BRCA2 and homologous recombination

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.

BRCA2
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]. Cells with mutant BRCA2 protein are, like many cancer cells, genetically unstable and accumulate gross chromosomal rearrangements [5,6]. The sequence of this large protein (3418 amino acids) offers very little clue to its function, although ther