Did the Lenski experiments result in additional genetic information?

Question

In the debate between Bill Nye and Ken Ham on Feburary 4, 2014, Ham claimed the Richard Lenski experiments added no new genetic data. He went on to show a clip from Dr. Andrew J. Fabiach, a creationist that teaches at Liberty University,

When I look at the evidence that people cite of E. Coli supposedly evolving over 30 years, over 30,000 generations in the lab, and people say that it is now able to grow on citrate I don't deny that it grows on citrate but it is not any kind of new information. The information is already. It is just a switch that gets turned on and off. That is what they reported and it's nothing new.

Later in the Q/A exchange between Nye and Ham, Ham reiterates this claim,

What Bill Nye needs to do for me is to show me an example of something -- some new function -- that arose that was not previously possible from the genetic information that was there. I would claim and challenge you that there is no such example that you can give. That's I brought up the example in my presentation of Lenski experiments in regards to E. coli; and, there were some that seemed to develop the ability to exist on citrate but as Dr. Fabiach (sp?) has said from looking at his research he has found that that information was already there. It was just a gene that switched on and off. There is no example because information that's there in the genetic information of different animals and plants and so on there is no new function that can be added. Certainly great variation within a kind, but you'd have to show an example of brand new function that never previously was possible. There is no such example that you can give anywhere in the world.

So did the E. coli long-term evolution experiment result in new genetic data from mutation, or not?

Answer 1

I'll avoid trying to define what "additional genetic information" means and focus on what the Lenski experiment actually shows. The claim from Ken Ham that an existing gene was switched on is essentially correct, although there is a bit more to the whole thing.

The genetic background for the evolution of the Cit⁺ trait is examined in Detail in the paper "Genomic Analysis of a Key Innovation in an Experimental E. coli Population" from Lensky. They state:

The Cit1 trait originated in one clade by a tandem duplication that captured an aerobically expressed promoter for the expression of a previously silent citrate transporter.

The E. coli strain in this experiment is unable to use citrate as a carbon source under aerobic conditions, a major reason for that is that it can't transport citrate though the membrane. This E. coli strain has a copy of the citT gene which can function as a citrate/succinate antiporter, but this gene is under the control of a promoter that is not active under aerobic conditions.

What the bacteria did that evolved the ability to use citrate under aerobic conditions is that they duplicated the citT gene. The duplicated gene was inserted in a way that put it under the control of an entirely different promoter, which is active under aerobic conditions.

But this is not the whole story, they write in this paper:

The evolution of the Cit1 trait involved three successive processes: potentiation, actualization and refinement.

The process I described is the actualization step. But before this some unspecified mutations were necessary to make this step possible. They didn't identify exactly which mutations those were, but they could show that they must have existed. The third step, refinement was also necessary as the initial phenotype was very weak, and several other mutations substantially increased the ability to use citrate.