[Participation of the product of gene dnaG in the slow nonmutagenic repair pathway for gamma-induced single-stranded DNA breaks in Escherichia coli cells].

The survival of cells and yield of DNA single-strand breaks after the completion of DNA repair in growth medium M9 and in the buffer at 30 degrees and 43 degrees C has been investigated in four strains of alpha-irradiated Escherichia coli: PC3 dnaGts, NY73 dnaGts polA1, W3110 pol+, P3478 polA1. The survival of the dnaGts mutant at 43 degrees in M9 and the buffer is lower and the yield of single-strand breaks is higher than at 30 degrees. In the polA1 mutant, the yield of single-strand breaks in M9 and in the buffer at both the temperatures is significantly higher, and the survival is significantly lower than in pol+- and dnaGts strains. These data indicate that dnaG gene product (primase, rifampicin-resistant RNA polymerase) and DNA polymerase I are involved in different pathways of DNA single-strand break repair. DNA polymerase I is the key enzyme for the fast, growth medium-independent repair of DNA single-strand breaks. Thus, the dnaG gene product is involved in the slow, growth medium-dependent polA-independent DNA single-strand break repair. The yield of breaks in double mutant polA1 dnaGts in M9 and in the buffer does not differ from that in single mutant polA1. Thus, DNA polymerase I in fast repair of DNA single strand breaks is not changed by the dnaG gene product. It has been demonstrated that the dnaG gene product does not participate in the UV-induced mutagenesis.