Do you mean that Behe has a habit of ignoring his critics?
All your claims here are perfectly unsubstantiated.
Now, could you tell me what very different story, according to you, is told by the evidence from the malaria example?
No, the paper by Summers et al was definitely very good news for the thesis developed by Behe in the EoE.
For the records, here is Behe’s response to Moran’s often confused critic you pointed to.
That response is very interesting. I will quote one passage:
I wrote in my last post that I had cited chloroquine resistance in Edge as a likely example of the two-mutation phenomenon, and that Summers et al. recently “confirmed” that it did need two mutations to pump chloroquine. Moran responds, “This is a little bit misleading and possibly a little bit disingenuous. Everyone understood that chloroquine resistance was rare and that it almost certainly required multiple mutations.”
I’m afraid it is he who is playing the ingénue. There’s a big difference between simply requiring serial additive mutations for some maximal effect and requiring multiple mutations before you get an effect at all. The first is a run-of-the-mill, gradualist Darwinian scenario: one mutation comes along, helps a bit, spreads in the population by selection, which increases the base from which the second mutation may arise; the second appears, helps a bit more, spreads, and so forth. Lather, rinse, repeat.
But if the first required mutation (or second, or third) doesn’t help, or positively hurts, then the gradualist scenario is interrupted. The first mutation does not spread in the population (in fact it’s actively kept in check by negative selection), so the number of organisms with the mutation does not increase and can’t provide a larger base within which the second mutation can arise. The Darwinian magic is turned off.
Do you think that is an accurate understanding of Moran’s position? If so, please support your claim with quotations from Moran’s article. Thanks.
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I think ultimately the whole CQR debacle is a nothingburger because CQR evolved.
Behe’s case seems to be something like “If X scenario applies, Y would have great difficulty evolving within some timeframe” and then he points to CQR as an example of something that was very difficult to evolve because a somewhat restrictive scenario applied (hence it took longer for CQR to evolve than resistance to other antibiotics have arisen in other organisms). And if we imagine the scenario was even more restrictive, Y would never evolve in the lifetime in the universe.
Great. Cool. I agree. It’s just that we have zero evidence that such a scenario applies to any other known adaptation in any known form of life. We have literally NO data that indicates that for some known morphological or molecular adaptation from some known organism to have evolved, it would have had to do so through a series of events so unlikely as to be prohibitively implausble in the history of life.
Then what was the point? To handwave in the direction of an imaginary possibility and then pretend that, well then it just MUST be the case that something else out there in life is so prohibitively unlikely to evolve that ID is required for it?
Yes. Yes that was Behe’s point with it in the first place. Come let us imagine…
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Not only that, but it even provided a loss of fitness.
This is a straw man. ID proponents don’t believe that all adaptations are exceedingly difficult to evolve, not at all. They perfectly understand that adaptations that can be reached through a smooth route comprising baby steps wherein each individual step involves a beneficial mutation is quite easy to evolve naturalistically. The problem for evolution arises for adaptations that require several mutations that are, individually, detrimental or unselected, as the story of HCQ resistance in malaria documents.
Speaking of the time-lapsed agar petri dish video posted at 19 by @AllenWitmerMiller, I don’t know if the specific mutational paths that the different lineage of bacteria went through to evolve their capacity to survive in high antibiotics have been deciphered. But the prediction is that those mutational paths were all smooth and that none of them involved a step requiring even only two mutations individually detrimental or neutral.
I am curious as to how Gilbert knows that it is Moran’s “critic” [sic] (I assume he means critique) that is “confused”, rather than Behe’s own response to it – Behe is after all no more an expert on chloroquine resistance than he is on any of the other subjects he’s been pontificated on ineptly for the last thirty-odd years.
Has Gilbert been hiding his own expertise on chloroquine resistance ‘under a bushel’?
Or is it just yet more wishful thinking on his part?
Addendum: I forgot an obvious third option, Moran’s critque is “confused” because Behe says it is, and everything that Behe says must be the ‘gospel truth’
The Gospel According to Saint Michael of LeHigh – patron saint of Astrologers.
credulous adj
Over-ready to believe; apt to believe on weak or insufficient grounds.
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That might be Behe’s prediction, but it isn’t a prediction of evolutionary theory. Technically there are ways—if conditions are right—for deleterious mutations to go to fixation despite being individually selected against, when either they can hitchhike with benficial mutations, or they slip through population bottlenecks where their effects are masked by strong genetic drift.
Suppose you have an individual carrying a deleterious mutation (the K76T mutation for example) with a 1% fitness cost, have a few offspring, then one of these offspring has a more strongly beneficial mutation that overcompensates (gives a 2% fitness increase) in that environment, for example by giving strong resistance to another antibitioc present).
It’s clear that something like this must actually be quite prevalent in evolution as many adaptations are often compromises between multiple selection pressures, which can even some times fluctuate. The thick coat for fur might help you in the winter months, but be a detriment in the summers. The question is which condition “weighs” more over the lifetime of an individual. This is also relevant to why some organisms evolve to be generalists, and others specialize.
The bacteria adapting to antibiotics in the megaplate experiment could well be fixing deleterious mutations that potentiate later mutations, if they are hitchhiking with mutations that are beneficial for other reasons when diffusing through the agar plates.
This is why these thought-experiment’s of Behe’s a basically worthless for showing some sort of problem with evolution because reality is typically much more complex than these simplistic scenarios.
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Wrong.
Focusing on evolution in CPR, we sampled and phenotyped compensatory mutants, finding that many had not only compensated for growth but had also increased in resistance, often beyond the resistance levels of the propagating front (Fig. 4C). Yet, as these mutants were engulfed by their parental lineage, they stayed constrained to the immediate vicinity in which they appeared and were unable to overtake the moving front. To test whether these compensatory mutants were capable of outcompeting the propagating front, in an additional evolution experiment we sampled the trapped compensatory mutants and moved them forward, re-inoculating them ahead of the still-moving front. These compensatory mutants were able to grow in a region where the front could not (Fig. 4D). Similarly, some trapped compensatory mutants were able to outcompete their parent when placed side-by-side on a fresh gradient plate (fig. S5). Hence, as compensatory mutations often occur behind the front, they are spatially restricted from contributing to the ultimate evolutionary course of the population. Indeed, in the rare cases when these compensatory mutations appeared at the front, and were not physically blocked, they accelerated the adaptive process (movie S3, 00:53; fig. S3). Thus, the fitness of the population is not driven by the fittest mutants, but rather by those that are both sufficiently fit and arise sufficiently close to the advancing front.
I have to say, I cannot recall any ID’er saying that adaptations requiring multiple beneficial mutations commonly occur without the intervention of the “Designer.” Could you provide some citations?
In any event, that is not the only way, nor even the most common way, that adaptations occur. Can you think of another?
Well, sure. Are you under the impression that this is something ID’ers first realized?
Not so fast, there. We’re still discussing whether that is that case.
If so, so what?
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Not at all. He certainly does write many many blogs mentioning certain critics. But regarding studies like the one shown at the top, he will either ignore it or twist it to fit his narrative.
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You substantiate it below by avoiding the obvious evidence and pretending that Behe’s misrepresentations of the evidence are more important.
Behe claimed that only two mutations could work and that they had to have occurred simultaneously. The evidence in the paper Moran cited demolishes both of those claims.
Again:
Try engaging with the evidence YOURSELF, Gilbert. It tells a very different story.
I predict that you lack sufficient faith to do so.
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There were covid variants displaying synergistic mutations which were individually deleterious. It happens in the real world and petri dishes.
Real-time identification of epistatic interactions in SARS-CoV-2 from large genome collections
Interview - Synergistic mutations found in omicron variant of SARS-CoV-2
“Both escape mutations and increased infectivity were observed in the omicron variant of SARS-CoV-2,” says Galardini. “Epistatic interaction can enable pathogens to acquire favorable properties even though the individual mutations are deleterious.”
Compensatory epistasis maintains ACE2 affinity in SARS-CoV-2 Omicron BA.1
We find that immune escape mutations in BA.1 individually reduce ACE2 affinity but are compensated by epistatic interactions with other affinity-enhancing mutations, including Q498R and N501Y. Thus, the ability of BA.1 to evade immunity while maintaining ACE2 affinity is contingent on acquiring multiple interacting mutations. Our results implicate compensatory epistasis as a key factor driving substantial evolutionary change for SARS-CoV-2 and are consistent with Omicron BA.1 arising from a chronic infection.
Importantly, L455F single substitution significantly dampens receptor binding; however, the combination of L455F and F456L forms an adjacent residue flipping, which leads to enhanced NAbs resistance and ACE2 binding affinity. The perturbed receptor-binding mode leads to the exceptional ACE2 binding and NAb evasion, as revealed by structural analyses. Our results indicate the evolution flexibility contributed by epistasis cannot be underestimated, and the evolution potential of SARS-CoV-2 RBD remains high.
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Yes. As I have said elsewhere, he could just as easily have written an entire book on the fact that no malaria parasite has ever evolved the ability to do differential calculus, therefore this ability is beyond “The Edge of Evolution”, therefore evolution is false and ID is true.
But if he did that, it would be even more obvious than it already is how stupid his argument is. Though maybe his devoted fans will still think it was brilliant.
Also, to your last point: There likely have been some prohibitively improbable adaptations that have occurred over the course of evolutionary history, just by luck of the draw. For the same reason, even though the odds of winning the lottery are very low, someone eventually wins it.
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Here is the other thing when it comes to point of The Edge of Evolution. What is presented is the odds of a given specific adaptation. Where is the accounting of the billions of adaptations which could have happened, such as arms on bird creatures or human UV vision, but never materialized? Lottery winners rake in millions, exactly because it did not happen for millions of others. Other improbable mutations could have happened instead of the particular ones that led to familiar life. Instead of Earth, we could be Pandora, and creationist Pandorans then arguing about the odds of mountain banshees evolving while neglecting that there were an infinity of alternate possibilities.
Evolution, as Gould argued in Wonderful Life, is capricious. The odds were actually against every living thing we see around, but here we are. You and me are absurdly lucky in that every generation leading up, for hundreds of millions of years without a single exception, did not fail to adapt, survive, and successfully breed. Such fortune was beyond the edge of evolution for many species, genera, and even classes. No adaptation came to the rescue of trilobites. The history of life is replete with extinction, where variation was not sufficient to keep pace with change. Animals that were related but not descendant would fill the void, but that was the end of the line for the extinct. Recognizing that fact was one of the first observations that caused people to question a static and fixed creation to begin with.
The planet’s spoils go to the victors. Others fall by the way. Of course evolution has an edge, that is what is expected and found.
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Hasn’t CQR resistance evolved at least 4 times (or is it 7?) that we know of since we started keeping track? This seems to be yet another case of the more it happens the less likely it is to occur.
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Nope. It means that each new emergence of resistance is a miracle.
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Yes, Behe acknowledges this. His argument is not that CQR resistance required God to intervene as an “intelligent designer.” Rather, he argues that it represents “The Edge of Evolution.” There are, therefore, several possible reasons that a hypothetical adaptation would lie beyond this “edge”. For instance, an organism with a significantly smaller population and/or longer generation time would be unable to generate an adaptation of similar genetic complexity in a realistic time scale. Or, if the mutational steps have lower selection coefficients than those involved in CQR resistance, it would similarly be beyond Behe’s “edge” (all else being equal).
The informed reader will note that there is nothing novel about what Behe is claiming. No evolutionary biologist would deny that there are adaptations that, for these (and other) reasons, are prohibitively unlikely to evolve. But among the many failings of Behe’s argument is that he has not demonstrated that CQR, itself, represents such an “edge” (The reasons newly resistant strains have been identified as rarely as they have been go beyond the parasite’s population genetics). And, crucially, he has not demonstrated any observed traits that do lie beyond his “edge” and, therefore (by his logic), have been “intelligently designed.”
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This is not surprising given the high mutation rate of SARS-CoV-2, the huge number of people that have been infected and the huge number of virus particles in each infected person.
To me, that would be surprising since if you have enormous population sizes, natural selection is far more effective over genetic drift, such that it is actually more difficult for deleterious mutations to be fixed. I believe one of the main hypotheses for the highly divergent Omicron variant is that it evolved in prolonged infection within immunocompromised individuals, such that it existed in a weak selective environment allowing it to cross valleys within the fitness landscape.
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You can accumulate 2 synergistic mutations that are individually detrimental without genetic drift, can’t you?