Fig. 4: Outward-oriented CBSf regulates Pcdhβγ by blocking their aberrant looping from the outside of the TAD boundary. | Nature Communications

Fig. 4: Outward-oriented CBSf regulates Pcdhβγ by blocking their aberrant looping from the outside of the TAD boundary.

From: Outward-oriented sites within clustered CTCF boundaries are key for intra-TAD chromatin interactions and gene regulation

Fig. 4: Outward-oriented CBSf regulates Pcdhβγ by blocking their aberrant looping from the outside of the TAD boundary.The alternative text for this image may have been generated using AI.

a CTCF and Rad21 ChIP-seq profiles of the Pcdhβγ downstream TAD boundary in CBSf-deleted (ΔCBSf) homozygous mice compared to their wild-type (WT) littermates. b Close-up of CTCF and Rad21 ChIP-seq as well as ATAC-seq profiles in ΔCBSf mice compared to their WT littermates. c RNA-seq showing decreased expression levels of Pcdhβγ upon CBSf deletion. Data as mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001; two-tailed Student’s t test. For CBSf deletion mouse line, n = 4 biologically independent samples; for their WT littermate controls, n = 2. Source data are provided as a Source Data file. d, e 4C profiles using a repertoire of Pcdhβγ promoters as anchors, showing decreased chromatin interactions with HS18-20 enhancers (highlighted in blue, (e)) and increased chromatin interactions beyond CBSf (highlighted in pink, (e)). Note a sharp edge for the transition from decrease to increase at the location of CBSf. Differences (ΔCBSf versus WT) are shown under the 4C profiles.

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