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. 2019 Dec 27;6(1):41–53. doi: 10.1021/acscentsci.9b01063

Figure 1.

Figure 1

A CRISPR activation screen identifies Gch1 as ferroptosis antagonist. (A) Venn diagram of overlapping top 30 genes found in each overexpression screen against ferroptosis inducers 0.3 μM RSL3, 2 μM IKE, and Gpx4–/– by 1 μM tamoxifen. (B) Relative Gch1 mRNA expression levels and dose response curves against RSL3 treatment in Gch1-overexpressing MF-dCas9-Gch1 (Gch1 OE) cells and empty vector control (control) immortalized mouse fibroblasts. Addition of 10 μM α-tocopherol (αToc) serves as rescue control for ferroptosis. (C) Relative GCH1 mRNA expression levels and dose response curve against RSL3 treatment in HT-1080 cells overexpressing GCH1-IRES-Puro construct (GCH1 OE) and parental HT-1080 cells (parental) ± 2 μM ferrostatin-1 (Fer-1) rescue. Viability data are plotted as mean ± SEM of n = 3 (B) or n = 2 (C) technical replicates of at least three repetitions of the experiment with similar outcomes. Relative mRNA expression is shown as mean ± SD of n = 3 technical replicates of three independent repetitions of the experiment with similar results.