Interplay between Bacillus subtilis RecD2 and the RecG or RuvAB helicase in recombinational repair

•Bacillus subtilis RecD2 shows a poor-growth phenotype and a suppressor mutation maps to pcrA.•RecD2 is not epistatic with AddA, RecS, RecQ, PcrA, HelD, DinG, RecG and RuvAB.•A ΔrecD2 mutation could not be transferred to the ΔrecG or ΔruvAB backgrounds, but ΔrecD2 ΔrecU, ΔrecD2 ΔrecQ and ΔrecD2 ΔrecS were viable, which suggests that rather than HJ resolution or dissolution, a defect in HJ translocation revealed a synthetically lethal.•Specific RecD2 degradation reduced cell viability on the ΔrecG or ΔruvAB but not on the ΔrecU background.

Bacillus subtilis AddAB, RecS, RecQ, PcrA, HelD, DinG, RecG, RuvAB, PriA and RecD2 are genuine recombinational repair enzymes, but the biological role of RecD2 is poorly defined. A ΔrecD2 mutation sensitizes cells to DNA-damaging agents that stall or collapse replication forks. We found that this ΔrecD2 mutation impaired growth, and that a mutation in the pcrA gene (pcrA596) relieved this phenotype. The ΔrecD2 mutation was not epistatic to ΔaddAB, ΔrecQ, ΔrecS, ΔhelD, pcrA596 and ΔdinG, but epistatic to recA. Specific RecD2 degradation caused unviability in the absence of RecG or RuvAB, but not on cells lacking RecU. These findings show that there is notable interplay between RecD2 and RecG or RuvAB at arrested replication forks, rather than involvement in processing Holliday junctions during canonical double strand break repair. We propose that there is a trade-off for efficient genome duplication, and that recombinational DNA helicases directly or indirectly provide the cell with the means to tolerate chromosome segregation failures.

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