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. 2022 Nov 18;50(20):11635–11653. doi: 10.1093/nar/gkac1045

Figure 6.

Figure 6.

A n example of GR-dependent PGx-eQTLs with functional implications for disease risk. (A) PGx-eQTL SNP-gene pairs for rs1697139-MAST4. Adjusted P-values from Tukey's post-hoc multiple comparisons and represent differences between wildtype and variant genotypes. Cortisol induced the eQTL, and C297 antagonized the cortisol effect, normalizing eQTL expression across genotypes. (B) IGV plots of the PGx SNP-eQTL gene locus. Tracks for GR-targeted ChIP-seq in different treatment conditions are colored in blue, which show similar drug-dependent patterns as expression data: Cortisol induced GR binding at SNP locus, and C297 antagonized the cortisol effect, reducing GR binding. H3K4me1 is a histone mark associated with enhancers. H3K4me3 is a histone mark associated with promoters. H3K27ac is a histone mark associated with active promoters and enhancers. For the H3K27ac HiChIP tracks, loops directly interacting with the PGx SNP locus are highlighted in pink and others in blue. (C) SNP-dependent and drug-dependent enhancer activity of the PGx locus in LCLs as measured by STARR-seq. CPM stands for counts per million.