The products of the recG and ruvAB genes of Escherichia coli are both thought to promote branch migration of Holliday recombination intermediates by their junction specific helicase activities in homologous recombination and recombination repair. To investigate the in vivo role of the recG gene, we examined the effects of a recG null mutation on cell division and chromosome partition. After UV irradiation at a low dose (5J/m 2), ΔrecG mutant formed filamentous cells with unpartitioned chromosomes. A mutation in the sfiA gene, which encodes an SOS-inducible inhibitor of septum formation, partially suppressed filamentation of recG mutant cells, but did not prevent the formation of anucleate cells. The sensitivity to UV light and the cytological phenotypes after UV irradiation of a recA recG double mutant were similar to a recA single mutant, consistent with the role of recG, which is assigned to a later stage in recombination repair than recA. The recG ruvAB and recG ruvC double mutants were more sensitive to UV, almost as sensitive as the recA mutant and showed more extreme phenotypes concerning filamentation and chromosome nondisjunction, both after UV irradiation and without UV irradiation than either recG or ruv single mutants. The recG polA12 (Ts) mutant, which is temperature sensitive in growth, formed filamentous cells with centrally located chromosome aggregates when grown at nonpermissive temperature similar to the UV irradiated recG mutant. These results support the notion that RecG is involved in processing Holliday intermediates in recombination repair in vivo. We suggest that the defect in the processing in the recG mutant results in accumulation of nonpartitioned chromosomes, which are linked by Holliday junctions.
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