Fig. 1

Redistribution of chromatin-bound SUMO2/3 in heat stress. a SUMO2/3-modified cellular proteins accumulate in K562 and VCaP cells upon heat stress. Anti-SUMO2/3 antibody immunoblotting analysis of total cellular lysates from cells grown at control conditions (C; 37 °C) or exposed to heat shock (HS; 30 min at 43 °C), and from VCaP cells in recovery from HS (Re; HS followed by 1 h at 37 °C). Anti-lamin B1 antibody was used as a loading control. b Redistribution of chromatin SUMO2/3 in HS. SUMO2/3 (anti SUMO-2/3 antibody) ChIP-seq track examples of chromatin loci in K562 cells where SUMO2/3-binding decreases (ZNF gene cluster), is unaltered (tRNA gene cluster), or increases (HSP (heat shock protein) gene cluster) in HS. Numbers (on the left) depict maximal signal intensities of each track. c Distribution of SUMO2/3 peaks between annotated genomic loci in K562 and VCaP cells. SUMO2/3 peaks are from in control (blue), HS (red), and recovery (orange) conditions. d Chromatin environment of SUMO2/3 peaks categorized to SUMO2/3 C unique peaks (blue bar), SUMO2/3 C/HS-shared peaks (black bar), and SUMO2/3 HS unique peaks (red bar). Numbers on the left refer to the amount of peaks in each category. Heat map showing SUMO2/3-binding site, DNaseI and different histone mark signals in ±2 kb window using false-color scale (intensity increases from darker to lighter colors). Line profile of average ChIP-seq signal intensities at ±2 kb area surrounding the peak centers of different SUMO2/3 categories. ChIP-seq signals were normalized to 10 million reads