Lenski's E. Coli bacterial microevolution experiment
A short description of the experiment is here; a longer description is here -- comments may be left in both places. The experiment is being performed by Richard Lenski and colleagues at Michigan State University. The results are being debated on Uncommon Descent [1] [2] and Panda's Thumb . The comment thread under Carl Zimmer's article is probably the best because he provides the most details about the experiment. Michael Behe's response is here. The debate has barely begun and some Darwinists are already rejoicing -- that's very open-minded of them.
I have barely begun to read others' comments about the experiment, but here are my own observations and questions so far:
The mutations appear to have occurred at two or even three stages: the first -- or preliminary -- mutation at around the 27,000th generation (around the 20,000th generation according to some sources), the second at around the 31,500th generation, and possibly a third around the 33,000th generation.
Question: To what extent did the first mutation spread through the population, if it spread at all, considering that it apparently conferred no advantage?
There were around 44,000 generations in 20 years, or about 2,200 generations per year. So assuming that the first mutation occurred at 27,000 generations and the second occurred at 31,500 generations, that would be about 2 years from the first mutation until the second mutation. That seems to mean that the second mutation is rare -- however, on the other hand this second mutation appears to be common because it was repeated numerous times by starting with the unfrozen samples of previous generations. So how could the second mutation be both rare and common at the same time? Maybe the second mutation is really quite common but is rarely expressed because there are relatively few individuals with the first mutation, which confers no advantage.
Carl Zimmer said,
.
Carl Zimmer gives the following explanation for the preceding observations:
Actually, the rise and fall at 31,500 and 33,000 generations respectively is not what indicates that the citrate-eating trait is not just a one-mutation affair, because -- as noted above -- it appears that an essential preliminary mutation occurred at around 27,000 generations (around 20,000 according to some sources).
Also, in a sense the citrate-eating bacteria are not really competing with the glucose-eating bacteria, because the two kinds of bacteria have different food sources.
The citrate-eaters were initially getting quite good at competing with the glucose-eaters, rising to 19% before nearly vanishing and then becoming dominant. Zimmer does not adequately explain why the citrate-eaters nearly vanished.
Also, Zimmer said,
As I calculated above, there is an average of about 2,200 generations per year, so if a new population was started each day with a sample from an old population, then there were about 6 generations per population. With only 6 generations, there might be a significant possibility -- depending on the size of the sample -- that a mutation occurring in an old population would not be collected in the sample used to start the next population, particularly if the mutation occurred in one of the last generations of the old population. The populations should of course be well-stirred before collecting the samples to start the next populations - the Zimmer article says that the flasks full of E. coli were placed on a "gently rocking table," and I presume that means that the populations were well-stirred before collecting the samples.
.
I have barely begun to read others' comments about the experiment, but here are my own observations and questions so far:
The mutations appear to have occurred at two or even three stages: the first -- or preliminary -- mutation at around the 27,000th generation (around the 20,000th generation according to some sources), the second at around the 31,500th generation, and possibly a third around the 33,000th generation.
Question: To what extent did the first mutation spread through the population, if it spread at all, considering that it apparently conferred no advantage?
There were around 44,000 generations in 20 years, or about 2,200 generations per year. So assuming that the first mutation occurred at 27,000 generations and the second occurred at 31,500 generations, that would be about 2 years from the first mutation until the second mutation. That seems to mean that the second mutation is rare -- however, on the other hand this second mutation appears to be common because it was repeated numerous times by starting with the unfrozen samples of previous generations. So how could the second mutation be both rare and common at the same time? Maybe the second mutation is really quite common but is rarely expressed because there are relatively few individuals with the first mutation, which confers no advantage.
Carl Zimmer said,
.
Blount took on the job of figuring out what happened. He first tried to figure out when it happened. He went back through the ancestral stocks to see if they included any citrate-eaters. For the first 31,000 generations, he could find none. Then, in generation 31,500, they made up 0.5% of the population. Their population rose to 19% in the next 1000 generations, but then they nearly vanished at generation 33,000. But in the next 120 generations or so, the citrate-eaters went berserk, coming to dominate the population.
Carl Zimmer gives the following explanation for the preceding observations:
This rise and fall and rise suggests that the evolution of citrate-eating was not a one-mutation affair. The first mutation (or mutations) allowed the bacteria to eat citrate, but they were outcompeted by some glucose-eating mutants that still had the upper hand. Only after they mutated further did their citrate-eating become a recipe for success.
Actually, the rise and fall at 31,500 and 33,000 generations respectively is not what indicates that the citrate-eating trait is not just a one-mutation affair, because -- as noted above -- it appears that an essential preliminary mutation occurred at around 27,000 generations (around 20,000 according to some sources).
Also, in a sense the citrate-eating bacteria are not really competing with the glucose-eating bacteria, because the two kinds of bacteria have different food sources.
The citrate-eaters were initially getting quite good at competing with the glucose-eaters, rising to 19% before nearly vanishing and then becoming dominant. Zimmer does not adequately explain why the citrate-eaters nearly vanished.
Also, Zimmer said,
Lenski started off with a single microbe. It divided a few times into identical clones, from which Lenski started 12 colonies. He kept each of these 12 lines in its own flask. Each day he and his colleagues provided the bacteria with a little glucose, which was gobbled up by the afternoon. The next morning, the scientists took a small sample from each flask and put it in a new one with fresh glucose. And on and on and on, for 20 years and running.
As I calculated above, there is an average of about 2,200 generations per year, so if a new population was started each day with a sample from an old population, then there were about 6 generations per population. With only 6 generations, there might be a significant possibility -- depending on the size of the sample -- that a mutation occurring in an old population would not be collected in the sample used to start the next population, particularly if the mutation occurred in one of the last generations of the old population. The populations should of course be well-stirred before collecting the samples to start the next populations - the Zimmer article says that the flasks full of E. coli were placed on a "gently rocking table," and I presume that means that the populations were well-stirred before collecting the samples.
.
Labels: Citrate-eating E. coli, Intelligent design
posted by Larry Fafarman | 6/12/2008 03:02:00 AM
9 Comments:
Nobody, including Behe, denies that random mutations and natural selection produce some things. In The Edge of Evolution, he even argues that they have produced a form of "antifreeze" in certain cold-water fish.
Behe's argument is about the experimentally-determined rate at which new interactions between protein molecules, which depend upon "binding sites," can be produced by random mutations plus natural selection. He finds it to be much too slow to account for the many different kinds of binding sites in cells. See fig 7.4, p144, of his book for a summary.
Since Darwinism has gone belly-up anyway (see the interview with Massimo Piattelli-Palmirini, which I discussed here on June 10), the Darwin-fans have nothing left to rejoice about. It's true that Massimo, as a True-Believing Materialist, thinks that there must be some purely materialistic or mechanistic means by which all life evolved. But nobody knows what it is: so no materialistic theory of evolution now exists.
So what are the public schools supposed to teach now: "By True Faith in Materialism, we believe that all life evolved materialistically! But we don't know how in Hell that happened?"
I guess that will be the new theory that will be taught in Florida schools?
Massimo Piattelli-Palmarini and Jerry Fodor are writing a new book with the provisional title, What Darwin Got Wrong (I believe that's it.) Anyway, that's a better title for a book than What Darwin Got Right, in which case the book would be only a few pages long.
I think the guys had better be very careful about how they word their book. Or Eugenie Scott's Thought Police from the NCSE (the National Censors of Science Education,) might be right on their tails.
Jim Sherwood said...
>>>>> Nobody, including Behe, denies that random mutations and natural selection produce some things. <<<<<<
Behe claims that the ability of RM + NS to produce evolution is limited where multiple mutations are required to produce a single beneficial trait. He wrote of the Lenski-Blount-Borland study,
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.
I agree with Behe. Even though I think that the second mutation in the Lenski-Blount-Borland study is fairly common (because it often re-appeared in populations that descended from frozen samples of the 27,000th -- or 20,000th according to some sources -- generation or later), it took approx. 4,500-11,500 generations or approx. 2-5 years for the second mutation to be expressed, and I think that was because there was a scarcity of bacteria with the preliminary first mutation because the preliminary first mutation conferred no advantage in survival. So if more mutations are needed, the chance of getting all the right ones in one bacterium grows exponentially worse, as Behe said.
I wonder if there is any data on how quickly the second mutation was re-expressed in the populations descended from the unfrozen populations of 20,000-27,000 generations or later.
Behe also wrote,
The major point Lenski emphasizes in the paper is the historical contingency of the new ability. It took trillions of cells and 30,000 generations to develop it, and only one of a dozen lines of cells did so. What’s more, Lenski carefully went back to cells from the same line he had frozen away after evolving for fewer generations and showed that, for the most part, only cells that had evolved at least 20,000 generations could give rise to the citrate-using mutation. From this he deduced that a previous, lucky mutation had arisen in the one line, a mutation which was needed before a second mutation could give rise to the new ability. The other lines of cells hadn’t acquired the first, necessary, lucky, “potentiating” (1) mutation, so they couldn’t go on to develop the second mutation that allows citrate use. Lenski argues this supports the view of the late Steven Jay Gould that evolution is quirky and full of contingency. Chance mutations can push the path of evolution one way or another, and if the “tape of life” on earth were re-wound, it’s very likely evolution would take a completely different path than it has.
I haven't read Behe's book "The Edge of Evolution," but I think that the main idea of the book was to show that evolution has negligible power to produce change under conditions unfavorable to evolution (i.e., complex organisms, complex changes, few organisms, few generations, and many mutations for a single new trait) by showing that evolution has limited ability to produce change under conditions highly favorable to evolution (i.e., simple organisms, simple changes, many organisms, many generations, and very few mutations for a single new trait).
Looks like Larry got an encouraging review of his personality from PZ Meyers in his blog concerning the E. Coli bacterial experiment responses...
"If you don't know of him, you're fortunate. He's a mentally ill, permanently obtuse, persistent freakazoid creationist who, given a chance, will run the rational discussion right off the rails."
Seems a little immature from a professional but not surprising coming from him.
"If you don't know of him, you're fortunate. He's a mentally ill, permanently obtuse, persistent freakazoid creationist who, given a chance, will run the rational discussion right off the rails."
This shows that Behe knows Larry.
By the way, "feakazoid" means: a bizarre or very strange person; a person with outstanding or unusual skills but questionable sanity."
It appears PZ Meyers has some sort of admiration for Larry...The question is, will some follow PZ instructions and challenge Larry on the E. Coli bacterial experiment?
I envy Larry; PZ's attack indicates that Larry is doing good stuff. I regret that PZ has never insulted me. I feel left out. But then, I don't have a blog.
So I agree with Michael. And I marvel that Michael is able to be quite compassionate toward PZ. It seems that I just can't stand that guy.
The Michael/Sherwood/Larry mutual backpatting society is entertaining to say the least.
I wonder if any of the three of you understand how clueless you are?
No matter - I hguess that was just real 'unprofessional' of me. Instead, I suppose, I could post out of context quotes on my blog or write inane nonsense purporting to be insightful commentary, all to prop up my religion or my 'anti-materialism' or similar nonsense, for that wqould be very 'professional' in the wacky world of the creationist/anti-evolutionist/egomaniac.
Have fun, y'all!
Post a Comment
<< Home