Practice question

Mammalian double-strand break repair choice depends on cell cycle and end processing factors. Ku70-Ku80 heterodimer is initial sensor avidly threading onto free DNA ends with sequence-independent high affinity, physically blocking extensive resection by MRN-CtIP and Exo1. By recruiting DNA-PKcs, XRCC4, Ligase IV, Ku drives classical non-homologous end joining pathway which re-ligates ends with minimal processing generating small indels. Loss of Ku unmasks ends to homologous recombination or alternative microhomology-mediated end joining, shifting repair balance toward resection-dependent mechanisms particularly active in S phase, illustrating competitive pathway control.