DNA-damage-inducible (din) loci are transcriptionally activated in competent Bacillus subtilis.
DNA damage-inducible (din) operon fusions were generated in Bacillus subtilis by transpositional mutagenesis. These YB886(din::Tn917-lacZ) fusion isolates produced increased beta-galactosidase when exposed to mitomycin C, UV radiation, or ethyl methanesulfonate, indicating that the lacZ structural gene had inserted into host transcriptional units that are induced by a variety of DNA-damaging agents. One of the fusion strains was DNA-repair deficient and phenotypically resembled a UV-sensitive mutant of B. subtilis. Induction of beta-galactosidase also occurred in the competent subpopulation of each of the din fusion strains, independent of exposure to DNA-damaging agents. Both the DNA-damage-inducible and competence-inducible components of beta-galactosidase expression were abolished by the recE4 mutation, which inhibitS SOS-like (SOB) induction but does not interfere with the development of the competent state. The results indicate that gene expression is stimulated at specific loci within the B. subtilis chromosome both by DNA-damaging agents and by the development of competence and that this response is under the control of the SOB regulatory system. Furthermore, they demonstrate that at the molecular level SOB induction and the development of competence are interrelated cellular events.
D001412:Bacillus subtilis / Q000235:genetics*; D004260:DNA Repair; D004269:DNA, Bacterial / Q000235:genetics*; D004274:DNA, Recombinant; D005786:Gene Expression Regulation / Q000187:drug effects; D005798:Genes, Bacterial; D016685:Mitomycin; D008937:Mitomycins / Q000494:pharmacology; D014158:Transcription, Genetic; D001616:beta-Galactosidase / Q000235:genetics
D004269:DNA, Bacterial; D004274:DNA, Recombinant; D008937:Mitomycins; D016685:Mitomycin; D001616:beta-Galactosidase