Fig. 5: ChIP-seq analyses of H3K27me3 in chondrocytes. | Cell Death & Disease

Fig. 5: ChIP-seq analyses of H3K27me3 in chondrocytes.

From: Histone H3K27 demethylase UTX compromises articular chondrocyte anabolism and aggravates osteoarthritic degeneration

Fig. 5

Venn diagram showing the overlap of H3K27me3 peaks between UtxKO and WT mice. Total numbers of H3K27me3-enriched binding sites and their relative proportions (%) are indicated. Note that UtxKO mice revealed fewer binding sites compared to WT animals (a). Heatmaps of ChIP-seq analyses showing H3K27me3 DNA occupancy within 5 kb upstream and downstream, respectively, of transcriptional start site (TSS) (b). Scatter plots shows H3K27me3 ChIP-seq signals distribution in UtxKO and WT (c), next to the relative distribution of H3K27me3 occupancy across genomic regions in chondrocytes of WT and UtxKO animals, respectively (d). Gene set enrichment analysis of H3K27me3 marks revealed significant enhancement mitochondrion in UtxKO cells (e, f). Data are calculated from three mice. Tfam mRNA expression (g), Tfam immunostaining (h scale bar, 10 μm) mitochondrial respiration profiles (i), basal and maximal oxygen consumption rates (j), ATP production (k), and mitochondrial mass as evidenced in MitoTracker Green staining (scale bar, 20 μm) and electron transmission microscopy (scale bar, 200 nm) (l) in UtxKO chondrocytes were higher than in WT cells. Data are expressed as mean ± standard errors calculated from three to five mice. *P < 0.05; **P < 0.001.

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