evolve.
But this is a simple probability calculation for independent events, and if the events are independent, then they may happen in parallel, and the probability doesn’t change.
[quote=“Mercer, post:252, topic:15043, full:true”]
No, again, Behe observes what evolution did, including existing variation, etc. And I think the author of the paper Behe quotes was aware of intermittent selection, so that would be included too. This is borne out by the result of about 1 in 10^20 generations for chloroquine resistance, which we now know has two main paths to resistance, each requiring two basic mutations for it to work–versus atovaquone resistance, which arises in about 1 in 10^12 generations, and requires one mutation.
He includes them by observing what evolution actually did. I don’t know why this is opaque to you.
No, it’s a continuum, and Behe states that.
Based on what?
Not any given structure, just those that result from a series of changes that are within the expected range of variation of existing structures and are selectively advantageous. Most structures are not selectively advantageous.
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“The elegant immune system is designed to saturate shape space. But the situation is entirely different inside the cell. For cellular proteins there is no built-in mechanism to deliberately make new binding sites. Cellular proteins almost always are made with just one sequence, not billions of different sequences like antibodies. In general the only way to get a new sequence for a cellular protein is over many generations by random mutation. Searching through shape space with cellular proteins is glacially slow and abysmally inefficient.” (The Edge of Evolution, p. 133)
Yes, but I’m needed each step to survive in the wild, to become fixed, even.
Yes, there is. It’s called random mutations.
And yet well within the speed needed to produce the biodiversity we see today. The human and chimp genomes differ by less than 1% at the amino acid level, well within capacity of the observed mutation rates.
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Fixation is not required for selection.
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No, Lee. Behe observes what evolution did and attributes it entirely to new mutations. If you disagree, show me where he explicitly does so. “Behe observes what evolution did” is nonresponsive.
I know he is, which is why he pointed out that Behe was misrepresenting him.
You KNOW no such thing. You even know you don’t know, because you won’t risk any money.
It’s not opaque, it’s nonsense.
It is, but that it not evident in Behe’s math. For example, why did you make the claim that antibodies aren’t new?
So is evolution. Behe has no expertise in immunology. Why are you quoting him as an authority?
Only if you ignore existing variation, recombination, and sexual reproduction.
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Yes, so Behe generalizes from chloroquine resistance to new protein-protein binding sites, which he concludes need about 5 or 6 mutations to produce a tight binding to a given target. He then grants 2 mutations, saying we will call them neutral, and calls the remaining mutations deleterious (since most mutations will be deleterious). So two new binding sites would require 6 to 8 mutations, or several times the difficulty of producing chloroquine resistance, with 2 mutations.
That response of Behe’s is fantastically deceptive, and just reveals how dishonest Behe is because he should know better. The first sentence is just a question begging assertion(that the immune system is designed), and it’s known to be false that the diversity of antibody variation “saturates shape space”. It of course doesn’t, not by a long shot.
The amount of possible shapes far outnumber the diversity of antibodies, and new antibodies aren’t made with deliberation.
When a b-cell makes an antigen it’s also made with “just one seqeuence”.
And during the process of evolving new antibodies, your b-cells really do go through “many generations” of random mutation and natural selection.
The variation in sequences exist in different members of the population. In your immune system it is in the population of b-cells and t-cells the variation is found, in eukaryote and prokaryote populations the variation is found in different individuals that make up the populations of that species.
You’ll have noticed we’re not all clones of each other. There are individuals with different mutant versions of all the genes we have. So here the diversity exists between different individuals in the species population, rather than different cells in the b-cell or t-cell populations.
Now to be sure, the generation times for most large multicellular eukaryotes are much, much longer than the generation times of b-cells, and the mutation rate is much lower. But on the other hand there are many more genes mutating simultaneously.
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Which is ludicrous, because the primary mechanism underlying chloroquine resistance involves no protein-protein binding. The PfCRT (a transporter) is evolving.
Why do you keep citing this guy who clearly has no idea what he’s writing about, Lee?
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Let me step this back a bit …
OK. It’s a little more complicated than that, but we can work thru the simple example.
So 2000 steps is very improbable, if the steps are independent, even if each step is 99% certain.
Get a 100-sided die or percentile dice, each roll is independent. a roll of “1” is a failure, “2-100” is a success. Start rolling …
By the time you have rolled 2000 times, the probability you have rolled 2000 successes and zero failure is indeed very small, ~210^-9. On average after 2000 rolls you should have about ~1980 successes and ~20 failures. Roll 22 more times and you have about 50% chance of getting the 2000th success. Roll 22 more, for a total of 2044 rolls, and it’s nearly certain you will have at least 2000 successes. *
Your are calculating the probability of exactly 2000 successes in 2000 trials with p=0.99. Equivalently you could be calculating the probability of zero failure in a single roll of 2000 dice. Your math is correct but it means nothing; no one thinks evolution works this way.
There is some related math for calculating in the thread below. The topic comes up fairly often. 
** Operating in parallel, rolling more than one die in each trial with multiple trials, will obviously speed things up even more, requiring fewer than 2000 trial for 2000 successes. Exactly how much faster requires requires some sort of simulation of sexual mixing, which seems beyond the scope of current discussion.
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