A propos du livre de Behe: The Edge of Evolution
Publié : 29 juin 2007, 18:32
Bonjour, est-ce que quelqu'un aurait un accès au New York Times? Je cherche un article critique de R. Dawkins sur le nouveau livre de M. Behe "The Edge of Evolution". On en trouve quelques passages ici mais j'aimerai le lire entièrement si possible.
A mon avis, les arguments que l'on trouve sur la page de Pharyngula démontent assez bien les affirmations de Julien sur l'impossibilité des mutations "bénéfiques": si elle étaient aussi impossibles que Julien le prétend, la sélection intelligente humaine n'aurait pu façonner autant d'espèces domestiques (de chiens ou autres) par des moyens "naturels".
Le livre de Behe s'est fait pasablement éreinter dans Nature, dans une critique de K.R. Miller (28 (2007): 1055-1056; voir ici (demande sans doute un abonnement)). Miller dénonce aussi les pseudo-calculs qui ne visent, contre toutes observations, qu'à laisser-croire à l'impossibilité de l'évolution. Il prend un exemple de Behe concernant l'acquisition d'une résistance de l'agent causant de la malaria à un antibiotique:
"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."
Et, il démolit joyeusement l'argument... en égratignant la réputation de Behe au passage:
"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."
Suit un relevé d'erreurs similaires tirées d'un autre livre de Behe ("Darwin's Balck Box"). Puis:
"No doubt creationists who long for a scientific champion will overlook the parts of this deeply flawed book that might trouble them, including Behe's admission that "common descent is true", and that our species shares a common ancestor with the chimpanzee. Instead, they will cling to Behe's mistaken calculations, and proclaim that the end of evolution is at hand. What this book actually demonstrates, however, is the intellectual desperation of the intelligent-design movement as it struggles to survive in the absence of even a shred of scientific data in its favour."
Jean-François
A mon avis, les arguments que l'on trouve sur la page de Pharyngula démontent assez bien les affirmations de Julien sur l'impossibilité des mutations "bénéfiques": si elle étaient aussi impossibles que Julien le prétend, la sélection intelligente humaine n'aurait pu façonner autant d'espèces domestiques (de chiens ou autres) par des moyens "naturels".
Le livre de Behe s'est fait pasablement éreinter dans Nature, dans une critique de K.R. Miller (28 (2007): 1055-1056; voir ici (demande sans doute un abonnement)). Miller dénonce aussi les pseudo-calculs qui ne visent, contre toutes observations, qu'à laisser-croire à l'impossibilité de l'évolution. Il prend un exemple de Behe concernant l'acquisition d'une résistance de l'agent causant de la malaria à un antibiotique:
"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."
Et, il démolit joyeusement l'argument... en égratignant la réputation de Behe au passage:
"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."
Suit un relevé d'erreurs similaires tirées d'un autre livre de Behe ("Darwin's Balck Box"). Puis:
"No doubt creationists who long for a scientific champion will overlook the parts of this deeply flawed book that might trouble them, including Behe's admission that "common descent is true", and that our species shares a common ancestor with the chimpanzee. Instead, they will cling to Behe's mistaken calculations, and proclaim that the end of evolution is at hand. What this book actually demonstrates, however, is the intellectual desperation of the intelligent-design movement as it struggles to survive in the absence of even a shred of scientific data in its favour."
Jean-François