Fig. 4: Unsupervised clustering highlights differential responses to the absence of BPTF at the level of CTCF binding, chromatin opening and nuclear organization.
From: Systematic assessment of ISWI subunits shows that NURF creates local accessibility for CTCF

a, Boxplot displaying changes upon loss of BPTF or SNF2H in CTCF ChIP–seq and ATAC–seq signal at all bound CTCF sites, expressed as log2(FC) in respect to WT control cells. Measurements are shown for all sites (left) and separately for clusters 1–5. Black lines indicate median, boxes indicate first and third quartiles, and whiskers indicate maximum and minimum values of distribution after the removal of outliers. b, Distribution of chromatin states at sites surrounding bound CTCF motifs, as labeled by chromHMM (Methods) and split by clusters (as in a). Cluster numbers reported on top. c, Changes in observed/expected interactions at TADs (identified in ref. 46 mESCs dataset) following BPTF depletion, SNF2H depletion (data from ref. 14) and CTCF auxin-mediated degradation for 48 h (data from ref. 30), measured using Hi-C (ratios over respective controls are reported), at 10 kb resolution. d, Same analysis as in c at TAD boundaries (identified in ref. 46 mESCs dataset). e, Same analysis as in c and d at Hi-C loops. f, Changes in observed/expected interactions at CTCF sites divided by clusters (as in a) following BPTF depletion, SNF2H depletion and CTCF auxin-mediated degradation (48 h), measured using Hi-C (ratios over respective controls are reported). Cluster number is reported on the left. Canonical motif orientation (5′–3′) indicated by the arrow.