Figure 2.

H2A.Z highly correlates with H3K4 methylation and localizes to distal elements. (a) Venn diagrams show overlaps of H2A.Z-enriched genomewide intervals with H3K4me1, H3K4me2 and H3K4me3. (b) Composite plots of ChIP-Seq signals for H2A.Z across TSSs (±5 kb, left panel) and intergenic sites (±5 kb, right panel) enriched for H2A.Z. (c) Analogous composite plots showing enrichment of H3K4me1, a putative enhancer mark, at intergenic H2A.Z sites. (d) Analogous composite plots for H3K4me2, which shows enrichment in both TSSs and enhancers. (e) Analogous composite plots for H3K4me3, which is enriched at H2A.Z-occupied TSSs. (f) Analogous composite plots for histone variant H3.3, which is enriched at H2A.Z-occupied TSSs and enhancers. (g) Bar graph shows fractions of intergenic MTLs [28] occupied by H2A.Z in mES cells, suggesting the correlation between H2A.Z and regulatory genomic regions under nucleosome regulation. ChIP-Seq: chromatin immunoprecipitation coupled with high-throughput sequencing; H3: histone H3, K: lysine; kb: kilobases; me1: monomethylation; me2: dimethylation; me3: trimethylation; MTLs: multiple transcription factor binding loci; TF: transcription factor; TSSs: transcription start sites; mES: mouse embryonic stem.

Ku et al. Genome Biology 2012 13:R85   doi:10.1186/gb-2012-13-10-r85
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