Practice question

BRCA2 is prominent tumor suppressor containing BRC repeats that directly interact with Rad51. Under normal conditions RPA rapidly coats ssDNA preventing spontaneous Rad51 nucleation. After DNA damage, BRCA2 is recruited via PALB2 and BRCA1 to break sites where it mediates nucleation of Rad51 filament, stabilizing ATP-bound active conformation, blocking ATP hydrolysis mediated disassembly, and delivering Rad51 to ssDNA replacing RPA. This loader function is essential for strand invasion, D-loop formation, and homology-directed repair. Pathogenic BRCA2 mutations cause defective Rad51 recruitment, reliance on error-prone NHEJ, and breast-ovarian cancer susceptibility.