“…The type II CRISPR/Cas9 endonuclease system evolved in bacteria as a defensive measure against viruses to cleave invading foreign DNA ( Barrangou et al, 2007 ). This natural defense system has been engineered into a bipartite genome editing tool, consisting of a guide RNA (gRNA) that directs double stranded DNA cleavage by the Cas9 endonuclease at specific locations within the genome ( Jinek et al, 2012 ) and has been adapted for use in a myriad of organisms (reviewed in: ( Bassett and Liu, 2014 ; Doudna and Charpentier, 2014 ; Hsu et al, 2014 ; Overcash et al, 2015 ; Sander and Joung, 2014 ; Sternberg and Doudna, 2015 ; Zhang et al, 2014 ), including Drosophila ( Bassett et al, 2013 ; Gratz et al, 2013a ; Kondo and Ueda, 2013 ; Ren et al, 2013 ; Yu et al, 2013 ). Following gRNA/Cas9 cleavage at a given target site, mutations can be generated at that genomic location via one of two pathways: error-prone non-homologous end joining (NHEJ) DNA repair, which typically generates small insertions and/or deletions (indels) at the cut site, or the more precise homology-directed repair (HDR) pathway that copies sequences from a homologous DNA template ( Gratz et al, 2013 ).…”