Brca1 mutations in the coiled-coil domain impede Rad51 loading on DNA and mouse development.

Abstract

We recently developed a Brca1 coiled-coil mutant mouse model (Brca1^CC ). Brca1^CC/CC results in embryonic lethality, with a fraction of mice reaching birth but with defects that parallel Fanconi anemia. Brca1^CC/CC cells lacked Rad51 foci and were PARP inhibitor sensitive. Strikingly, inter-crossing with Brca1^Δ11 generated Brca1 ^CC/Δ11 mice that were developmentally normal.