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Fig. 4 | Epigenetics & Chromatin

Fig. 4

From: Hypoxia increases genome-wide bivalent epigenetic marking by specific gain of H3K27me3

Fig. 4

Transcription status is primarily controlled by H3K4me3. a Bar graphs depicting numbers of H3K27me3-marked genes at indicated experimental conditions (normoxia: 0 h, acute hypoxia: 8 h; chronic hypoxia: 24 h; reoxygenation: +8 h): H3K27me3-enriched loci were classified as (upper to lower panels): all H3K27me3-enriched genes (All categories), promoter (Promoter)-, transcription start site (TSS)- and gene body (Broad)-marked genes; b TSS-associated enrichment profiles (average number of reads) for the corresponding H3K27me3 classes (colored lines; solid: promoter, dashed: TSS, dotted: broad profile) represent all H3K27me3-marked genes. c Boxplots: H3K27me3 enrichment was plotted against median expression levels. Comparative analysis was done at (upper to lower panels) t = 0, t = 8, t = 24 h hypoxia and after reoxygenation (t = +8 h). Subscripts correspond to non-marked (no mark), all H3K27me3-marked genes (all), and to promoter, TSS and broad H3K27me3 profiles as indicated. d Boxplots: H3K4me3 + H3K27me3 and H3K27me3 enrichment only were plotted against median expression levels. Comparative analysis was done at (upper to lower panels) t = 0, t = 8, t = 24 h hypoxia and after reoxygenation (t = +8 h). Subscripts correspond to non-marked (no mark), all H3K27me3-marked genes (all), and to promoter, TSS and broad H3K27me3 profiles as indicated; gene numbers are indicated in insets. Asterisks (c, d) indicate statistically significant differences (p < 0.05)

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