Extended Data Fig. 8: UTX condensates regulate genomic histone modifications and enhancer transcription. | Nature

Extended Data Fig. 8: UTX condensates regulate genomic histone modifications and enhancer transcription.

From: UTX condensation underlies its tumour-suppressive activity

Extended Data Fig. 8

a. A Venn diagram for genomic sites bound by UTX WT and ΔcIDR. The overlap number refers to the number of WT peaks that overlapped with ΔcIDR peaks. b. Genomic features of all 15,554 UTX WT-bound sites. The number of sites for each feature is shown in the parenthesis. c. Number and percentage of the genomic sites bound by either UTX WT (normal) or specifically by ΔcIDR (aberrant, not bound by WT) that overlap (within indicated distance) with any of the activating histone marks (H3K4me1, 2, 3, and H3K27ac) merged across all cell samples. d. Heatmap (left) and composite plot (right) for all 15,554 UTX WT-binding peaks in indicated cells. Heatmap rows were ranked by UTX peak levels (MACS2 peaks q-value, high to low). UTX ChIP-seq signals per 20bp non-overlapped bins covering 4kb regions centered at UTX peaks were shown. Details in Supplementary Table 3. e, f. Heatmap (left) and composite plot (right) for H3K4me1 (e) or H3K27ac (f) peaks in indicated cells at the UTX-binding sites (number indicated) with higher H3K4me1 (e) or H3K27ac (f) intensity in WT than vector expressing cells. Heatmap rows were ranked by UTX peak significance (MACS2 q-value, high to low). ChIP-seq signals from indicated histone modification per 20bp non-overlapped bins covering 4kb regions centered at UTX peaks were shown. gj. Left, scatter plot using the indicated H3K4me3 (g), H3K4me2 (h), H3K27me3 (i), and MLL4 binding (j) signal level change in cells indicated on the x and y axes, for all 15,554 UTX WT-bound sites. Black dashed line indicates the linear fit with correlation coefficient (r) labeled. Right, composite plot for indicated modification or binding signals centered at UTX peaks in indicated cells. k. Scatter plots using the indicated histone modification signal level change in cells indicated on the x and y axes, for all 15,554 UTX WT-bound sites. Black dashed line indicates the linear fit with correlation coefficient (r) labeled. l. Top, scatter plot for PRO-seq signal change at all 4,806 UTX WT-bound enhancers in indicated cells. Black dashed line indicates the linear fit with correlation coefficient (r) labeled. Bottom, composite plot for the PRO-seq signals centered at PRO-seq peaks in indicated cells. m. Heatmap (left) and composite plot (right) for PRO-seq signals at UTX WT-bound enhancers that had increased (top row) or decreased (bottom row) PRO-seq signals over 1.2 fold in WT compared to vector expressing cells, in indicated cells. PRO-seq signals centered at PRO-seq peaks were shown.

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