Precise genome editing is essential for both basic and translational research. The recently developed CRISPR/Cas9 system can specifically cleave a designated site of target gene to create a DNA double-strand break， which triggers cellular DNA repair mechanism of either inaccurate non-homologous end joining， or site-specific homologous recombination. Unfortunately， homology-directed repair (HDR) is challenging due to its very low efficiency. Herein， we focused on improving the efficiency of HDR using a combination of CRISPR/Cas9， eGFP， DNA ligase IV inhibitor SCR7， and single-stranded oligodeoxynucleotides (ssODN) in human cancer cells.
Precise genome editing is essential for both basic and translational research. The recently developed CRISPR/Cas9 system can specifically cleave a designated site of target gene to create a DNA double-strand break， which triggers cellular DNA repair mechanism of either inaccurate non-homologous end joining， or site-specific homologous recombination. Unfortunately， homology-directed repair (HDR) is challenging due to its very low efficiency. Herein， we focused on improving the efficiency of HDR using a combination of CRISPR/Cas9， eGFP， DNA ligase IV inhibitor SCR7， and single-stranded oligodeoxynucleotides (ssODN) in human cancer cells.
