Operator-constitutive mutation in the recA gene enhances radiation resistance of Escherichia coli

Operator-constitutive mutation in the recA gene enhances radiation resistance of Escherichia coli Plasmid pUC19-recAoc carrying a mutant allele of the recA gene, which plays the key role in the control of the SOS repair system and homologous recombinational repair, causes a 1.5-fold increase in radiation resistance of Escherichia coli ΔrecA cells, as compared to the wild-type recA + cells. The protective effect of this plasmid is drastically reduced in mutant lexA3 recAΔ21 deficient in the LexA protein and in induction of the SOS regulon. Plasmid pUC19-recAoc effectively suppresses UV sensitivity of the ΔrecA mutant. Mutation recAo20 allows constitutive high-level synthesis of the RecA protein. This mutation impairs the SOS box in the operator site of the recA gene and enhances heterology of the dimer LexA binding site. These data confirm that high level of the RecA protein synthesis per se is not sufficient for the expression of γ-inducible functions and that the derepression of lexA-dependent genes, other than recA gene, is necessary for the complete induction of the SOS repair system. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Russian Journal of Genetics Springer Journals

Operator-constitutive mutation in the recA gene enhances radiation resistance of Escherichia coli

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Publisher
SP MAIK Nauka/Interperiodica
Copyright
Copyright © 2009 by Pleiades Publishing, Ltd.
Subject
Biomedicine; Microbial Genetics and Genomics; Animal Genetics and Genomics; Human Genetics
ISSN
1022-7954
eISSN
1608-3369
D.O.I.
10.1134/S1022795409080043
Publisher site
See Article on Publisher Site

Abstract

Plasmid pUC19-recAoc carrying a mutant allele of the recA gene, which plays the key role in the control of the SOS repair system and homologous recombinational repair, causes a 1.5-fold increase in radiation resistance of Escherichia coli ΔrecA cells, as compared to the wild-type recA + cells. The protective effect of this plasmid is drastically reduced in mutant lexA3 recAΔ21 deficient in the LexA protein and in induction of the SOS regulon. Plasmid pUC19-recAoc effectively suppresses UV sensitivity of the ΔrecA mutant. Mutation recAo20 allows constitutive high-level synthesis of the RecA protein. This mutation impairs the SOS box in the operator site of the recA gene and enhances heterology of the dimer LexA binding site. These data confirm that high level of the RecA protein synthesis per se is not sufficient for the expression of γ-inducible functions and that the derepression of lexA-dependent genes, other than recA gene, is necessary for the complete induction of the SOS repair system.

Journal

Russian Journal of GeneticsSpringer Journals

Published: Aug 25, 2009

References

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