The epistatic relationship between BRCA2 and the other RAD51 mediators in homologous recombination.
PLoS Genet
; 7(7): e1002148, 2011 Jul.
Article
in En
| MEDLINE
| ID: mdl-21779174
ABSTRACT
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.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
BRCA2 Protein
/
Epistasis, Genetic
/
Rad51 Recombinase
/
Homologous Recombination
Limits:
Animals
Language:
En
Journal:
PLoS Genet
Journal subject:
GENETICA
Year:
2011
Type:
Article
Affiliation country:
Japan