Torres Rubén, Romero Hector, Rodríguez-Cerrato Violeta, Alonso Juan C
Department of Microbial Biotechnology, Centro Nacional de Biotecnología (CNB-CSIC), 3 Darwin Str., 28049, Cantoblanco, Madrid, Spain.
Department of Microbial Biotechnology, Centro Nacional de Biotecnología (CNB-CSIC), 3 Darwin Str., 28049, Cantoblanco, Madrid, Spain.
DNA Repair (Amst). 2017 Jul;55:40-46. doi: 10.1016/j.dnarep.2017.05.004. Epub 2017 May 12.
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.
枯草芽孢杆菌的AddAB、RecS、RecQ、PcrA、HelD、DinG、RecG、RuvAB、PriA和RecD2是真正的重组修复酶，但RecD2的生物学作用尚不清楚。ΔrecD2突变使细胞对导致复制叉停滞或崩溃的DNA损伤剂敏感。我们发现这种ΔrecD2突变会损害生长，而pcrA基因中的一个突变（pcrA596）可缓解这种表型。ΔrecD2突变对ΔaddAB、ΔrecQ、ΔrecS、ΔhelD、pcrA596和ΔdinG不具有上位性，但对recA具有上位性。特定的RecD2降解在缺乏RecG或RuvAB时导致细胞无法存活，但在缺乏RecU的细胞中则不会。这些发现表明，在停滞的复制叉处，RecD2与RecG或RuvAB之间存在显著的相互作用，而不是参与经典双链断裂修复过程中的霍利迪连接的处理。我们提出，为了实现高效的基因组复制存在一种权衡，并且重组DNA解旋酶直接或间接地为细胞提供了容忍染色体分离失败的方法。
