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. 2021 Aug 9;4(10):e202000940. doi: 10.26508/lsa.202000940

Figure S2. Modeling of tumorigenic mutations in intestinal organoids by prime editing.

Figure S2.

(A) Mutations targeted for tumor modeling in organoids in TP53 and APC and the number of observed clones as observed after either selection with both the addition of nutlin-3 (TP53) or removal of wnt and Rspo1 (APC) from the culture medium. (B) Bright-field images of prime-editing experiments targeting the TP53-C176F compared with a negative-scrambled sgRNA control. (C) Sanger sequencing trace of selected clonal organoids harboring the TP53-C176F mutation compared with WT. (D) Prime-editing efficiency on TP53-C176F as measured by Sanger sequencing of 36 hygromycin-resistant clones. (E) Bright-field images of prime-editing experiments targeting the APC R1450* mutation compared with a negative-scrambled sgRNA control (Scale bar: = 2,000 μm). (F) Sanger sequencing trace of selected APC R1450* clone. Insertion is shown in yellow, protospacer adjacent motif is shown in red, and spacer sequence is shown in blue.