Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2

Inherited mutations in the human BRCA2 gene cause about half of the cauca of early-onset breast cancer. The embryonic expression pattern of the mouse Brca2 gene is now defined and an interaction identified of the Brca2 protein with the DNA-repair protein Rad51. Developmental arrest in Brca2- deficient embryos, their radiation sensitivity, and the asssociation of Brca2 with Rud51 indicate that Brca2 may be an essential cofactor in the Rud51- dependent DNA repair of double-strand breaks, thereby explaining the tumour- suppressor function of Brca2.