I see you did some homework...
I'm a scientist in training. That's my job
I cannot say I have ever heard Dr. Behe state it but I suspect that he believes his strongest arguments lie with the idea of genetic manipulation (via intelligent intervention) as opposed to simply the magical appearance of organisms/systems.
Ok, where was the genetic manipulation in this?
Dr. Behe notes the need for an artificial inducer IPTG in order to produce Hall's results. The two noted evolutionary mutations required this inducer in order for the beneficial adaptations to occur. IPTG was injected in the medium which (according to Dr. Behe) is not something that would ever occur in nature. I am certain you can follow the logic from here. The mutations were a direct result of intelligent intervention thereby reinforcing the idea that adaptation occurs only with significant intervention. The systems studied will not function (much less display advantagious adaptations) without several other pre-existing components and significant manipulation.
I follow the logic, but I still don't agree. I hope you can follow my logic in turn. First, the most important idea necessary to understand the situation:
E. coli normally eat glucose for energy. They'll keep the
lac operon switched off even if there is lactose around so long as glucose is also present. (I think that's because lactose is a disaccharide, and to get energy from it they first have to break it into glucose + galactose, while glucose they can just use as it is)
Presumably, they could eat glucose before they could eat lactose. In any case, let's assume they got the abilities in that order.
Given that the glucose-only bacteria would die without a source of glucose,
they would not live in glucose-limited environments. (Just like the
Δgalactosidase mutants would not live in the IPTG-free medium). Which means they would not need a
lac operon to survive where they normally lived.
The ability to digest lactose in this situation is an
extra: not essential under "normal" circumstances, but allows the bacteria to explore new habitats or (more likely in the beginning) to get through shortages with more success.
But this ability would only be selected in the right environment. Which also includes that the bacteria would have to
survive there in the first place. It could be a normally glucose-rich place with lactose also present.
What Hall did was not "genetic manipulation" (I gather he had no idea what the mutations were until he examined the lactose-digesting mutants), but providing the right environment! It was a simulation of what could just as easily happen in nature (not in the specific components, maybe, but the general situation of bacteria barely being able to survive, and an as yet inaccessible nutrient available in plenty).
As for the permease problem,
E. coli lac permease belongs to a
family of proteins that also transport a variety of other related molecules. In the evolution of the original
lac operon, the permease could have come from a gene duplication. Whether the permease or the galactosidase appeared first (likely as a protein that originally did other jobs and just happened to be able to deal with lactose as a byproduct, like Hall's ebg), the evolution of the other would have given the critters an advantage in glucose-limited environments.
I'm pretty sure the sophisticated regulation of the
lac operon came
last; so the original operon would have been switched on as a whole, and probably switched on regardless of the presence of glucose or lactose, and the permease would not have been independently regulated of the galactosidase - therefore no need for the regulatory function of the galactosidase. Regulation would have been an additional step to ensure that the cell does not waste energy on lactose metabolism when it can manage in other ways.
The point of this mental exercise is that the need for IPTG is a feature of the experimental setup (in which the pre-existing system depended on a regulator to express the permease), not an absolute requirement for the appearance of a
lac operon.
Also, look again at the citrate-digesting
E. coli. To my knowledge, they got nothing but citrate to stimulate them. It took them over 30 000 generations (rather longer than Hall's experiments, I think, though a digital copy of the original paper doesn't seem to exist), but they figured it out.
I will read between the lines a bit but I cannot help but note during several reading of Dr. Behe on this subject that Dr. Behe implies that certain beneficial mutations can occur in E. coli given the right circumstances; but these changes may very well be preprogrammed or selected to occur under the correct conditions. I would not be surprised if this train of thought was applicable to all living organisms. This really is significant because it IS an alternative paradigm to materialistic evolution.
No, it's only an alternative paradigm to the randomness of mutations with respect to fitness, as I don't see why adaptive mutation necessarily implies a "non-materialistic" source.
What
is "materialistic evolution" anyway?
Back to the "wishful thinking" that I mentioned before. I share this wishful thinking at a "gut" level~~It may not be very scientific but imagining the entire universe and all living matter arising from nowhere seems an absurdity.
A lot of things in science seem an absurdity. I mean, gravity can bend light???
Yes, it can. That doesn't mean gravity is a supernatural force, just that common sense isn't always the best guide to the natural world.
Oh, and the "I can't imagine" argument says more about your imagination than the thing you can't imagine.
The mechanism of evolution itself (especicially at the genetic level) is a fantastic system that seems far to complex and mechanical to simply have arisen from nothingness.
What nothingness, and in what ways is it too complex? Just asking because evolutionary biology is going to be my degree in a year and a half, and I haven't seen any such sign so far.
