Role of RPOS Regulon in Resistance to Oxidative Stress and Near- UV Radiation In ΔOXYR Suppressor Mutants of ESCHERICHIA COLI

Escherichia coli ΔoxyR mutants are hyper-sensitive to oxidative agents but this sensitivity is reversed to hyper-resistance in ΔoxyR suppressor strains (ΔoxyRsup; Greenberg, J.T. and Demple, B. 1988. EMBO J. 7:2611- 2618). Also, ΔoxyR mutants have increased mutation rates that are also reversed in ΔoxyRsup. We now report that the rpoS regulon may have a role in determining hyper-resistance and loss of hyper-mutability of ΔoxyRsup. ΔoxyRsup cells were also resistant to near-ultraviolet radiation (near-UV) and survived longer in stationary phase than ΔoxyR cells. In ΔoxyRsup cells elevated β-galactosidase expression from a rpoS::lacZ promoter fusion and significant overproduction of RpoS protein was observed. These increases were accompanied by substantial elevation in transcription of rpoS-dependent genes as determined by β-galactosidase expression from katE::lacZ, dps::lacZ, and xthA::lacZ promoters. Catalase HPI and HPII activities were also increased. When rpoS::Tn10 was transduced into ΔoxyRsup, phenotypes switched back to hyper-sensitive, hyper-mutable and reduced catalases I and II. Individual ΔoxyR colonies exhibited significant clonal variability in β-galactosidase expression from rpoS::lacZ promoter. These results provide further evidence of the functional and regulatory overlap between two major anti-oxidant defense systems of bacteria.