29 June 2007

Neues zu Michael "The Edge" Behe.

Zwei weitere Kommentare zu Behes neuem Buch sind erschienen, einer bei Dawkins in der New York Times und ein weiterer von Kenneth Miller in Nature [Miller KR (2007). Falling over the edge. Nature 447:1055-1056].
Dawkins Beitrag ist nur für Abonnenten zugänglich, so dass ich ihn nicht lesen konnte. Es gibt aber Ausschnitte daraus, z. B. hier. Der Nature-Artikel ist ebenfalls nicht frei zugänglich, aber über die Arbeit komme ich da natürlich ran.

Hier ein relevanter Ausschnitt:
[...] To Behe, the genetic changes in both parasite and host represent the absolute limit of what darwinian processes can accomplish, and mark the "edge of evolution". [...]
Where does this leave evolutionary explanations of more complex systems? Behe tells us frankly that darwinism cannot account for even a modest share of the complexity of life, and therefore design is absolutely required as an explanation. Yet, at the heart of his anti-darwinian calculus are numbers not merely incorrect, but so spectacularly wrong that this badly designed argument collapses under its own weight.

Behe cites the malaria literature to note that two amino-acid changes in the digestive-vacuole membrane protein PfCRT (at positions 76 and 220) of Plasmodium are required to confer chloroquine resistance. From a report that spontaneous resistance to the drug can be found in roughly 1 parasite in 1020, he asserts that these are the odds of both mutations arising in a single organism, and uses them to make this sweeping assertion:

"On average, for humans to achieve a mutation like this by chance, we would need to wait a hundred million times ten million years. Since that is many times the age of the universe, it's reasonable to conclude the following: No mutation that is of the same complexity as chloroquine resistance in malaria arose by Darwinian evolution in the line leading to humans in the past ten million years."

Behe, incredibly, thinks he has determined the odds of a mutation "of the same complexity" occurring in the human line. He hasn't. What he has actually done is to determine the odds of these two exact mutations occurring simultaneously at precisely the same position in exactly the same gene in a single individual. He then leads his unsuspecting readers to believe that this spurious calculation is a hard and fast statistical barrier to the accumulation of enough variation to drive darwinian evolution.

It would be difficult to imagine a more breathtaking abuse of statistical genetics.

Behe obtains his probabilities by considering each mutation as an independent event, ruling out any role for cumulative selection, and requiring evolution to achieve an exact, predetermined result. Not only are each of these conditions unrealistic, but they do not apply even in the case of his chosen example. First, he overlooks the existence of chloroquine-resistant strains of malaria lacking one of the mutations he claims to be essential (at position 220). This matters, because it shows that there are several mutational routes to effective drug resistance. Second, and more importantly, Behe waves away evidence suggesting that chloroquine resistance may be the result of sequential, not simultaneous, mutations (Science 298, 74–75; 2002), boosted by the so-called ARMD (accelerated resistance to multiple drugs) phenotype, which is itself drug induced.

A mistake of this magnitude anywhere in a book on science is bad enough, but Behe has built his entire thesis on this error. Telling his readers that the production of so much as a single new protein-to-protein binding site is "beyond the edge of evolution", he proclaims darwinian evolution to be a hopeless failure. Apparently he has not followed recent studies exploring the evolution of hormone-receptor complexes by sequential mutations (Science 312, 97–101; 2006), the 'evolvability' of new functions in existing proteins — studies on serum paraxonase (PON1) traced the evolution of several new catalytic functions (Nature Genet. 37, 73–76; 2005) — or the modular evolution of cellular signalling circuitry (Annu. Rev. Biochem. 75, 655–680; 2006). Instead, he tells his readers that there is just one explanation that "encompasses the cellular foundation of life as a whole". That explanation, of course, is intelligent design.
Nett.

Auf Dawkins gibt es schon eine Reaktion des Disco Institutes, wo sich übrigens auch zwei "Antworten" auf Sean Carrolls Buch-Review finden (Part I and Part II). Behe selbst hat auch schon auf einige Kritiken reagiert (die von Coyne, Carroll und Ruse), vielleicht wird er ja zu den neuen Kritiken auch noch was schreiben.

Eine Linkliste zu Reaktionen auf Behes Buch gibt's bei Science After Sunclipse.

MfG,
JLT

[Bild-Quelle: Tom Toles]



UPDATE 02.07.07:
Professor Jerry Coyne addresses Michael Behe's reply to Coyne's review of Behe's new book.

Darin fasst er die Hauptkritikpunkte noch einmal zusammen:

  1. There is no evolutionary expectation that complex protein-protein interactions will evolve in a parasite adapting to a new drug. Any mutation that improves fitness is acceptable, regardless of what it does.
  2. Behe's probability calculations, on which his entire argument rests, are flatly wrong because they assume that adaptation cannot occur one mutation at a time. He uses chloroquine resistance of malaria (CQR) as an example, saying that the parasite always must have two mutations arising together to evolve resistance. As Ken Miller shows, this assumption is false, because one of the two mutations that Behe claims are "required" for CQR is not actually required (Chen et al. 2003, reference accidentally omitted from Miller's piece). It is therefore bogus to take the 1/10e20 number as the estimate of the probability of the evolution of a single binding site for CQR. And it is even more bogus to use this as a generic estimate for the evolutionary probability of getting any protein-protein binding site.
  3. The probability calculations are also wrong because Behe's argument is based on specifying a priori exactly which mutations have to occur to be adaptive: the identical pair of mutations that occur in chloroquine-resistant malaria. He neglects the possibility (indeed, the certainty) that many other mutations that cause interactions between proteins and other molecules can also be adaptive.

1 Kommentare:

Thomas Waschke said...

Die Rezension von Dawkins ist inzwischen frei zugänglich:

http://richarddawkins.net/article,1360,Inferior-Design,Richard-Dawkins

Mein Eindruck ist ein wenig gespalten. Dawkins brilliert zwar im Ausdruck, aber nicht in der Sache. Das Hunde-Beispiel wird einen aufrechten ID-ler oder gar Kreationisten nicht überzeugen: Mikroevolution innerhalb eines Grundtyps wird schon seit Darwins Zeiten anerkannt.

Auch wenn ich von Lönnigs 'Gesetz der rekurrenten Variation' nichts halte, gehe ich doch davon aus, dass Dawkins etwas zu optimistisch ist, was die Möglichkeiten der künstlichen Auslese anbelangt. Soweit ich informiert bin, stößt man immer an Grenzen. Was dann ins Spiel kommt (Mutationszüchtung, Einkreuzungen, 'grüne' Gentechnik), ist dann eher ein Beispiel für Design als für 'selection in the wild'.

Man darf auch mit Fug und Recht bezweifeln, dass die 'Heilige Dreifaltigkeit der Populationsgenetik' und deren Epigonen wirklich gezeigt haben, dass die Selektion hinreichend 'schöpferisch' sein kann. Wenn ich richtig informiert bin, gaben deren Modelle gerade das nicht her. Zudem muss man bedenken, dass diese Forscher unter 'Evolution' die 'Verschiebung von Allelfrequenzen in Populationen' verstanden. Die spannende Frage war schon immer, ob das die gesamte Evolution erklärt, oder ob da bookkeeping mit Mechanismen verwechselt wird.