Extended Data Fig. 5: Absence of BPTF affects SNF2H localization at CTCF sites.

a. Detection of BPTF by ChIP–seq at distal bound CTCF sites shown as average signal for WT (gray) and BptfΔ (orange). Input signal is shown in blue. Canonical motif orientation 5′–3′ indicated by the arrow. b. Same analysis as in a for bound CTCF sites within ±500 bp from annotated promoters. c. CUT&RUN signal for SNF2H in WT, Snf2hΔ and BptfΔ cells, shown as alignment densities centered on bound CTCF motifs (black arrowhead). IgG signal is shown for each background as negative control. d. SNF2H CUT&RUN average signal at bound CTCF sites for WT, BptfΔ, Snf2hΔ and IgG. e. Boxplot (as in Fig. 4a) showing SNF2H CUT&RUN signal (log₂ fold change over IgG control) for WT (gray), BptfΔ (orange), Snf2hΔ (purple) at bound CTCF sites grouped by ATAC changes in BptfΔ. Groups are displayed from left to right starting with regions with stronger ATAC loss on the left (n= number of sites in each group, range of ATAC changes in each group is reported in the x-axis). f. Detection of SNF2H by CUT&RUN at distal DNaseI hypersensitive sites that do not overlap with CTCF motifs shown as average signal for WT (gray), BptfΔ (orange), Snf2hΔ (purple). IgG signal is shown in blue as negative control. CTCF sites are excluded to illustrate consistent binding of SNF2H in WT and BptfΔ lines outside of CTCF-bound sites. g. Boxplots (as in Fig. 4a) showing SNF2H CUT&RUN signal (log₂ fold change over IgG control) for WT (gray), BptfΔ (orange), Snf2hΔ (purple) at distal DNaseI hypersensitive regions not overlapping with CTCF sites (left) and at bound CTCF sites (right), illustrating specific reduction in SNF2H signal over CTCF sites in the BptfΔ line. Significance between WT and Bptf∆ conditions was calculated by a one-sided Wilcoxon signed-rank test.