Fig. 1

Genome-wide analysis of H3.3-ARID1A chromatin co-regulation. A Genomic annotation of 40,006 genome-wide H3.3 ChIP-seq peaks in 12Z cells (n = 2). B Distribution of H3.3 peak widths. Median H3.3 peak width is 1830 bp. C Genome-wide overlap of ARID1A and H3.3 ChIP-seq peaks. D Genome-wide association between H3.3 and other previously measured chromatin features, per genomic bp, quantified as [observed / expected]. Statistic is hypergeometric enrichment. E Enrichment for H3.3 and ARID1A co-regulation across 18 chromatin states previously modeled via ChromHMM [27]. Left, enrichment of H3.3 peaks; center, enrichment of H3.3+ARID1A binding; right, enrichment of ARID1A binding at sites with vs. without H3.3. Statistic is hypergeometric enrichment. F Left, ARID1A binding levels (ChIP/input fold-enrichment, FE) at H3.3+ vs. H3.3− ARID1A peaks. Right, H3.3 abundance (ChIP/input fold-enrichment) at ARID1A+ vs. ARID1A− H3.3 peaks. Statistic is two-tailed, unpaired Wilcoxon’s test. G Top, enrichment of H3.3 at genes promoter-proximally bound by ARID1A. Bottom, enrichment of ARID1A+H3.3 co-binding at genes DE following ARID1A loss (siARID1A treatment). Statistics are hypergeometric enrichment test and pairwise two-tailed Fisher’s exact test. H Example hg38 browser shots of genes and regulatory elements co-regulated by H3.3 and ARID1A. y-axis is log-likelihood ratio (logLR) of assay signal (compared to input chromatin for ChIP-seq or background genome for ATAC-seq). Small bars under tracks indicate significant peak detection by MACS2 (FDR < 0.05). Super-enhancers were detected by ROSE from H3K27ac ChIP-seq. * p < 0.05, ** p < 0.01, *** p < 0.001