MOESM11 of A yeast phenomic model for the influence of Warburg metabolism on genetic buffering of doxorubicin

Additional file 11. Integration of yeast phenomic and cancer cell line pharmacogenomic data to predict human genes that modify doxorubicin toxicity in cancer cells. (A) Tables of UES and OES human genes and whether their yeast homologs were found to be deletion enhancing or deletion suppressing, respectively. (B-C) Overlap between the gCSI and GDSC1000 databases with regard to UES and OES human genes (B) across all tissues or (C) for individual tissues. Note: the intersection of UES with OES between gCSI and GDSC was used as a negative control for assessing UES and OES overlap. (D-E) Yeast phenomic doxorubicin-gene interaction profiles for homologs of human UES or OES genes, sub-classified according to interaction type (deletion enhancing or suppressing) and Warburg-dependence of the interaction, for the (D) gCSI or (E) GDSC1000 databases. Similar to Fig. 11, yeast-human homology relationships are shown to the left of heatmaps (blue - one to one; green - one to many; red - many to many). (F-I) Interactive plots for yeast-human homologs, comparing the p-value of human genes to L interaction scores for yeast counterparts in (F, G) HLD or (H, I) HLEG from (F, H) gCSI or (G, I) GDSC1000. For the standardized coefficient (‘estimate’; color gradient), a negative value (purple) indicates UES, while a positive value (orange) indicates OES. Thus, the model would predict causality for a human gene if its yeast homolog has a positive L interaction (deletion enhancing) and is colored purple (UES), or a negative L interaction (deletion suppressing) and colored orange (OES). Genes are only plotted if the human homolog was significant (p-value < 0.05).