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      recO and recR mutations delay induction of the SOS response in Escherichia coli.

      Molecular & general genetics : MGG
      Bacterial Proteins, analysis, biosynthesis, genetics, metabolism, DNA-Binding Proteins, Escherichia coli, radiation effects, Escherichia coli Proteins, Gene Expression Regulation, Bacterial, Mutation, Promoter Regions, Genetic, Recombinant Fusion Proteins, Repressor Proteins, SOS Response (Genetics), Serine Endopeptidases, Ultraviolet Rays, beta-Galactosidase

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          Abstract

          RecF, RecO and RecR, three of the important proteins of the RecF pathway of recombination, are also needed for repair of DNA damage due to UV irradiation. recF mutants are not proficient in cleaving LexA repressor in vivo following DNA damage: therefore they show a delay of induction of the SOS response. In this communication, by measuring the in vivo levels of LexA repressor using anti-LexA antibodies, we show that recO and recR mutant strains are also not proficient in LexA cleavage reactions. In addition, we show that recO and recR mutations delay induction of beta-galactosidase activity expressed from a lexA-regulated promoter following exposure of cells to UV, thus further supporting the idea that recF, recO and recR gene products are needed for induction of the SOS response.

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