Regulation and SOS induction of division inhibition in Escherichia coli K12.
When Escherichia coli is subjected to treatments that damage DNA or perturb DNA replication considerable cell filamentation occurs. It has been postulated that this phenomenon is associated with the presence of a division inhibitor induced coordinately with the SOS functions. The role of this induction would be to delay septation during DNA repair to prevent the formation of DNAless cells. In this communication, we present evidence for such a division inhibitor based on the properties of a division mutant which is hyperactive in the septation delay. Cells of this mutant filament extensively after a nutritional shift-up, have drastically reduced colony-forming abilities on a rich medium but not on a minimal medium following treatment with ultraviolet radiation and, are deficient in the lysogenization of phage lambda; phenotypes which are characteristic of but expressed to a much lower extent in another type of division mutant called Ion. Cells harboring the division mutation plus either one of the lexA mutant alleles, spr-51 or tsl-1, are filamentous suggesting that they are permanently derepressed for division inhibition. These results are in agreement with models that assign the regulation of cell division to a division inhibitor which is regulated by the lexA repressor protein.
D010582:Bacteriophage lambda / Q000235:genetics; D004260:DNA Repair; D004261:DNA Replication; D004926:Escherichia coli / Q000235:genetics* / Q000254:growth & development / Q000528:radiation effects; D005838:Genotype; D007700:Kinetics; D008242:Lysogeny; D009154:Mutation; D013045:Species Specificity