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Plasmid (pKM101)-mediated enhancement of repair and mutagenesis: Dependence on chromosomal genes in Escherichia coli K-12

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Summary

The drug resistance plasmid pKM101 plays a major 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 λ 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°. The presence of the plasmid raises the level of the Weigle-reactivation curve for the reactivation of ultraviolet-irradiated λ in E. coli and causes a shift 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.

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  1. Graham C. Walker

    Present address: Biology Department, Massachusetts Institute of Technology, 02139, Cambridge, Mass., USA

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  1. Biochemistry Department, University of California, 94720, Berkeley, Cal., USA

    Graham C. Walker

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Communicated by E. Witkin

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Walker, G.C. Plasmid (pKM101)-mediated enhancement of repair and mutagenesis: Dependence on chromosomal genes in Escherichia coli K-12. Molec. Gen. Genet. 152, 93–103 (1977). https://doi.org/10.1007/BF00264945

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