Effect of a null mutation in the priA gene on the radiation resistance of Escherichia coli

According to Kogoma's model of DNA recombination by replication, the PriA p rotein is involved in the RecBCD pathway of double-strand break (DSB) repai r, which is associated with extensive DNA degradation, at the stage of prim osome assembly in D-loops (intermediates of strand exchange at the ends of DSB) for the subsequent switch to DSB-induced DNA resynthesis. Comparable d ata on possible involvement of the PriA protein in the repair of gamma-ray- induced lethal lesions in cells of the wild-type strain of Escherichia coil (strain AB1157) and in two radiation-resistant mutants Gam(r)445 and Gam(r )444 were obtained. In all three strains examined, the null priA2::kan muta tion in the structural priA gene was shown to markedly enhance the radiatio n sensitivity, causing a two- to threefold increase in the slopes of linear dose-survival curves. In the AB1157 strain, the inactivation of PriA is ma nifested most clearly in the range of low doses (up to 0.15 kGy) when the p riA2::kan mutation had only a slight effect on the radiation resistance of Gam(r) mutants. It can be assumed that, in these mutants with a decreased l evel of postradiation DNA degradation, the PriA-dependent RecBCD pathway of DSB repair associated with extensive DNA resynthesis is not essential for the repair of lethal lesions at low doses. However, this pathway becomes cr ucial at higher doses (>0.5 kGy) even for radiation-resistant strains, espe cially for the most resistant Gam(r)444 mutant.