Let’s see here, “If the development of many of the features of the cell required multiple mutations during the course of evolution” which we have here a feature which required at least 2, if we know that this trait required multiple steps, others almost certainly did as well. “Then the cell is beyond Darwinian explanation.”

Behe didn’t say that an evolution requiring two mutations is impossible — he just called it “a big evolutionary problem” and said that the problem gets exponentially worse when more mutations are needed. Here is what he actually said,

I think the results fit a lot more easily into the viewpoint of The Edge of Evolution. One of the major points of the book was that if only one mutation is needed to confer some ability, then Darwinian evolution has little problem finding it. But if more than one is needed, the probability of getting all the right ones grows exponentially worse. “If two mutations have to occur before there is a net beneficial effect — if an intermediate state is harmful, or less fit than the starting state — then there is already a big evolutionary problem.” (4) And what if more than two are needed? The task quickly gets out of reach of random mutation.

You didn’t even quote me correctly! I actually said,

— the bacteria were given lots of citrate and little glucose to eat in order to give a big advantage to bacteria that develop the ability to eat citrate.

– and you misquoted me as follows:

the bacteria were given lots of citrate and little glucose to eat in order to have a population of bacteria that was not supposed to grow.

Why were the bacteria “not supposed to grow”?

The whole point is that it was not intended to “give a big advantage to bacteria that develop the ability to eat citrate”.

Giving the bacteria lots of citrate and insufficient glucose — as was done in this experiment — does give a big advantage to bacteria that develop the ability to eat citrate. I am still trying to get an answer to my question of whether evolution of citrate-eating E. coli bacteria was one of the goals of the experiment.

You need to read up on what a “control” is in science.

I did not use “control” in the sense of, say, a “control group.” What I meant was that the conditions of the experiment were closely controlled.

The evolution of Cit+ was, in this case, completely unexpected.

Zachary Blount, a co-author of the paper, said that evolution of Cit+ was not unexpected — such evolution had been observed once before. What I am trying to find out is whether trying to induce such evolution was one of the purposes of the experiment — as I said, the condition of lots of citrate and insufficient glucose tends to promote such evolution.

Then I guess I didn’t understand when he said that “If the development of many of the features of the cell required multiple mutations during the course of evolution, then the cell is beyond Darwinian explanation”.

Let’s see here, “If the development of many of the features of the cell required multiple mutations during the course of evolution” which we have here a feature which required at least 2, if we know that this trait required multiple steps, others almost certainly did as well. “Then the cell is beyond Darwinian explanation.” -This I read as “successive random mutations coupled with selection cannot explain the cell”. By including this line in an article (or blog entry) about development of a trait in a specific strain of E. coli, it leads one to conclude that he’s using the phrase to refer to the topic at hand (aka citrate eating bacteria).

Or perhaps my assumption that “successive random mutations coupled with selection” is what he meant by “Darwinian explanation”, was wrong. If that is the case please explain to me what is meant by “Darwinian explanation”.

the bacteria were given lots of citrate and little glucose to eat in order to have a population of bacteria that was not supposed to grow.

Fixed. The whole point is that it was not intended to “give a big advantage to bacteria that develop the ability to eat citrate”.

You need to read up on what a “control” is in science. The evolution of Cit+ was, in this case, completely unexpected.

This was just as serendipitous as the discovery of penicillin.

Larry,

That’s not all, it appears as though there were subsequent mutations that made the citrate uptake weaker and then even stronger than previous generations.

But some of the citrate-eating bacteria would not have been affected by any subsequent mutations that made the citrate uptake weaker, and these unaffected citrate-eaters should have continued to thrive. Instead the citrate-eaters nearly disappeared after rising to 19% of the population.

Taken together with what is above he seems to be saying that this strain of E. coli—which Lenski demonstrates clearly arose from successive random mutations coupled with selection—couldn’t have possibly arisen out of successive random mutations coupled with selection.

Michael Behe never said or implied that “this strain of E. Coli . . . .couldn’t have possibly arisen out of successive random mutations coupled with selection.” And so far as I know he never argued before that this couldn’t happen — he only argued that evolution becomes increasingly difficult exponentially as the number of mutations required for a single beneficial trait increases — and I agree with him.

melior said (June 13, 2008 12:47 PM) –

These bacteria comprise roughly one fourth, by mass, of human feces.

So you and I and all of us are evolutionary playscapes for it as well.

OK, but this is a controlled experiment — the bacteria were given lots of citrate and little glucose to eat in order to give a big advantage to bacteria that develop the ability to eat citrate.

I read the Slate article, and then looked for the original paper. I think it must be Manning et al. PNAS 105:4868. But I can’t find anything in either that suggests the genes were acquired in 15 years. Rather, the authors of the Manning et al paper estimate the most recent common ancestor to have lived about 20,000 years ago.

Can anyone clear this up?

I can’t resist adding a fascinating E. coli bit to ponder that I picked up reading one of Jay Ingram’s collections of strange science tales:

These bacteria comprise roughly one fourth, by mass, of human feces.

So you and I and all of us are evolutionary playscapes for it as well.

That’s not all, it appears as though there were subsequent mutations that made the citrate uptake weaker and then even stronger than previous generations.

And re Behe’s response:

“One of the major points of the book was that if only one mutation is needed to confer some ability, then Darwinian evolution has little problem finding it. But if more than one is needed, the probability of getting all the right ones grows exponentially worse.

A mutation occurred at around 20,000 generations and the citrate-eating ability appeared when one of the bacteria bearing that mutation had a different mutation at around 31,500 generations. IMO the first mutation was very unusual or rare because (1) it apparently took about nine years to occur (44,000 generations in 20 years is about 2200 generations per year) and (2) it apparently appeared in only one of twelve lines of bacteria, even though all twelve lines were descended from a single individual. I think that the second mutation is a fairly common one because it was often expressed again in populations started by the unfrozen preserved populations of 20,000 generations or later, and the reason why this second mutation took so long to be expressed the first time — about 11,500 generations (from the 20,000th to the 31,500th) or 5 years — was that bacteria with the preliminary first mutation were scarce because the preliminary first mutation conferred no advantage in survival. After the preliminary first mutation occurs, appearance of the citrate-eating ability would be just a matter of time if the second mutation were a common one.

Also, I am disturbed by numerous claims that the results of this study refute the ideas of Michael Behe — IMO that is not the case. Michael Behe’s response to this study is at –

http://www.amazon.com/gp/blog/post/PLNK3U696N278Z93O

I thought this was to help “people over in China” understand you as an English speaker.

You can also find most of Lenski’s papers on his own website: https://www.msu.edu/~lenski/

Here’s a press release on it that Google dug up:
http://newsroom.msu.edu/site/indexer/672/content.htm

And/or ask nicely online. Amazing what you can turn up that way.

And in response to Nate’s remaining question to me, I got a PhD in molecular microbiology and after a number of years as a post-doc, left the sciences and am now working in public health.

Oh, and that leads to my last point – question for Carl… Now that I’m out of the sciences, and now that I’m becoming interested in reading papers again, I suddenly sadly aware that not being in a science dept means – no access to papers… including PNAS. Waaaah (again)! Can’t read it

So, how on Earth DOES a non-scientist get to see such papers?

He started starving bacteria in Roberto Kolter’s lab in Harvard (about 15 years ago) and is still starving those same cultures to this day. The difference between his experiments and Lenski’s, is that Lenski adds back fresh nutrients. Finkel lets E. coli starve for years, and watches the interesting communities that develop (and he does indeed find cannibals – cool!).