Behe claims evolution can’t produce IC structures through direct pathways where each step confers a survival advantage. That’s a rather meaningless point since it’s been empirically demonstrated evolution can produce IC structures through indirect pathways.
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This is not his claim. Listen and understand his discussion w Swamidass.
Welcome to Peaceful Science @Sam 
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That discussion was a travesty. I’m surprised Behe’s nose didn’t grow so long is smashed thru my monitor.
@swamidass showed admirable self-restraint.
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7 posts were split to a new topic: Side squabbles from Sam Asks About Behe
So your position here is that Michael Behe believes it is possible for biological structures he considers to be “irreducibly complex” to have arisen thru undirected evolutionary processes, with no interveneion required by an “intelligent designer.”
Could you please quote where he has written this?
I don’t know what you mean by an “indirect pathway.”
Anything other than the sequential addition of invariant parts. Scaffolding, for example, is an indirect pathway.
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But does the base alone have to eliminate mice to serve a useful function? Is that piece of wood by itself absolutely useless? I don’t think so. It might not make for a functional mousetrap at all, and it might not even have any use that has anything to do with mice, but that alone does not tell you it is useless.
Same goes with the base and one more component. Does it have to now function as a mousetrap, or can that combination of parts not also serve some other useful function?
I hope you can see where I am going with this.
The problem with irreducibly complexity as an argument against evolution is not that some things aren’t irreducibly complex in that sense of the word. There are irreducibly complex things in biology, but that does not mean they could not have evolved. I agree that, for example, the bacterial flagellum is irreducibly complex. If you remove the hook and filament from the flagellum, then it stops working as a flagellum. But that does not mean it stops working entirely. What sits below the hook and filament is a protein secretion system that can pump proteins out of the bacterial cell. So it still has a function. It can secrete, for example, pilus proteins, adhesion proteins, or enzymes.
This is actually a well-known phenomenon in molecular biology. Existing “components” (such as individual proteins) can be combined in novel ways that produce new functions in a phenomenon called exaptation. An enzyme that used to catalyze a chemical reaction can change function and become a type of structural protein, or pieces of two different proteins doing totally different functions, can be combined into a new protein with a novel function of it’s own.
Almost all of the proteins that make up the flagellum evolved from ancestral proteins that used to perform different functions, often times as part of simpler pre-flagellum structures.
Nick Matzke wrote a very good article on the evolution of the bacterial flagellum back in 2003:
It’s a long article that goes well into depth with explaining how the bacterial flagellum could have evolved gradually, and what evidence we can infer it’s possibly evolutionary history from, but in it’s most succinct form the model is captured in this figure:
Figure 7: Summary of the evolutionary model for the origin of the flagellum, showing the six major stages and key intermediates. White components have identified or reasonably probable nonflagellar homologs; grey components have either suggested but unsupported homologs, or no specific identified homologs, although ancestral functions can be postulated. The model begins with a passive, somewhat general inner membrane pore (1a) that is converted to a more substrate-specific pore (1b) by binding of proto-FlhA and/or FlhB to FliF. Interaction of an F1F0-ATP synthetase with FlhA/B produces an active transporter, a primitive type III export apparatus (1c). Addition of a secretin which associates with the cytoplasmic ring converts this to a type III secretion system (2). A mutated secretion substrate becomes a secreted adhesin (or alternatively an adhesin is coopted by transposition of the secretion recognition sequence), and a later mutation lets it bind to the outer side of the secretin (3a). Oligomerization of the adhesin produces a pentameric ring, allowing more surface adhesins without blocking other secretion substrates (3b). Polymerization of this ring produces a tube, a primitive type III pilus (4a; in the diagram, a white axial structure is substituted for the individual pilin subunits; all further axial proteins are descended from this common pilin ancestor). Oligomerization of a pilin produces the cap, increasing assembly speed and efficiency (4b). A duplicate pilin that loses its outer domains becomes the proto-rod protein, extending down through the secretin and strengthening pilus attachment by association with the base (4c). Further duplications of the proto-rod, filament, and cap proteins, occurring before and after the origin of the flagellum (6) produce the rest of the axial proteins; these repeated subfunctionalization events are not shown here. The protoflagellum (5a) is produced by cooption of TolQR homologs from a Tol-Pal-like system; perhaps a portion of a TolA homolog bound to FliF to produce proto-FliG. In order to improve rotation, the secretin loses its binding sites to the axial filament, becoming the proto-P-ring, and the role of outer membrane pore is taken over by the secretin’s lipoprotein chaperone ring, which becomes the proto-L-ring (5b). Perfection of the L-ring and addition of the rod cap FlgJ muramidase domain (which removes the necessity of finding a natural gap in the cell wall) results in 5c. Finally, binding of a mutant proto-FliN (probably a CheC receptor) to FliG couples the signal transduction system to the protoflagellum, producing a chemotactic flagellum (6); fusion of proto-FliN and CheC produces FliM. Each stage would obviously be followed by gradual coevolutionary optimization of component interactions. The origin of the flagellum is thus reduced to a series of mutationally plausible steps.
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An indirect pathway is one where every evolutionary step doesn’t have to be beneficial to the organism in leading directly to the end IC product. A pathway where an original function has been co-opted and repurposed (exaptation) by evolution. As example would be the feathers on wings of extant birds. Most extant birds wings are IC since extant birds can’t fly without feathers but feathers existed long before flight evolved.
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3 posts were merged into an existing topic: Side squabbles from Sam Asks About Behe
He does not make the “can’t evolve” argument. Behe understands argument strategy very well. You are not going to win this rhetorically. The best you can do is understand and discuss strength and weaknesses to his argument. @Swamidass does this very well.
A post was merged into an existing topic: Side squabbles from Sam Asks About Behe
Since you are very familiar with his arguments, can you briefly state them?
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Behe’s claim is that irreducibly complex structures are a powerful challenge to evolution. This does not claim they “can’t evolve”. If one wants to claim they can evolve then it is up to the one making the claim to demonstrate it as @Art did with his demonstration of plants evolving a gated ion channel through genetic recombination.
As far as irreducibly goes he states that irreducibly complex structures (structures that require all parts to perform the observed function) offer a powerful challenge to the Darwinian mechanism.
As far as the design argument:
Design is detected by the purposeful arrangement of parts. By purposeful we are talking about an observed function whose direct purpose can be inferred.
He sees that design detection is easier for some observations than others. If you look at his discussion `18 minutes in you will see examples of different observations with different levels of design detection.
This debate is one the best evolution design debates ever held in my opinion.
Behe was already conclusively proven wrong on this ID-Creationist claim decades ago.
No one has ever shown a purposeful arrangement of parts in a biological system. Bill still keeps confusing function for purpose no matter how many times he is corrected. It’s just one more iteration of the Bill-cycle you were warned of. 
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That’s not his argument, that’s the conclusion to his argument. He states reasons why it, in his view, offers a powerful challenge to “the Darwinian mechanism”.
I agree.
24 Nov Behe - A Mousetrap for Darwin
Didn’t see this linked to - delete if already linked.