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Mutagenesis and repair deficiencies of Escherichia coli umuC mutants are suppressed by the plasmid pKM101 by Graham C. Walker; Patricia P. Dobson is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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The presence of the drug resistance plasmid pKM101 restored the ability of Escherichia coli umuC mutant strains to be mutated by methyl methanesulfonate. Inducible (Weigle) reactivation of ultraviolet-irradiated bacteriophage lambda was not observed in uvrA6 umuC mutant strains lacking pKM101 but was observed if the plasmid was present in the strains. In a uvrA+ umuC36 strain pKM101 increased the efficiency of the Weigle reactivation process. Plasmid-mediated UV-resistance and plasmid-mediated phage reactivation were observed in umuC(pKM101) strains both in uvrA+ and uvrA6 backgrounds. No restoration of methyl methanesulfonate mutability by pKM101 was observed in umuC36 recA56 strains. pKM101 mutants unable to enhance mutagenesis in umuC+ backgrounds also had no effect on methyl methanesulfonate mutagenesis in umuC mutant strains. Neither a umuC mutation nor the presence of pKM101 affected the UV induction of protein X, the recA protein. Hypotheses relating the mode of action of pKM101 to the process of mutagenesis and inducible phage reactivation are discussed.

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Author

Graham C. Walker; Patricia P. Dobson

Publisher

Springer; Springer-Verlag; Springer Verlag; Springer Science and Business Media LLC (ISSN 0026-8925)

Published

1979

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)