Isn’t that what Behe says can’t happen in the blog post you cited?
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No. Behe says that this can happen for organisms with huge population sizes and very short generation times such as P.falciparum or SARS-CoV-2. On the other hand, he says that this is forbiddingly unlikely for any class of large animals such as mammals because of the much lower population sizes and longer generations times compared to that of P.falciparum or SARS-CoV2.
Wasn’t there a calculation that was based on CQ resistance only having arisen twice?
(Am usung phone so can’t search easily)
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Diametrically opposite to fact, as large populations make deleterious mutations more visible to selection and more difficult to fix.
However, mammals typically have much larger genomes that suffer higher pr. genome mutations pr. generation (humans typically have ~100 novel mutations), increasing the odds that beneficial mutations co-occur with deleterious ones, facilitating hitchhiking. Additionally due to lower efficacy of selection from smaller effective populations, drift can mask deleterious effects allowing deleterious mutations to persist for longer and even go to fixation.
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Can you be more specific what you believe he means by “this”? Also, to your knowledge, has Behe demonstrated that “any class of large animals such as mammals” actually possess a trait that would have been so “forbiddingly unlikely” according to his understanding of evolution?
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That was likely Behe’s calculation. Here is the more recent paper, educational copy available on request.
I agree that there is inescapable hazard in guestimating microbe counts, rate of fixation, and how often a given trait actually arises, and applying those basis numbers to macroscopic animals which have very different genetic characteristics, reproductive strategies and ratios, but of course this is exactly what Behe attempted.
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I think there are two different but ultimately closely-related stories here.
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There doesn’t appear to be a strong solid consensus on the number of independent origins of CQR, but a key review from 2009 points to at least six (see Fig 5 in that paper).
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The 2023 paper cited by @Dan_Eastwood (which is open access, BTW) might explain how there could be so many (and probably more) independent origins of CQR. As mentioned regularly, CQR from the 20th century seems to depend completely on one key mutation (pfcrt1 K76T). Parasites carrying that mutation have reduced fitness, but like all mutations in all organisms everywhere all the time, the fitness cost is determined by genetic background. (No gene or polymorphism is an island, which should always be obvious but seems to be the first fact elided by apologists.) The 2023 paper reveals a huge role for another gene, pfaat1, in determining the fitness of parasites carrying the pfcrt1 K76T mutation (polymorphism, more accurately), and in the process explains some big differences between continents.
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Yes. I do not see how Behe can honestly cling to his simplistic claim that CQR only results from two specific,individually deleterious mutations that occur simultaneously* (or nearly so), in the same parasite, or at least the same host.
Of course, there are any number of dishonest ways he could continue to make this claim. I trust that @Giltil will be providing us with some examples.
*I am aware that, at some points, Behe says only one of the two mutations must be deleterious. But that is just nonsense. If that were the case, then all that would be required is that the neutral/beneficial mutation occur prior to the deleterious one. Similarly, Behe at other times says it makes no difference to his probability calculations if the trait requires four or more mutations rather than just two. Really?
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What are Behe’s probability calculations you are referring to here?
Can you explain what it is with the different genetic characteristics, reproductive strategies and ratio of large animals that according to you would allow them to develop more easily the type of adaptation exemplified by CQ resistance in malaria?
Picking reproductive strategies, sexual selection can make mutations that would be deleterious for other reasons (negatively affects survival, such as the Peacock’s large tail), go to fixation anyway, either due to hitchhiking with a “sexy allele”, or because it’s a “sexy” allele itself.
That’s just one way. Another would be their considerably lower effective population sizes that means deleterious mutations are less visible to selection, so they can stick around for longer on average, increasing the probability that they can go to fixation due to reciprocal sign epistasis when the other mutation occurs.
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I am referring to what he wrote here (the first quote is from Larry Moran):
The recent paper by Summers et al. (2014) shows that seven of the chloroquine resistant strains that have been observed have at least four mutations and some of them are relatively neutral. This refutes and discredits the scenario that Michael Behe put forth in his book.
It’s hard to see why Professor Moran thinks the second sentence in this quote belongs after the first. Close your eyes and envision a pathway to a malaria parasite that has four mutations. The first mutation is deleterious, the second rescues the first and makes the parasite marginally chloroquine resistant. Subsequent steps are all beneficial by dint of either improving chloroquine resistance or of stabilizing the structure of the mutated PfCRT, which is required for malaria survival. Once a parasite can survive at least marginally in the presence of chloroquine, further mutations can be added one at a time (no longer two at a time) in each cycle of infection because the population size (1012) greatly exceeds the inverse of the mutation rate.
You first need to be more clear what you mean by “the type of adaptation exemplified by CQ resistance in malaria”. It would help if you gave an example of an adaptation found in “large animals” that you believe lies at or beyond Behe’s “Edge of Evolution,” and how you determined this to be the case.
I think it’s important to note that Behe’s writing suggests that he believes evolution is supposed to work like this:
A mutation occurs that produces a beneficial effect.
This mutation spreads in the population and is eventually fixed.
Then another mutation occurs that improves on the effect of the first.
This mutation then spreads to fixation
This process is repeated for every subsequent mutation. If there is an adaptation that involves four mutations, then, each mutation would first have to be fixed before another one has any effect.
Any scenario that differs from this does not meet his personal definition of “Darwinian evolution” and therefore shows that evolution is false and ID is true.
As incredible as it may seem, he really appears to believe this, or at least something close to it. If so, it would help explain why he writes such nonsense.
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Well I think at best Behe has been somewhat inconsistent in his use of terminology. In his interview with @dsterncardinale, Behe explicitly stated that he considers ALL forms of unguided evolution to be “Darwinian” evolution, even all the neutral evolution and so on:
It’s all “Darwinian” evolution to Behe. If it’s unguided it’s Darwinian. And he thinks it can’t work if it’s unguided. Because Behe commits the Texas sharpshooter fallacy.
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That’s another of his silly tricks. He will claim (sometimes, but not always, correctly) that something cannot occur thru Darwinian evolution. And then, since he has unilaterally declared that all evolution that doesn’t involve the direct intervention of God is “Darwinian evolution”, he has thereby proven that it can only occur thru ID.
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It is an apple to oranges comparison. As it is Behe who is committed to the idea, it is his burden to make the case, but it would be challenging to control for all the variables. Microbe parasites have a huge offspring count, with multiplying within the body posing a very different setting than the challenge of contagion, whereas large animals have very small offspring counts with a much higher level of individual success, in relatively constant environments. The reproductive cycle of malaria is nutty complicated. What effect does all that that have respectively on the ratio of mutations occurring to fixation? This is a question. I do not know the answer - does Behe?
Then the matter of two deleterious sequential mutations. Fitness is relatively easy to measure in a petri dish, with large, fast replicating and expanding populations. Large animals are not so conveniently disposed. So how deleterious are we talking here? It is not binary. If it is embryonic re-absorption, stillbirth, or lethal, that is the end of the road. If it is slight, then several factors can impact selection and escape.
As well, most of the distinctions between populations are regulatory. Many subspecies isolated on islands will be appreciably larger or smaller than their mainland counterparts, but their proteins will be close if not identical. A Dutch dude is likely to be taller than me, but we would share essentially the same proteins. Related animals look very alike as embryo’s and grow more visually distinctive as they mature. Regulatory evolution is by its nature more a matter of timing and proportionality, and typically does not have to cope with some double step barrier. So as has been asked earlier in the thread, what example does Behe have for large animals? Are cats and dogs beyond the edge?
Then, lest we forget, in play is the ample time of millions of years to bungle in the jungle.
We know that adaptations which are beneficial in combination occur; covid and Behe’s own example are demonstrations of concept; the matter is then one of degree. In that regard, rigor is absent, with a hopelessly dodgy calculation supposedly posing a challenge to a much more established body of evidence.
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Just to clarify, the calculation itself wasn’t dodgy. It was referring to fixation, not mutation. It’s Behe misrepresentation of it that’s dodgy.
Yes. The calculation was not dodgy, Just trivially, childishly simple:
If the odds of a specific mutation occurring in an individual are 10-10, then the odds of two such mutations occurring simultaneously in the same individual are 10-20.
Nothing more there than freshman genetics and high school math.
The dodgy parts: Someone makes an offhand comment in a paper that CQR in malaria has arisen in human patients, by a very rough estimate, every 1019 to 1020 generations.
Behe says “Hey, 1020 ! That’s the same number as two mutations with odds of 10-10 occurring at once! Therefore, CQR requires two 10-10 mutations at once! Therefore God!”
And writes a book about this.
Can someone explain why this ought to be taken at all seriously?
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Interesting.
But I thought Darwinism was dead, and intelligent design people were using it as a straw man.
What is this in response to? I did a search for “Darwinism” and no one has talked about it in this thread.
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