The Epistatic Relationship between BRCA2 and the Other RAD51 Mediators in Homologous Recombination
Creators
- 1. Kyoto University
- 2. University of Chicago
- 3. Sichuan University
Description
RAD51 recombinase polymerizes at the site of double-strand breaks (DSBs) where it performs DSB repair. The loss of RAD51 causes extensive chromosomal breaks, leading to apoptosis. The polymerization of RAD51 is regulated by a number of RAD51 mediators, such as BRCA1, BRCA2, RAD52, SFR1, SWS1, and the five RAD51 paralogs, including XRCC3. We here show that brca2-null mutant cells were able to proliferate, indicating that RAD51 can perform DSB repair in the absence of BRCA2. We disrupted the BRCA1, RAD52, SFR1, SWS1, and XRCC3 genes in the brca2-null cells. All the resulting double-mutant cells displayed a phenotype that was very similar to that of the brca2-null cells. We suggest that BRCA2 might thus serve as a platform to recruit various RAD51 mediators at the appropriate position at the DNA–damage site.
Files
journal.pgen.1002148.pdf
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Additional details
Identifiers
- DOI
- 10.1371/journal.pgen.1002148
- Other
- oai:uchicago.tind.io:10774
Funding
- Ministry of Education, Culture, Sports, and Science of Japan
- Grant-in-Aid for Scientific Research on Priority Areas
- Ministry of Education, Culture, Sports, and Science of Japan
- Grant-in-Aid from the Special Coordination Funds for Promoting Science and Technology
- The Uehara Memorial Foundation
- The Naito Foundation