Fig. 1: Genome-wide CRISPR-Cas9 dropout screening identifies genetic determinants of AZA-sensitivity. | Nature Communications

Fig. 1: Genome-wide CRISPR-Cas9 dropout screening identifies genetic determinants of AZA-sensitivity.

From: TOPORS E3 ligase mediates resistance to hypomethylating agent cytotoxicity in acute myeloid leukemia cells

Fig. 1: Genome-wide CRISPR-Cas9 dropout screening identifies genetic determinants of AZA-sensitivity.

A Schematic of the genome-wide CRISPR-Cas9 dropout screen workflow performed in AZA-treated Cas9-expressing MDS-L. B MAGeCKFlute nine-square correlation plot using cell-cycle normalized β scores calculated for each gene target (n = 2), highlighting sgRNAs specifically (red) enriched, or (blue) depleted following AZA selection. C ClueGO pathway term network highlighting biological processes enriched in dropout hits. D Competitive proliferation assay workflow. MDS-L/Cas9 cells were transduced with lentiviral vectors encoding a single sgRNA plus a tagRFP657 (tagRFP657) reporter from separate promoters. E Validation of AZA-selection against TOPORS-, UBE2K-, and UBXN7-editing using the competitive proliferation assay shown in D. In each plot, y = %tagRFP+ in AZA/mean %tagRFP+ in vehicle; n = 3 technical replicates. Source data are provided as a Source Data file. Panels A and D created with BioRender.com released under a Creative Commons Attribution-Non Commercial-No Derivs 4.0 International license.

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