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. Author manuscript; available in PMC: 2024 May 1.
Published in final edited form as: Nat Cell Biol. 2023 Oct 9;25(11):1616–1624. doi: 10.1038/s41556-023-01250-5

Fig. 2: Chemical genomic screens link HEM25 to the mevalonate pathway.

Fig. 2:

a, Gene fitness correlations with HEM25. Genes involved with ergosterol and CoQ biosynthesis are highlighted. b, Fitness ranking of geneΔ strains in the presence of 78.68 μM atorvastatin. c, Relative CoQ abundances of WT and hem25Δ cells treated with either vehicle (DMSO) or 10 μM atorvastatin (*P = 0.0002 DMSO-treated WT versus DMSO-treated hem25Δ, **P = 1.1 × 10−6 DMSO-treated hem25Δ versus atorvastatin-treated hem25Δ, mean ± s.d., n = 3 biologically independent samples, two-sided Student’s t-test; NS, not significant). ALA was present in the growth medium to support haem biosynthesis. d, Growth assay of WT and hem25Δ yeast in synthetic complete medium containing 0.1% (wt/vol) glucose, 3% (wt/vol) glycerol and 300 μM ALA. The media were further supplemented with either vehicle (DMSO) or atorvastatin, as indicated (mean, n = 3 biologically independent samples). Under these conditions, yeast enter respiratory growth after approximately 8 h. Raw data for a and b are from the HIPHOP chemogenomics database34. Fitness defect scores reflect the homozygous deletion profiles for atorvastatin (compound SGTC_2648). Numerical data are available as Source data.