Practice question

Pathway choice for double-strand break repair depends strongly on cell cycle stage and resection control. In G0 quiescence and G1 gap where sister chromatids absent, extensive 5' resection blocked by 53BP1-RIF1-Shieldin complex and Ku end-binding factor prevents homology search. Therefore non-homologous end joining dominates, initiated by Ku70/Ku80 rapidly capping ends and recruiting DNA-PKcs and ligase IV. In S/G2, CDK phosphorylation activates CtIP enabling resection favoring homologous recombination. Thus NHEJ predominance in G0/G1 reflects availability of template and protective mechanisms limiting homologous recombination when homolog unavailable.