A new mutation in Escherichia coli K12, isfA, which is responsible for inhibition of SOS functions.
A new mutation in Escherichia coli K12, isfA, is described, which causes inhibition of SOS functions. The mutation, discovered in a delta polA+ mutant, is responsible for inhibition of several phenomena related to the SOS response in polA+ strains: UV- and methyl methanesulfonate-induced mutagenesis, resumption of DNA replication in UV-irradiated cells, cell filamentation, prophage induction and increase in UV sensitivity. The isfA mutation also significantly reduces UV-induced expression of beta-galactosidase from recA::lacZ and umuC'::lacZ fusions. The results suggest that the isfA gene product may affect RecA* coprotease activity and may be involved in the regulation of the termination of the SOS response after completion of DNA repair. The isfA mutation was localized at 85 min on the E. coli chromosome, and preliminary experiments suggest that it may be dominant to the wild-type allele.
Bebenek
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A
Institute of Biochemistry and Biophysics, Polish Academy of Science, Warsaw.
Pietrzykowska
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I
D010582:Bacteriophage lambda / Q000235:genetics; D002874:Chromosome Mapping; D003227:Conjugation, Genetic; D004926:Escherichia coli / Q000235:genetics* / Q000528:radiation effects; D017353:Gene Deletion; D005798:Genes, Bacterial; D009154:Mutation; D011061:Poly A / Q000235:genetics; D011938:Rec A Recombinases / Q000378:metabolism; D011995:Recombination, Genetic; D013014:SOS Response, Genetics; D014466:Ultraviolet Rays; D001616:beta-Galactosidase / Q000235:genetics
D011061:Poly A; D011938:Rec A Recombinases; D001616:beta-Galactosidase