Fig. 1: Disrupted occupancies of CTCF and SMC1 due to CTCF depletion in BMDCs.
a Schematic showing in vitro DC differentiation models, where cultures of naïve BM in the presence of GM-CSF leads to differentiation of precursors into BMDCs. We added 4-hydroxytamoxifen (4-OHT) to the BM cultures on the first day of differentiation to remove loxP-flanked Ctcf alleles for Ctcf conditional knockout cells (CreER;CTCFfl/fl) but not for WT cells (CreER;CTCFwt/wt). Following in vitro differentiation, WT and CTCF-deficient BMDCs were activated using LPS. WT: untreated wild-type BMDC, WTL: wild-type BMDC treated with LPS for 3 h, KO: untreated CTCF knock-out BMDC, KOL: CTCF knock-out BMDC treated with LPS for 3 h. b, c Efficient depletion of CTCF at the mRNA (b) and protein (c) levels in CTCF-deficient BMDCs. Error bars represent mean ± standard error of the mean (s.e.m.). n = 2 biologically independent samples were used for each group. d Heatmaps of ChIP-Seq signal called for CTCF (left) and SMC1 (right) showing disrupted global occupancy of each protein in CTCF-deficient BMDCs. Histogram showing the average tag density of CTCF or SMC1 ChIP-seq peaks are displayed on top of each heatmap. e Snapshot of ChIP-seq signal tracks for CTCF and SMC1 in the representative genomic region. Source data are provided as a Source Data file.
