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. 2020 Nov 27;11:6049. doi: 10.1038/s41467-020-19878-4

Fig. 5. Transcription-dependent cohesin island formation during RIS and macrophage differentiation.

Fig. 5

a Representative genome browser images of indicated THOR-normalized ChIP-seq at the IL1 locus with and without DRB treatment in RIS IMR90 cells. b Averaged SMC3 and CTCF ChIP-seq signal in indicated conditions in IMR90 cells over all scaled cohesin islands identified, flanked by extra 5 kb regions. c Pol II ChIP-seq profile in growing and RIS over all cohesin islands, as in (b). d Differential aggregated interaction neighbourhoods (at 20 kb resolution) between RIS and in growing. The left panel represents all interactions between cohesin islands and nearby cohesin peaks within 150 kb of each other. Compare to the right panel, which represents only significantly increasing Hi-C interactions during RIS between each cohesin island and nearby cohesin peaks (within 250 kb either side). e Cohesin islands at IL1B during macrophage terminal differentiation and loop representations determined by Phanstiel et al.44. Reanalysis of Hi-C matrices (5 kb resolution) of THP-1 monocytes and PMA-induced macrophages from Phanstiel et al.44 as well as RAD21 ChIP-seq from Heinz et al.45 in the same cell context. f RAD21 ChIP-seq signals in monocyte and macrophage45 over 65 cohesin islands shared by PMA-induced THP-1 macrophages and RIS IMR90 cells.