Genome-scale CRISPR screens are efficient in non-homologous end-joining deficient cells.

摘要: The mutagenic repair of Cas9 generated breaks is thought to predominantly rely on non-homologous end-joining (NHEJ), leading insertions and deletions within DNA that culminate in gene knock-out (KO). In this study, by taking focused as well genome-wide approaches, we show pathway dispensable for the such lesions. Genetic ablation NHEJ fully compensated alternative end joining (alt-EJ), a POLQ-dependent manner, resulting distinct signature with larger may be exploited large-scale genome editing. Moreover, cells deficient both alt-EJ were still able CRISPR-mediated double-strand breaks, highlighting how little yet known about mechanisms CRISPR-based