http://myxo.css.msu.edu/lenski/pdf/2008, PNAS, Blount et al.pdf
It's pretty clear on pages 7899 and 7900 of Lenski's inaugural PNAS paper that he is speaking of the same bacteria. In fact, on page 7900 of the paper, there is a reference (#31) to the paper where I got the information from originally. Go to the following link and click on the link for #122
Richard Lenski's Web Page
I'm sorry, but I cannot think of a single way to say this nicely. You are wrong. Period, end of story. In fact, your claims go directly against much of what Lenski's written in his own work. Not even the paragraph you're referring us to would support your claim; its simply a description of some of the strains they've published along with a description of general changes observed across all strains. In fact, the paper doesn't even make reference to ribose metabolism, as those are completely different experiments, never mind the strain issue.
In fact, if you'd bothered to read the methods section of the two papers you continually refer to you'd have seen that the ribose-defective strains and cit+ strains arose from completely different experiments; with the respective strains being
selected out of mixed populations using different techniques.
I may be wrong, but didn't the cit+ bacteria come from those original 12 lines?
I don't get why this is so hard to explain; these are pretty standard techniques most biologists use frequently (I nearly left my old position to work for a company that uses this kind of "directed evolution" for commercial purposes). So let me try again, lets see if we can teach a little undergrad microbiology here:
1) You start out with 12 strains. On average each of cells in these strains experiences a mutations or two each generation, meaning every generation the number of genetically unique strains increases several thousand fold. So after one generation you are no longer working with 12 strains, but rather 12 populations (of 2 cells each) containing 2 unique "strains" of cells. After the next generation you have 12 populations of 8 unique cells. A few days later you have 12 populations of billions of unique cells.
2) After a while you then take those 12
mixed populations and look for bacteria with mutations of interest, using a selective screen. What this does is select the tiny proportion (usually on the order of 1-in-a-billion) of mutants which have the characteristic you are looking for.
3) You then analyze those mutants, and based on what you find you can determine how frequent those mutations are, how the occurred, etc.
The key point in the above is that you generate a mixed population, and then select out the
rare mutants of interest. And while the Rib- mutant was more common than the Cit+ mutation, both are still rare mutations. Rib- being 1:8x10
-5/generation, Cit+ being 1:10
-13/generation. to put that in context, the mutation rates of humans is 1:10
-8/generation, exactly mid-way between the two mutation rates observed here.
And yet, strangely enough, most of us catabolize ribose just fine...
Bryan