The Clustered regularly interspaced short palindromic repeats (CRISPR) and the associated protein (Cas9) are naturally found in nature as an adaptive immune system in some bacteria and Archaea (Terns & Terns, 2011). The mechanism has been biotechnologically adapted as a tool for precise genetic edition and applied to diverse species including viruses, bacteria, plants and animals (Barrangou & Doudna, 2016). CRISPR-Cas9 system is comprised of a ribonucleoprotein complex formed by the Cas9 protein, an endonuclease that cleaves DNA in a specific manner directed by its associated short guide RNA (sgRNA) (Gasiunas et al., 2012), complementary to the target DNA sequence which is followed by the nucleotides NGG, known as the protospacer adjacent motif (PAM) (Mojica et al., 2009). This system produces double-strand breaks (DSB) that induce alterations (insertions or deletions) in the genomic DNA mainly driven by the error-prone cellular repair mechanisms: non-homologous end joining (NHEJ) or homologydirected repair (HDR) (Ceccaldi et al., 2016;Chang et al., 2017).
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