Fig. 3: CTCF binding at strong motifs largely persists in the absence of BPTF despite loss of accessibility.
From: Systematic assessment of ISWI subunits shows that NURF creates local accessibility for CTCF
a, Average CTCF ChIP–seq signal at bound CTCF sites in Bptf∆ (orange) and parental ES cells (gray; top). The same analysis is in Snf2h∆ (purple) and parental ES cells (gray; bottom; data from ref. 14). Inputs are shown as control (blue). Canonical motif orientation (5′–3′) indicated by the arrow. b, Representative genomic loci illustrating changes in CTCF binding (ChIP–seq indicated by shades of red) and chromatin accessibility (ATAC–seq indicated by shades of blue) in Bptf∆, Snf2h∆ and parental ES cells. c, Average SMF signal at an unbound site (left) and at the same sites (as in b; right), in BPTF-deleted cells (orange) and WT control (gray). Shaded line represents s.d. d, A CNN-based model used to predict changes in CTCF binding in Bptf∆ cells. Influence of particular nucleotides is shown as average contribution scores, highlighting the role of an extended CTCF motif (M1 and M2) in retaining binding in the absence of BPTF. Canonical motif orientation (5′–3′) indicated by the arrow.
