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Haapaniemi E, Botla S, Persson J, Schmierer B, Taipale J
Nat. Med. 24 (7) 927-930 [2018-07-00; online 2018-06-11]
Here, we report that genome editing by CRISPR-Cas9 induces a p53-mediated DNA damage response and cell cycle arrest in immortalized human retinal pigment epithelial cells, leading to a selection against cells with a functional p53 pathway. Inhibition of p53 prevents the damage response and increases the rate of homologous recombination from a donor template. These results suggest that p53 inhibition may improve the efficiency of genome editing of untransformed cells and that p53 function should be monitored when developing cell-based therapies utilizing CRISPR-Cas9.
CRISPR Functional Genomics [Collaborative]
NGI Stockholm (Genomics Applications) [Service]
NGI Stockholm (Genomics Production) [Service]
National Genomics Infrastructure [Service]
Protein Science Facility (PSF) [Service]
PubMed 29892067
DOI 10.1038/s41591-018-0049-z
Crossref 10.1038/s41591-018-0049-z
pii: 10.1038/s41591-018-0049-z