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Mutation in the cspH-cspG gene cluster enhances expression of heat-shock proteins and SOS repair system of Escherichia coli

  • Genetics of Microorganisms
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Abstract

The recessive radioresistance allele gam12 cloned in plasmid pBC4042-gam12 slightly increases the radiation resistance of Escherichia coli wild-type cells. Meanwhile, irradiation by γ-rays induces transition of gam r 12 mutation to the homozygous state and causes a 3.37-fold increase in radiation resistance of these cells. The mutation gam r 12 was located at 22.68 min of the chromosomal map in the region of cspH-cspG gene cluster of cold-shock proteins. Sequence analysis of gam12 allele revealed the nucleotide sequence of cold-shock gene cspG and insertions in the C-terminal part of the gene. Translation of mutant cspG gene can lead to synthesis of a truncated product that represents the N-terminal protein fragment with motifs governing binding with DNA and RNA. Analysis of the Escherichia coli genome revealed motifs recognized by proteins of the cspA family in genes of cold shock, heat shock, SOS regulon, and other systems. These data suggest the possibility of involvement of mutant RNA-chaperones of type CspA′ and CspG′ in the expression of key genes in systems of SOS repair and recombination or auxiliary stress systems, including heat-shock proteins, in radiation resistant mutants of E. coli.

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Authors and Affiliations

  1. St. Petersburg Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, 188300, Russia

    V. N. Verbenko, L. V. Kuznetsova, L. A. Luchkina & N. V. Klopov

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  1. V. N. Verbenko
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  2. L. V. Kuznetsova
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  3. L. A. Luchkina
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  4. N. V. Klopov
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Correspondence to V. N. Verbenko.

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Original Russian Text © V.N. Verbenko, L.V. Kuznetsova, L.A. Luchkina, N.V. Klopov, 2009, published in Genetika, 2009, Vol. 45, No. 9, pp. 1194–1202.

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Verbenko, V.N., Kuznetsova, L.V., Luchkina, L.A. et al. Mutation in the cspH-cspG gene cluster enhances expression of heat-shock proteins and SOS repair system of Escherichia coli . Russ J Genet 45, 1047–1054 (2009). https://doi.org/10.1134/S102279540909004X

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  • DOI: https://doi.org/10.1134/S102279540909004X

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