Fig. 2

Mechanisms of double strand break repair exploited for gene editing. a Illustration of the results of the error-prone repair process during non-homologous end joining (NHEJ), which can introduce a mutation at the site of the double strand break through either the incorporation of random non-complementary nucleotides, or the deletion of nucleotides (indels). The goal is to either render a protein non-functional (e.g. knockout of diseased protein or preferentially knockout a functional protein for therapeutic benefit) or to (re-)activate a gene by either correcting/eliminating a deleterious nucleotide in the region of the break site or knocking out a repressive/inactivating element due to the introduction of an indel within that element. b Depiction of the results of homology-directed repair. Here a double strand break is induced in the presence of donor DNA. The donor DNA has nucleotide sequences flanking the gene to be inserted that are homologous to those upstream and downstream of the site of the break, enabling addition of the gene based on complementarity during the repair process