Plasmid (pKM101)-mediated enhancement of repair and mutagenesis: dependence on chromosomal genes in Escherichia coli K-12.
The drug resistance plasmid pKM101 plays a mojor role in the Ames Salmonella/microsome carcinogen detecting system by enhancing chemical mutagenesis. It is shown that in Escherichia coli K-12 the plasmid pKM101 enhances both spontaneous and methyl methanesulfonate-caused reversion of an ochre mutation, bacterial survival after ultraviolet irradiation, and reactivation of ultraviolet-irradiated lambda in unirradiated cells. All these effects are shown to be dependent on the recA+ lexA+ genotype but not on the recB+ recC+ or recF+ genotypes. The recA lexA-dependence of the plasmid-mediated repair and mutagenesis suggests an interaction with the cell's inducible error-prone repair system. The presence of pKM101 is shown to cause an additional increase in methyl methanesulfonate mutagenesis in a tif mutant beyond that caused by growth at 42 degrees. The presence of the plasmid raises the level of the Weigle-reactivation curve for the raactivation of ultraviolet-irradiated lambda in E. coli and causes a shif of the maximum to a higher UV fluence. These observations suggest that pKM101 does not exert its effects by altering the regulation of the cell's error-prone repair system but rather by supplying a mechanistic component or components.
D002876:Chromosomes, Bacterial; D004260:DNA Repair; D004269:DNA, Bacterial; D004926:Escherichia coli / Q000187:drug effects / Q000378:metabolism*; D005111:Extrachromosomal Inheritance / Q000187:drug effects; D005838:Genotype; D008741:Methyl Methanesulfonate / Q000494:pharmacology; D009154:Mutation; D010957:Plasmids / Q000187:drug effects; D014161:Transduction, Genetic
D004269:DNA, Bacterial; D008741:Methyl Methanesulfonate