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

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 Delta recD2 mutation sensitizes cells to DNA-damaging agents that stall or collapse replication forks. We found that this Delta recD2 mutation impaired growth, and that a mutation in the perA gene (perA596) relieved this phenotype. The Delta recD2 mutation was not epistatic to Delta addAB, Delta recQ, Delta recS, Nte1D, perA596 and Delta dinG, 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.