Genetic variability in a bacteria species

From the original Lederberg paper:"In a typical experiment, a dense broth culture was grown from a single colony on plain agar."
http://profiles.nlm.nih.gov/BB/A/B/F/J/_/bbabfj.pdfSo you start out with an isolated, single bacterium that then produces a colony big enough to see. This colony is then transferred to a liquid medium to increase the population size. It is the only practical conclusion. If the original bacterium used to grow the original colony was resistant then all of it's descendants (barring the in 1 a few million mutations that would knockout the resistance gene) would also carry that resistance. Instead, only 1 in 10 billion of the descendants of that single bacterium are resistant to spectinomycin, as they discussed in the paper above. Therefore, the resistance had to originate in one of the descendants of that single bacterium. The descendants of that single bacterium were tested. If the resistance gene were present in the parent then it should also be present in the offspring. Yes, there was. Log phase represents the period during which bacteria are dividing exponentially (hence the use of "log" as in "logarithmic"). Since there was more than one bacteria from each spot on the master plate that was resistant it represents a mutation during the period of division, not during the stationary phase where the bacteria are not dividing. If the mutation occurred during stationary phase then we should not see the same spot producing colonies on multiple plates at the same position. This is why the bacteriophage resistance is a nice corrolary in the Lederberg paper. Bacteriophage resistance often results from an indel in the tonB gene. This results in a lack of the full tonB gene product which happens to be the binding site for bacteriophage, so these mutations confer bacteriophage resistance. It is interesting to note that these mutants occurred in 1 in every 10 million divisions.So we would expect the same for the antibiotic resistance gene, if it was present in the founding bacterium. One in every 10 million descendants would have a mutation that knocks this gene out and makes it non-functional. Therefore, one in every 10 million descendants of a resistant bacterium should be antibiotic sensitive. Given such long odds for this occuring in the first few generations it is rejected in favor of the resistance coming about in the descendants and not in the founding bacterium. The difference being is that we have the numbers on our side, while you don't. Why would bacteria have mutations conferring resistance to antibiotics that they have never seen? Sounds like mutation is random with respect to fitness afterall.Edited by Taq, : No reason given.

Will try not to overlap with previous posts . . . Because that mutation allowed the bacteria to survive in the presence of antibiotic. I would think that this should be obvious. If it was a neutral mutation in an environment containing antibiotic then it would have been killed by the antibiotic. If you used the same master plate to stamp out colonies on plates containing bacteriophage you would find that there are bacteriophage resistant mutants on the same master plate, but they are not the same bacteria that are antibiotic resistant. All of the bacteria are mutating, but not all are gaining the same mutations. That's the whole point. It is in the DNA. It is in the DNA of the descendants of the founding bacterium, but it was not in the DNA of the founding bacterium. Therefore, the DNA necessary for antibiotic resistance had to come about through mutation of ancestral DNA. Not only that, but these mutations occurred in the ABSENCE of antibiotics demonstrating that mutations are random with respect to fitness. Because people are diploid organisms. Bacteria are haploid. Bacteria use clonal reproduction. People use sexual reproduction.