Fig. 4: Chromatin remodeling between single-cell states.
a Number of peaks with significantly different chromatin accessibility between scH (n = 2526), scH/LP (n = 4013), scLP (n = 2436), scM (n = 1964) tumor cells and non-tumor hepatocytes from the two non-tumor liver samples (NT, n = 1518). ‘sc-epithelial’ corresponds to the union of scH, scH/LP and scLP. Activated peaks are colored in red, repressed peaks in blue. b Characterization of differential peaks between scM and sc-epithelial cells. From top to bottom: Volcano plots showing the FDR-adjusted p value as a function of the log fold-change (ArchR getMarkerFeatures test), with significantly ( | log2FC| ≥ 1 & FDR ≤ 10-3) activated (resp. repressed) peaks show in red (resp. blue); Enrichment of normal liver chromatin states (from ROADMAP consortium) in differential peaks (the dotted circle represents enrichment=1); Transcription factor binding motifs enriched in differential peaks; Footprints of normalized Tn5 insertions around transcription factor binding motifs enriched in sc-epithelial (HNF1A) and sc-M peaks (NR5A1). c Characterization of differential peaks between scLP and scH cells, formatted as in (b). d Significant overlap between differentially accessible ATAC-seq peaks and transcription factor ChIP-seq peaks from ReMAP database. The 4 examples shown include HNF1A associated with sc-epithelial cells (overlap between HNF1A ChIP-seq peaks and ATAC-seq peaks more accessible in sc-epithelial cells: q = 3.0e–122), LEF1 with scM cells (q = 1.9e–15), CEBPB with scH cells (q = 4.5e–6) and MAZ with scLP cells (q = 1.4e–5). Additional examples are shown in Supplementary Fig. 11, and all significant associations are reported in Supplementary Data 7. ChIP-seq coverage tracks were obtained from ENCODE (HNF1A in HepG2 cells: ENCFF502ACF; CEBPB in HepG2 cells: ENCFF406BBU; MAZ in HepG2 cells: ENCFF527EZL) or GEO (LEF1 in hESC: GSM1579343). Source data are provided in the Source Data file.
