Impact of a stress-inducible switch to mutagenic repair of DNA breaks on mutation in Escherichia coli

摘要: Basic ideas about the constancy and randomness of mutagenesis that drives evolution were challenged by discovery mutation pathways activated stress responses. These could promote specifically when cells are maladapted to their environment (i.e., stressed). However, clearest example--a general stress-response-controlled switch error-prone DNA break (double-strand break, DSB) repair--was suggested be peculiar an Escherichia coli F' conjugative plasmid, not generally significant, occur alternative stress-independent mechanism. Moreover, mechanisms spontaneous in E. remain obscure. First, we demonstrate this same mechanism occurs chromosomes starving F(-) coli. I-SceI endonuclease-induced chromosomal DSBs increase 50-fold, dependent upon general/starvation- DNA-damage-stress responses, DinB polymerase, DSB-repair proteins. Second, DSB repair is also mutagenic if RpoS general-stress-response activator expressed unstressed cells, illustrating a repair. Third, survival improved or DinB, indicating inescapable byproduct Importantly, fourth, fully half frame-shift base-substitution during starvation requires stress-response, DSB-repair, data indicate DSB-repair-dependent stress-induced mutation, driven breaks, pathway usually use major source mutation. rule out models for Mechanisms couple responses can allow evolve rapidly responsively environment.