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. Author manuscript; available in PMC: 2012 Mar 26.
Published in final edited form as: Cell. 2011 Dec 23;147(7):1628–1639. doi: 10.1016/j.cell.2011.09.057

Figure 5. Comparisons of CR binding and modular associations in K562 and ES cells.

Figure 5

(A) CRs distribute to distinct loci in ES and K562 cells. For each CR (left) or histone modification (right), bar graph indicates proportions of binding intervals that are ES cell-specific (‘H1 only’, light blue), K562-specific (‘K562 only’, gray) or overlapping between cell types (‘H1 and K562’, navy). The bars are vertically centered according to the overlap regions. (B) CR-CR associations and CR-histone modification associations are largely preserved between K562 and ES cells. Scatter plot presents the correlations in localization profiles between every pair of CRs (black dots) and every CR-histone modification pair (red dots) in either K562 cells (X axis) or ES cells (Y axis). Linear regression lines and correlation coefficients are indicated for each type of combination. (C) CRs associate with similar chromatin states in ES and K562 cells with some distinctions. Pie charts indicate the proportion of CR binding sites that correspond to a given chromatin state annotation; green – active/competent promoter, gold – distal regulatory element/candidate enhancer, red – repressed chromatin (including bivalent state), blue – transcribed region. CRs are grouped according to the modules in Figure 3. (D) Combinatorial binding profiles are shown for CRs in ES cells. Fine-scale binding profiles are shown for each CR across 1189 target promoters (rows) in ES cells, after hierarchical clustering and re-ordering of major promoter clusters as in Figure 4A (original ordering shown in Figure S4). Functional gene set annotations (right) curated from enriched sets (Table S5B). CR labels colored as in Figure 4A, with ES cell-specific CRs in black.