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. 2021 Jan 21;12:499. doi: 10.1038/s41467-020-20830-9

Fig. 5. Bivalent LOCKs in primitive cells are enriched at TAD boundaries and bound by regulators of chromatin interactions.

Fig. 5

A Enrichment of LOCKs of active marks with low or high H3K27me3 ChIP-seq signal at TAD boundaries defined within H1-hESC, GM12878 or K562 cell types (−log10(FDR)). B Enrichment of regulators of chromatin interactions (CTCF, RAD21, ZNF143 and YY1) in H3K4me1 LOCKs with low or high H3K27me3 ChIP-seq signal in H1-hESC, GM12878 and K562 cell types (−log10(FDR)). C Case example of a bivalent LOCK at a TAD boundary in H1-hESC cells on the chromosome 16q22.1 locus. The ChIP-seq signal intensities for H3K4me1, H3K27me3 and regulators of chromatin interactions are shown. D Comparison of the median of H3K4me1, H3K27me3 and H3K9me3 ChIP-seq signal overlap of H1-hESC, GM12878 and K562 cell lines on the H3K4me1 bivalent LOCKs (with high H3K27me3 signal overlap) in H1-hESC. The signal is normalized to the depth of ChIP-seq profiles and size of the LOCKs. In the heatmap, every value for each ChIP-seq profile is also divided by the maximum value of that profile across the cell lines.