Fig. 2

Activation of AR induces GATA3 chromatin binding at AR/GATA3 co-occupied loci in ER-positive breast cancer cells. Volcano plots reporting the FDR adjusted p-value and the log₂ fold change (Log₂ FC) of GATA3 chromatin binding events in (A) T-47D breast cancer cells treated with DHT vs Veh or (B) GAR15-13D PDX tumors from [8] collected 5 days after treatment with the selective androgen receptor modulator (SARM), enobosarm vs Veh. For visualization of differential binding patterns, the threshold for gain or loss in volcano plots is shown as FC > 1 (vertical lines) with an FDR cut-off of 5 × 10⁻³ (horizontal line). C Venn diagram showing overlap of enriched (FDR < 0.05, no fold-change threshold) AR and GATA3 binding sites after stimulation with DHT. D Two-factor log-ratio (M) plot displaying DHT (T-47D, left)- or SARM (GAR15-13D PDX, right)-induced changes in GATA3 and AR enrichment at consensus chromatin binding sites. Point color denotes treatment-induced changes in transcription factor occupancy (called peaks); GATA3 unique (orange, plotted in the rear), AR unique (grey) and Veh + DHT (or Veh + enobosarm; SARM) shared (pink), DHT- or SARM-induced GATA3 peaks that are not shared with AR (blue), and shared AR/GATA3 peaks that are significantly gained with DHT or SARM stimulation (red). Point co-ordinates are derived from the average enrichment score of three independent ChIP-seq replicates for each consensus binding site. Example binding sites near known AR target genes are highlighted. E Consensus GATA3, AR, and H3K27ac ChIP-seq data showing heatmaps demonstrative of a DHT- (T-47D, left) or enobosarm-induced (GAR15-13D, right) gain in GATA3 chromatin binding sites that are shared with AR. F Example genome browser images showing GATA3, AR, and H3K27ac ChIP-seq signals at loci associated with AR target genes ZBTB16 (left panel) and SEC14L2 (right panel) in T-47D cells. Data represents the average signal of three replicates