Fig. 1.

CRISPR/Cas9-induced DSBs cause apoptosis or cell cycle arrest in a p53-dependent manner. Schematic representation of the possible outcomes of CRISPR/Cas9-induced genome editing in p53 wild-type (upper panel) or p53-inactivated (bottom panel) edited cells (human pluripotent stem cells (hPSCs)/human retinal pigment epithelial cells (RPE1)). In p53 wild-type cells, DNA double-strand breaks (DSBs) trigger the activation of the DNA damage response (DDR) pathway with consequent accumulation of p53 and the induction of its target gene p21. Most cells with DSBs undergo apoptosis or cell cycle arrest and only a small number of gene-corrected cells are obtained. p53 genetic inactivation reduces DSB-mediated apoptosis and cell cycle arrest and increases the number of gene-edited cells. No DSBs indicate unedited cells