Sadly, there is no Nobel Prize in biology, much less evolutionary biology.
Aren’t those two sentences contradictory? If they aren’t, it seems as if the hypothetical ID/creationist is proposing that Lenski’s experiments are evidence against ID.
Oh yeah
He has, at least, been elected to the NAS:
http://www.nasonline.org/member-directory/members/7066.html
Doudna and Charpentier won the Nobel for their work on CRISPR. They won in the field of chemistry, but that’s biology. It seems biology gets shuffled into other categories, be it medicine or chemistry.
I should have made that clearer. ID/creationists have suggested that we should have seen the step by step natural evolution of a highly complex IC system in the Lenski experiment if IC systems can evolve. If that is so, then why shouldn’t we also see the sudden emergence of a complex IC system in a single generation through intelligent design? It seems the knife cuts in both directions on this one.
Yes, but only if those discoveries can be shuffled. Lenski’s work can’t legitimately be called either.
And of course the rejoinder is that God does his stuff whenever he wants to, and he happens never to want to when anyone is looking. Mysterious ways.
Worth mentioning too, I think, that John Sanford’s “genetic entropy” doesn’t seem to have affected any of the twelve tribes in the twenty odd years and 75,000 generations of the experiment.
Hilariously Sanford thinks they’re suffering from GE. But that apparently makes him stand out as too cooky for various apologists at ICR and AIG who dislike having to argue against a curve that looks like this:
So they’ve elected to start saying that maybe sorta kinda bacteria don’t suffer from GE. Somehow the biblical “fall” didn’t affect bacteria. Everything else in the universe is slowly dying to the beams of rust and decay-magic emanating from Adam and Eve eating magical fruits, that have affected all of creation, but somehow not bacteria.
Hey Rum, could you provide a link to the diagram source?
im one of them. indeed, why dont we see a complex IC system evolving in the lab? after all, we are talking about bacteria. in addition, how many such experiments we should made to refute the claim they cant evolve? another question is why complexity evolved in the first place if the simplest form (bacteria) has the largest population.
And the answer is “that’s exactly what we saw, thank you for asking.”
This has actually become a serious argument. No it doesn’t make any sense. You can actually find Rob Carter claiming that, since E. coli have such a low mutation rate, the original “created” genome still exists, because there could be an unmutated lineage.
(Don’t do the math on that one. Okay, here it is: There’s ~60% chance that E. coli replicates its DNA without error. If we’re being really conservative and saying one replication per year, the probability of a string of perfect replications since creation would be about 0.6 to the 6000 power. Google gives up and just calls that “zero”.)
The other argument is that bacterial population sizes are so big that selection can operate efficiently, preventing extinction via GE. But if that’s the case than it’s conceding the argument. Once you acknowledge there are conditions under which GE is not inevitable, the whole idea crumbles. The point, as articulated by Sanford, is that it is inevitable. Once mutations don’t have to be, on net, harmful, GE fails.
Why don’t we see intelligent design produce an IC system in this experiment?
Exactly.
We did. The aerobic Cit+ trait meets Behe’s criteria. Thanks for asking.
@scd , I am wondering - just how would one go about looking for such an event?
It appears in this paper:
We did. The aerobic Cit+ trait meets Behe’s criteria. Thanks for asking.
This also happened in nature: the HIV vpu protein, as you know.
Hey Rum, could you provide a link to the diagram source?
Sure. It’s from:
Wielgoss S, Barrick JE, Tenaillon O, et al. Mutation rate dynamics in a bacterial population reflect tension between adaptation and genetic load. Proc Natl Acad Sci U S A . 2013;110(1):222-227. doi:10.1073/pnas.1219574110
https://www.pnas.org/content/110/1/222.short
Full figure: