What does “probability of evolving an eye” refer to? The probability of getting a 6 on a six-sided die is 1 in 6 upon rolling it once.
The probability of evolving an eye is .1, upon… what? “Rolling an evolution”? Something is missing here. The probability of evolving an eye must be specified in the context of some circumstance and length of time. Statements about probabilities of evolving something can only make sense when you detail the relevant factors and circumstances.
Sure, if the probability of evolving an eye is .1 out the total history of life on Earth, finding that it has evolved 50 times is very surprising. However, why should we think it is .1? Finding that it has evolved 50 times independently can at least as well tell you that the probability is so high that we would expect it to evolve 50 times in the history of life on Earth.
So what justification do you have for thinking it is .1 in the entire history of life? Or whatever you think is the real number, and why.
The model works regardless of what you set the transparency and refractive index to be. “Useful” just means not completely opaque and doesn’t completely bend and reflect all light away, that is to say some light penetrates through, and doesn’t shine directly into a perfect mirror. Regardless of how poor you set the initial conditions, if you allow variation to arise, selection can favor improvement.
Incidentally skin is almost completely transparent, particularly for microscopic animals where eyes are thought to have first evolved, and changing it’s opacity and refractive properties is a trivial matter of up or downregulating the concentration of the molecules that most affect those, and/or changing how those molecules interact with light.
It’s worse than that! The intermediate hosts were not being treated with chloroquine, so the selection was intermittent. Behe pretends that it was constant.
And as the parasite is going through phases with and without chloroquine, the selection landscape is very complex. Behe just pretends that none of that is happening.
So new surfaces on HIV proteins would have been made that could bind to any other viral protein in every orientation. Yet of all the many molecules its mutated proteins must have bound, none seem to have helped it; no new protein-protein interactions have been reported.
That was an objectively false statement when Behe wrote it, Lee.
Really? I count five, all of which are beneficial. How much would you bet that you are right and I am wrong?
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Why doesn’t HIV convincingly demonstrate it? It seems to me that it is pretty convincing, or Behe and you wouldn’t be going to such lengths to misrepresent the evidence itself.
How many completely different flagella do we already know about?
It’s an ironclad empirical prediction of Behe’s hypothesis. If two are required to increase resistance, one can’t possibly increase resistance by itself. How much are we betting?
I think that you haven’t looked at the relevant evidence. Nor did Behe before making ridiculous claims. By the way, what exactly is a “trial of the malarial parasite”? That looks like word salad to me.
He claims that, but he doesn’t compute anything of the sort.
Yet HIV evolved five, while Behe claimed zero, in real time.
Ah. Looks like another Texas sharpshooter, then. The model supposes nothing except that there is variance in quantitative characters, and that this variance will be maintained by new mutations in all directions. And we observe just such things in nature.
The change has to increase in frequency and eventually become fixed, but selection can act on many loci at once. You seem to be assuming that allele A must be fixed, and then allele B must be fixed after that, and so on. That isn’t how quantitative traits work. What’s moving here is the population mean.
Why do you assume either of those things? And why must a model of the eye incorporate neural evolution anyway? Everything in the organism is connected, so why stop there?
Events can’t be both unique and repeated, so it’s hard to parse that claim. Nor have you given any justification for supposing design.
You cannot generalize this number to all fixation even if, for sake of argument, you allow it for chloroquine resistance, because as you have discussed yourself, a mutation rate is not the fixation rate. A fixation rate is anything but constant. Do you have any idea how many chloroquine resistant mutations dead ended with a mosquito which just flitted around aimlessly until it expired, or in the gullet of a fish or bat, per successful fixation? Fixation can be expected to vary widely. Why would that exact ratio apply to mutations resulting in favorable vision or mobility, or to creatures whose reproduction strategy is few offspring high investment vs. large offspring broods to offset high mortality?
That is generally a fruitful approach. Biologists note what evolution actually did, resulting in progressive understanding of vision and flight, adaptation to new environments, and the rich history and diversity of life on earth.
?!? What? Where else would you expect it to go? What use is an opaque lens?
But you claimed that was a definition of ‘design’. It was not.
You don’t understand the problem, or even that there might be a problem. Repeating your self-contradictory claim won’t help you, but that’s all you seem capable of.
That’s fine, and a rock could be shaped by a human for a particular purpose, and that could be undetectable as design. That does not mean that we cannot detect design in other instances.
If you are interested in the details, I refer you to Behe’s book The Edge of Evolution. Behe finds from considerations of protein shape space:
“That means that if just five or six positions changed to the right residues—the ones that would allow the two proteins to bind—that would be an event of approximately the right frequency, since twenty multiplied by itself five or six times (205 or 206) is about three million or sixty million, respectively—relatively close to the ten to a hundred million different sites we need. So one way to get a new binding site would be to change just five or six amino acids in a coherent patch in the right way. This very rough estimation fits nicely with studies that have been done on protein structure.” (The Edge of Evolution, p. 134)
Let us assume you are right, and that the protein - protein binding sites shape space involving more than a couple of mutations must be due to divine design. This would apply to the identified covid variants - alpha, beta, delta, omicron, BA.1 and BA.2, and I have not listed them all. Several identical key mutations repeated in independent lineages, so that would definitely mean reuse of design, right? The covid spike protein binds to human ACE2 receptors in a way that triggers active conformational changes to permit invasion of the cell. I presume you have not been living in a cave the past two years. Why and how do you think these variants were all in succession divinely designed?
The spike - ACE2 binding can be presented as classic ID rhetoric. The two proteins must interface; if the one changes the other will not match. Blah There is information. Blah blah. There is a sequence space. Blah blah blah. What is to prevent me from proclaiming, behold omicron, evidence of design ?
Of course such a line of argument would not be pursued because it would make ID look ridiculous even to the choir. The reality is that protein - protein interfaces are generally not so brittle, one protein can change while the other remains static, co-adaptation happens all the time, there are often many viable paths, there can be many royal flushes in the deck, a good enough hand need not be a flush to win, and what is stunted in one environment can flourish is another.
Behe never found anything of the sort, and you have zero evidentiary basis for claiming that he found anything. That’s why there are no citations in this passage. It’s fiction, like Behe’s claim that no new protein-protein binding sites have been evolved by HIV.
That’s an utterly absurd fabrication and does not describe what we have learned from structural biology at all.
Binding sites are anything but digital–they come in all shapes and sizes. By combining genetics with biochemistry, as I have done throughout my career, we know that binding is routinely created, altered, or destroyed by changing single amino-acid residues.
Anyone who has ever purified any protein (even undergraduates, @Eddie) is well aware that the greatest problem is that of the protein aggregating NONspecifically (binding to itself).
Yeah unfortunately that doesn’t make sense as a response to what I said, and regardless it’s very strange for Behe to think a new protein binding site is beyond the edge of evolution while simultaneously admitting it has evolved in HIV. 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.
Let’s assume each step in the evolution of the eye is 99% probable, now Nilsson and Pelger estimate about 2,000 steps to evolve an eye, without regard to the neural processing changes that would be needed, so let’s add another 4,000 steps for neural processing, which is more complex than simple changes to an orbital cavity.
This results in a 1 in 6.5 x 10^27 chance for the eye to evolve, even if every step is 99% probable! Now there have been about 10^40 total organisms in all life’s history, as I have heard, so for the eye to evolve twice (never mind 50 times), we would need more organisms than have been present on earth.
But covering the eye opening? We can’t assume that evolution knows where to put the lens.
No, “Nicholas White of Mahidol University in Thailand points out that if you multiply the number of parasites in a person who is very ill with malaria times the number of people who get malaria per year times the number of years since the introduction of chloroquine, then you can estimate that the odds of a parasite developing resistance to chloroquine is roughly one in a hundred billion billion.16 In shorthand scientific notation, that’s one in 10^20.” (The Edge of Evolution, p. 57)
Here is the relevant quote from White’s paper: " Resistance to chloroquine in P. falciparum has arisen spontaneously less than ten times in the past fifty years (14). This suggests that the per-parasite probability of developing resistance de novo is on the order of 1 in 1020 parasite multiplications."
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I see no reference to a paper on p. 158.
I would need to see the details, the one instance I am aware of is the (disputed) Vpu gene.
No, two are required to provide basic resistance, and just one mutation does not provide this. Otherwise, resistance would occur at about the rate of atovaquone resistance, about 1 in 10^12 as I recall.
One parasite organism.
I must refer you to his argument in his book, where he examines protein shape space.
What does it mean to say a step is 99% probable? What is the “event” in question? Under what circumstance? What length of time?
No, let’s not agree to made up numbers. Justify the assumptions.
You seem to think the lens an object that would spontaneously develop anywhere on the body and that you sort of have to wait for it to develop in the right spot. That betrays a complete misunderstanding of development, naturally existing variation in traits, and gene expression.
While variation would exist in attributes all over the body (thickness of skin, concentration of all sorts of proteins and metabolites in cells, etc.) obviously there is no selection for transforming those tissues into lenses where they have no effect.
The formation of the lens is the product of selection operating on the naturally existing variations that exist in the tissue covering the light-sensitive spot. The expression and properties of the genes that control the development of the tissues covering the light-sensitive spot is what is subject to selection and leads to formation of the lens there instead of elsewhere. Sure, mutations that could in principle contribute to lens formation elsewhere on the body are bound to occur, but will not be selected for in those locations. You are aware, I hope, that genes control the attributes and development of tissues all over an organism’s body?
Behe does not apply that ratio (1 in 10^20) directly to other structures or creatures. From considerations of protein shape space, he deduces that arriving at a new, beneficial protein-protein binding site is also on the order of 1 in 10^20. Thus two new such binding sites is beyond the edge of evolution.
Here you assume that evolution did these things! But if Behe’s edge of evolution is correct, then these are unlikely to be the products of evolution.
I’m just saying that a lens appearing just where it is needed, with an appropriate set of parameters, is a big step, not to be expected as a matter of course.