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. Author manuscript; available in PMC: 2022 Jun 2.
Published in final edited form as: Nat Chem Biol. 2021 Dec 2;18(4):360–367. doi: 10.1038/s41589-021-00900-9

Fig. 4 |. Deep mutational scanning and CRISPR/Cas9 directed editing of binding site residues reveals mutations which confer resistance to ammocidin and apoptolidin.

Fig. 4 |

a, Illustration of the Bxb1 landing pad system consisting of an attP containing landing pad integrated at a single site in the genome and an attB transfer plasmid containing the variant gene of interest (ATP5x), colored genes are expressed in the presence of doxycycline; b, Tile plot of allelic enrichment after selection, filled based on the highest dose at which >10-fold enrichment was observed; c, Comparison of drug sensitivity between K562 Parental and K562 CRISPR/Cas9 knock-in resistant mutants demonstrating cross resistance to glycomacrolides with retained sensitivity to Oligm and puromycin (n = 3 per dose, P values computed for lower-bound of fitted log-logistic model, two-sided); d, Modeling of L83R and I387R mutations in the ammocidin cryoEM model (~ human residues in parenthesis).