Supplementary Figure 4: KDM1A K114me2 and CHD1 co-occupy AR-binding sites.

(a,b) Venn diagrams showing number and overlap of KDM1A K114me2 (a) and CHD1 (b) peaks in LNCaP cells with or without RNAi mediated knockdown (KD) of KDM1A (a) or CHD1 (b). (c) Venn diagram illustrating number and intersection of KDM1A K114me2 and CHD1 peaks that are refractory to RNAi-mediated knockdown of KDM1A and CHD1. (d) Venn diagram depicting number and intersection of AR peaks with RNAi-refractory KDM1A K114me2 and CHD1 peaks. (e) Venn diagram showing number and intersection of the KDM1A K114me2-CHD1-AR co-locations with SUZ12 in LNCaP cells cultured in the presence of DHT. (f) Venn diagram showing number of KDM1A K114me2 locations remaining in the KDM1A K114me2-CHD1-AR intersection (Fig. 3c, 2941 locations) upon RNAi of EHMT2 in LNCaP cells. (g) Venn diagram showing the intersection and number of genes where AR and the RNAi-refractory KDM1A K114me2 and CHD1 peaks co-localize with genes that are differentially regulated in LNCaP cells upon treatment with DHT. (h,i) Box-and-Whisker plots of KDM1A K114me2 (h) and CHD1 (i) ChIP-seq tags around AR peaks in LNCaP cells treated without (-DHT) and with DHT (+DHT). (j) Average KDM1A K114me2 and CHD1 ChIP-seq read density profiles of the 861 genes, which are co-occupied by KDM1A K114me2, CHD1 and AR and differentially expressed upon treatment with DHT. (a-j) Results of genome-wide analyzes are representatives of 2 independent experiments. *** p<0.0001; ** p<0.001 by two-tailed Student’s test.