Accumulation of mutants in "aging" bacterial colonies is due to growth under selection, not stress-induced mutagenesis.
Several bacterial systems show behavior interpreted as evidence for stress-induced mutagenesis (adaptive mutation), a postulated process by which nongrowing cells temporarily increase their general mutation rate. Theoretical considerations suggest that periodic stress-induced general mutagenesis would not be advantageous in the long term, due to the high cost of deleterious mutations. Alternative explanations have been tested for very few of the systems used as evidence for stress-induced mutation. In one prominent system, mutants resistant to rifampicin (Rif(R); rpoB; RNA polymerase) accumulate in cell populations that "age" on solid medium with little net growth. Mutant accumulation was initially attributed to stress-induced general mutagenesis in nongrowing cells. Evidence is presented that these Rif(R) mutants accumulate because they grow faster than parent cells during the aging period. Direct tests revealed no increase in the frequency of other mutant types during the aging period.
Wrande
Marie
M
Department of Cell and Molecular Biology, Box 596, The Biomedical Center, Uppsala University, S-75124 Uppsala, Sweden.
Roth
John R
JR
Hughes
Diarmaid
D
D000220:Adaptation, Biological; D015169:Colony Count, Microbial; D024881:Drug Resistance, Bacterial / Q000187:drug effects; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics* / Q000254:growth & development*; D016296:Mutagenesis; D009154:Mutation / Q000235:genetics; D012293:Rifampin / Q000494:pharmacology; D019779:Salmonella enterica / Q000187:drug effects / Q000235:genetics* / Q000254:growth & development*; D012641:Selection, Genetic
D012293:Rifampin