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. Author manuscript; available in PMC: 2018 Mar 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2017 Aug 24;38(1):12–18. doi: 10.1161/ATVBAHA.117.309326

Figure.

Figure

Schematic of possible outcomes of genome editing that are relevant to the prevention and treatment of atherosclerosis. On the left, standard CRISPR-Cas9 is directed to a genomic site by the protospacer-adjacent motif (PAM) in the DNA and protospacer sequence in the guide RNA, whereupon it generates a double-strand break (location indicated by arrows pointing to DNA strands). The break is repaired by either nonhomologous end-joining (NHEJ) or homology-directed repair (HDR), which yield different outcomes. On the right, the base editor does not generate a double-strand break but rather converts a cytosine base (or bases) into a uracil base, which is ultimately replaced with a thymine base (with a complementary change of guanine-to-adenine on the opposite strand).