Abstract
DNA double-strand break (DSB) is considered most deleterious among radiation-induced DNA damages and most relevant to the biological effects of radiation. In eukaryotic cells, DSB is repaired mainly through two pathways: non-homologous end-joining (NHEJ) and homologous recombination (HR). These repair pathways seem to play complementary roles. NHEJ is considered less accurate than HR, but HR is available only in late S and G2 phases in vertebrates. Recent studies elucidated how cells choose one from these two pathways depending on the circumstance: cell cycle phase, complexity of DNA damage and chromatin structure.
