Abstract
Two recent papers provide new evidence relevant to the role of the breast cancer susceptibility gene BRCA2 in DNA repair. Moynahan et al provide genetic data indicating a requirement for BRCA2 in homology-dependent (recombinational) repair of DNA double-strand breaks. The second paper, by Davies et al, begins to address the mechanism through which BRCA2 makes its contribution to recombinational repair. BRCA2 appears to function in recombination via interactions with the major eukaryotic recombinase RAD51 [1,2,3]. We briefly review the context in which the two studies were carried out, we comment on the results presented, and we discuss models designed to account for the role of BRCA2 in RAD51-mediated repair.
Highlights
BRCA2 was the second breast cancer susceptibility gene to be discovered, and was isolated through positional cloning using data from families with inherited breast cancer [4]
Following the landmark discovery by Scully et al that the homologous recombinase RAD51 colocalizes at subnuclear sites with BRCA1 [9], a number of additional results have provided evidence that both BRCA1 and BRCA2 are involved in recombinational repair of DNA damage
Cell lines defective in either BRCA1 or BRCA2 are sensitive to damaging agents that form double-strand breaks (DSBs), as are other cell lines defective in recombinational repair
Summary
BRCA2 was the second breast cancer susceptibility gene to be discovered, and was isolated through positional cloning using data from families with inherited breast cancer [4]. Following the landmark discovery by Scully et al that the homologous recombinase RAD51 colocalizes at subnuclear sites with BRCA1 [9], a number of additional results have provided evidence that both BRCA1 and BRCA2 are involved in recombinational repair of DNA damage. Cells lacking BRCA1/2 fail to form damage-induced subnuclear RAD51 foci with normal efficiency, suggesting that these proteins are required for the formation of recombinase complexes at the sites of DNA damage [20,21].
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