Interplay between Bacillus subtilis RecD2 and the RecG or RuvAB helicase in recombinational repair |
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| Affiliation: | 1. Department of Bacteriology, University of Wisconsin-Madison, Madison, WI 53706, USA;2. Department of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706, USA;3. Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX 77030, USA;4. Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA;1. Department of Microbiology and Immunology, University of Illinois at Chicago, Chicago, IL 60612-7344, USA;1. Focal Area Infection Biology, Biozentrum, University of Basel, 4056 Basel, Switzerland;2. Focal Area Structural Biology and Biophysics, Biozentrum, University of Basel, 4056 Basel, Switzerland;3. Centre for Cell and Molecular Biosciences, Newcastle University, NE2 4AX Newcastle upon Tyne, UK;4. Proteomics Core Facility, Biozentrum, University of Basel, 4056 Basel, Switzerland;5. Department of Biology, University of Copenhagen, 2200 Copenhagen, Denmark |
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| Abstract: | 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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| Keywords: | Double strand break repair DNA damage tolerance Replication fork stalling End resection RecA regulation |
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