Viability of Escherichia coli K-12 DNA adenine methylase (dam) mutants requires increased expression of specific genes in the SOS regulon.
We have examined the level of expression of the SOS regulon in cells lacking DNA adenine methylase activity (dam-). Mud (Ap, lac) fusions to several SOS operons (recA, lexA, uvrA, uvrB, uvrD, sulA, dinD and dinF) were found to express higher levels of beta-galactosidase in dam- strains than in isogenic dam+ strains. The attempted construction of dam- strains that were also mutant in one of several SOS genes indicated that the viability of methylase-deficient strains correlates with the inactivation of the SOS repressor (LexA protein). Consistent with this, the wild-type functions of two LexA-repressed genes (recA and ruv) appear to be required for dam- strain viability.
D004260:DNA Repair; D004269:DNA, Bacterial / Q000235:genetics*; D004926:Escherichia coli / Q000201:enzymology / Q000235:genetics* / Q000254:growth & development; D005796:Genes; D005798:Genes, Bacterial; D005838:Genotype; D008780:Methyltransferases / Q000235:genetics*; D009154:Mutation; D011938:Rec A Recombinases / Q000235:genetics; D015265:Site-Specific DNA-Methyltransferase (Adenine-Specific); D013045:Species Specificity; D014161:Transduction, Genetic; D001616:beta-Galactosidase / Q000235:genetics
D004269:DNA, Bacterial; D008780:Methyltransferases; D015265:Site-Specific DNA-Methyltransferase (Adenine-Specific); D011938:Rec A Recombinases; D001616:beta-Galactosidase