"Bacteria make major two step evolutionary nutritional shift in the lab."

Then why wouldn't it have been in the original from which Lenski's twelve clones came from? When you say: I remember Lenski saying that all such mutations should have occurred. What I don't understand is why any of them should have any generally beneficial effects that would apply in the wild, because any such mutation would have happened in the wild many times (and long ago) so would presumably be in the original ancestor of all Lenski's cultures. Some were certainly beneficial in the new circumstances, as described in the paper. Thanks anyway. It sounds as though it might be a while before we know the full story. Interesting stuff.

Because the advantage might not be so substantial that it has become fixed in all E. coli, in fact given the massive population of E. coli it seems very unlikely. The original 12 populations were all derived from 2 clones differing by only one single point mutation, hardly a wide sample of all the variation in E. coli in the wild.TTFN,WK

I looked back at the discussion of the paper (Blount et al., 2008) and they go into further detail on the exact approach they intend to take ... TTFN,WK

Hi,Since no Creationists are taking up the reins, I need to do it myself, so as to perhaps find out about anything I may be missing on the subject.I would think that a current weakness to the E. coli long-term evolution experiment (Prof. Lenski's experiment), is its lack of a direct demonstration that specific mutations within the genome are the exact reason for the newly heritable trait of citrate consumption.Until the scientists can show in an inescapable concrete way the direct chain of causality, the Creationists will be able to ascribe some sort of divine causality; like, saying that the necessary genetic material was already present in the genome; no mutation was needed.I can understand that the citrate consumption started in the 40k+ generation and then only after 20 years in, but the causes for that still cannot be ascribed directly to the currently presumed mutation to the genome.I am playing devil's advocate as I may not be seeing something obvious (and I need to see everything, before I get pwned in another debate).Thx Edited by CosmicChimp, : Corrected misspelling of "reins."

I would strongly suspect that this is exactly what Lenski is investigating right now, the genetic basis for this shift in phenotype. Given the conditions surrounding the emergence of this phenotype it argues strongly that mutation is involved, even if this involves a recombination event that results in ehanced expression of an already existing gene.In general, scientists often publish papers before they have all the answers. The data presented in the paper is certainly sufficient for a single publication. It is also important to remember that when it comes time for grant submissions a scientist is judged by how many publications they have produced over the last 3-5 years in addition to the work they are proposing to do. IOW, it makes sense for scientists to get as many publications from their work as possible.Also, Lenski has quite a few great papers that do describe specific genetic evolutionary mechanisms. Go to http://www.pubmed.com and use the following search string (copy and paste it): "Lenski RE"[Author]

Good info Taq, you never fail to satisfy. This tip is especially useful: I hope he can hurry up and finish the sequencing of the various genomes for his E. coli as that data will come in handy with many of his other papers as well. I also found something interesting in WIKI I hope It is true and that I can count on this little blurb:

quote:

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Lenski chose an E. coli strain that reproduces only asexually, without bacterial conjugation; this limits the study to evolution based on new mutations and also allows genetic markers to persist without spreading except by common descent.^[2]

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2. Lenski, Richard E. (2004). "Phenotypic and genomic evolution during a 20,000-generation experiment with the bacterium Escherichia coli" (PDF). Plant Breeding Reviews 24 (2): 225—265. http://myxo.css.msu.edu/...0Breeding%20Reviews,%20Lenski.pdf. Retrieved on 2008-06-18.

Well, of course he did. that's easy. You start with an E. coli without a pilus.Moreover, he started with one bacterium. It's a clonal line. Even if they could undergo recombination, any new gene would have to originate by mutation.

Good info Dr Adequate, thx.Taq mentioned above "recombination" and you just above as well. At first I took it to mean the usual (crossover) and thought the usage wrong, so I looked it up. Wiki (I think it was) says there is something called "genetic recombination" and after reading carefully the info took Taq's usage to mean what I had read there. I kind of offhandedly figured it must be some sort of unequal distribution of the bacterial chromosome leading to gene duplication in one of the daughter cells (the shorted cell not passing off genes thereafter). Could you say if that is wrong? Does that type of thing happen and to what sort of consequences can it lead? Is this not an example of mutation, too?Edited by CosmicChimp, : punctuation

Just to update this thread. Lenski et al. have now published the data on the resequencing of a number of the bacterial lines at different generations (Barrick et al., 2009). Unfortunately they don't explicitly look at the Citrate metabolism trait in this paper but they do identify multiple specific genetic mutations with demonstrable beneficial effects. I assume that we can expect more papers to be forthcoming.TTFN,WK

Cheers, WK, and a bump for those interested.There's some interesting comment on the apparent discordance between mutation rates and fitness gains. Also, they discuss a sharp increase in the mutation rate that occurred at ~26,000 generations.They have identified all the mutations in the first 20,000 generations. For those who don't have access to the paper, the ever useful SteveF over at TalkRational has copied some interesting charts into a thread HERE.Of course (they will presumably be ongoing indefinitely, like the experiment!) and you're right that this isn't quite what we were discussing, but I hope that will come soon. Because of the rapid increase I mentioned, they now have over 600 mutations at the 40,000 generation stage, so it could take a while I suppose.