DaveScot asked for the rhetorical game by asking me to propose situations in which evolution could be falsified.

I agree that the dichotomy is stupid, but the creationists/IDiologists insist on making it one. Science isn’t trying to disprove that there is a intelligent designer, after all. It just can’t create a falsifiable model of one. The IDiologist can play all the rhetorical games they want, but in the end the science (and that means evolution) wins.

Perhaps research papers should be written by groups of interdisciplinary scientists as to not give any lenience to the IDists rampant, ignorant, and deliberate rhetorical games in order to makeup and insert flaws that were not intended but meant to be understood on a more basic level. After all Lenski is not an expert in mathematical/information theory among other things that could be picked apart.

The part about unexpressed enzymes already being there was an interesting point you should have started out with but the rhetorical nitpicking was just stupid. By your standard absolutely no paper could or would make it through a peer review process, everyone would be analyzing everyone else’s definitions and verbiage to much to get anything done.

I could just say the whole dichotomy you have over creation vs evolution shows a bias in itself. A creator is just another assumption I could pick apart with rhetorical games as well.

I don’t really think that simple bias error (which was missed by the peer reviewers too) detracts from the methods or conclusions, per se. It’s simply an indicator of sloppy thinking, sloppy peer review, and doctrinal bias in authors and reviewers that may or may not be a factor in the rest of the paper. It probably is judging by the sensationalist spin given to something that bacteria are very, very good at - adapting digestive enzymes to the predominant nutrients in the substrate. In this case though, E.coli already had the enzymes - all it was missing was the aerobic expression of a citrate transport protein (it already had the citrate transport protein too).

If you ask nicely I’ll give you a design theoretic guess at why the transport protein is repressed in the presence of oxygen. Ask on my blog though. I’m cheap but not free. :-)

Sorry my friend but I’m afraid the FAIL is yours. Specifically you didn’t bother to check into subsequent research at Scripps.

I responded to you here

http://www.uncommondescent.com/intelligent-design/first-paragraph-of-lenski-paper-contains-an-error/#comment-291468

It does indeed target certain genes and excludes others.

Just because the 2005 Scripps paper didn’t point that out, a followup paper in 2006 did (you’ll have to visit my site at the link above to get the link to the 2006 Scripps paper - consider another visit to my website the cost of your lesson).

In a nutshell the response is the derepression of certain specialized polymerases Pol II, Pol IV, and Pol V. Notably missing is Pol III. Pol III, you see, is involved in ribosomal DNA (rDNA) repair. If you were a designer and you wanted to give your design the ability to deal with unknown toxins in the environment you sure wouldn’t want to start mutating the crap out of your ribosomes. That’s a pretty quick and certain kill with no chance of solving the toxin problem. Not all bits of DNA are as forgiving of mutations as others and rDNA is one of the least forgiving. So you would want to exclude that from your rapid mutation targets. And indeed that’s the way it was found to play out. If you didn’t have such a blind spot you’d be able to guess what a good designer might do and look for that instead instead of looking for what a blind watchmaker would do. Take off the blinders, my friend. Life was intelligently designed and it’s a fruitful heuristic to adopt as I’ve just demonstrated.

Sorry for any embarrassment this may cause you but you asked for it.

Cheers

I’m pretty sure that there proposed model has something to do with repressing correction machinery, but I didn’t want to misrepresent the research, unlike some people (ahem).

At any rate, decreasing error correction results in increased mutation rate, so the point stands without knowing the exact mechanism (which I don’t think has been proven yet).

I’ve voiced similar sentiments in the comments section at Uncommon Descent… I wonder if the comment will be approved for posting.

Way to cut through DaveScot’s logic, too.