Well I have been debating this topic on the net for about 4 years now and am still convinced that Dr. Behe has answered his critics to an extent. On the question of the evolution of the eye he basically failed but most of the other points he made he is still flailing away.
I cannot post links as of yet but Dr. Behe's response to Ken Miller "A True Acid Test" (the back and forth between them) is the perfect example of how Dr. Behe basically debates his opponents to a standstill.
*
reads*
The mechanism(s) of adaptive mutation are currently unknown. While they are being sorted out, it is misleading to cite results of processes which "violate our most basic assumptions about the randomness of mutations" to argue for Darwinian evolution, as Miller does.
I think this is the only good point Behe makes, but I haven't read anything about adaptive mutations. I know their existence has been claimed, and I vaguely remember that a few experiments failed to find them, and that's about it.
If, however, adaptive mutations have perfectly normal biochemical mechanisms then they are an even stronger argument against ID than mere natural selection: it's much easier to put together a useful novelty if you can use a larger proportion of all mutations.
Behe's essay said:
The mutations reported by Hall simply enhance pre-existing activities of the proteins.
Which a central point of the argument
against IC. That "new" things are not built from scratch, but from old things accidentally predisposed to working in a new way.
(A huge exception is nylonase, I think, which is the result of a frameshift. Incidentally, nylonase is a prime example that complete novelty is not impossible in evolution, although I wouldn't think complex machines arise that way; that would be a true tornado in the junkyard scenario)
A critical caveat not mentioned by Kenneth Miller is that the mutants that were initially isolated would be unable to use lactose in the wild--they required the artificial inducer IPTG to be present in the growth medium. The reason is that a permease is required to bring lactose into the cell. However, ebg only has a B-galactosidase activity, not a permease activity, so the experimental system had to rely on the pre-existing lac permease.
[...]
With further growth and selection, Hall isolated secondary mutants with improved B-galactosidase activity. These mutants all had the same two changes (mentioned above) at positions 92 and 977 of ebg B-galactosidase. Hall discovered that, in addition to hydrolyzing lactose, the double mutants could also synthesize some allolactose, just as the homologous lac B-galactosidase can do, allowing them to induce expression of the lac operon without further need of IPTG.
Behe shoots himself in the foot. Overcoming the "critical caveat" was
a matter of further selection. Lactose is not the normal foodstuff of
E. coli anyway. Being able to digest it is an advantage where glucose is limited, but not being able to digest it doesn't make a bacterium inviable in its normal environment. Which leads us to neutral evolution...
The chance of fixation of neutral mutations is far from negligible (IIRC, 1/2
N in diploid populations, so I'd imagine 1/
N in bacteria?). While bacteria have huge population sizes that aren't conducive to genetic drift, they also mutate and reproduce faster than bigger things. Plus, IIRC, they switch off a lot of their mutation-checking mechanisms during hard times, so they can produce the most mutations when raw material for evolution is most needed.
What really shakes Behe's argument about neutral evolution is
this experiment, though. It's simulated organisms rather than real bacteria, but the function they evolve is highly complex, they evolve it in a surprisingly large proportion of trials, and sometimes via outright
deleterious mutations. The only incentive towards complex functions is a selective advantage to complete, working functions.
(In case you think a ×2 selective advantage is unrealistic, IIRC that's about the pressure on dark vs. light peppered moths on the wrong-coloured bark. And yes, they do rest on bark and they do get predated, and yes, selectively based on colour. If you want to look at primary sources, I can probably find a paper or two.)
Something similar might be going on with the
citrate-digesting E. coli, but I don't know if the actual mutations have been found since the new ability was reported.
Another important point to consider is that the experiment Miller and Behe are discussing is the reconstruction of
specific functions in a
specific machine. This limits the number of solutions observed, as it's easier to fill the gaps with components that are predisposed to interact with the pre-existing system than make up an entirely new system.
If bacteria without any
lac operon at all would be pressed to use lactose, I'm sure they'd figure it out (just like the Lenski team's
E. coli figured out citrate), and probably in several different ways. Evolution "in the wild" is far less restricted in the range of useful possibilities than this artificial scenario.
So, yeah, Hall's experiments may not be the most spectacular example against IC, but they don't make Behe's point either.
Really, the only thing that is missing is his initiation of a true ID research study.
Really. I wonder
why it's missing
BTW, if it's Dr. Behe, let Prof. Miller have his title too
