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Fig. 2 | Cancer & Metabolism

Fig. 2

From: A yeast phenomic model for the influence of Warburg metabolism on genetic buffering of doxorubicin

Fig. 2

Q-HTCP provides cell proliferation parameters as phenotypes to quantify gene interaction. a, b Average pixel intensity and standard deviation for 768 reference strain cultures at indicated times after exposure to escalating doxorubicin concentrations in a HLD or b HLEG media. c, d Semi-log plots after fitting the data plotted above for c HLD or d HLEG to a logistic function (see Fig. 1d). el CPP distributions from data depicted in panels A-D for eh HLD and i, j HLEG, including L (e, i), K (f, j), r (g, k), and (h, l) AUC. m, n Comparison of doxorubicin-gene interaction scores using the L vs. K CPP in the context of either m HLD or n HLEG media. Score distributions of knockout (YKO, green), knockdown/DAmP (YKD, red), and non-mutant parental (Ref, purple) strain cultures are indicated along with thresholds for deletion enhancement and suppression (dashed lines at ± 2). o Differential doxorubicin-gene interaction (using L as the CPP) for HLD vs. HLEG, classified with respect to Warburg metabolism as non-specific (NS), respiratory-specific (R), or glycolysis-specific (G) deletion enhancement (Enh) or deletion suppression (Sup). pr Comparisons between genome-wide studies of doxorubicin-gene interaction: p Genes reported from Westmoreland et al. (green), Xia et al. (red), or both studies (purple) are plotted overlying L interaction scores (gray) in HLD vs. HLEG. q, r L interaction scores (gray) for genes reported by Westmoreland et al. (green), Xia et al. (red), or both studies (purple) in q HLD or r HLEG media. s, t Doxorubicin-gene interaction from whole-genome (WGS) and validation (V) studies on s HLD or t HLEG media

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