ABSTRACT
In Escherichia coli, the repair of lethal DNA damage induced by H2O2 requires exonuclease III, thexthA gene product. Here, we report that both endonuclease IV (the nfo gene product) and exonuclease III can mediate the repair of lesions induced by H2O2 under low-iron conditions. Neither the xthA nor thenfo mutants was sensitive to H2O2in the presence of iron chelators, while the xthA nfodouble mutant was significantly sensitive to this treatment, suggesting that both exonuclease III and endonuclease IV can mediate the repair of DNA lesions formed under such conditions. Sedimentation studies in alkaline sucrose gradients also demonstrated that both xthAand nfo mutants, but not the xthA nfo double mutant, can carry out complete repair of DNA strand breaks and alkali-labile bonds generated by H2O2 under low-iron conditions. We also found indications that the formation of substrates for exonuclease III and endonuclease IV is mediated by the Fpg DNA glycosylase, as suggested by experiments in which thefpg mutation increased the level of cell survival, as well as repair of DNA strand breaks, in an AP endonuclease-null background.