Fig. 5

Super-enhancers affected by PML-RARα. a Boxplots of H3K9K14ac ChIP-seq intensity at the PML-RARα (P/R, purple) interaction binding sites or not as identified in PR9+Zn cells. The control (gray) represents H3K9K14ac signals at non-PML-RARα anchor loci (None). Paired t test was used to test the difference. **p < 0.001. b Distribution plots of H3K9K14ac ChIP-seq signals and the super-enhancers (SEs) identified in PR9 and PR9+Zn cells. SEs were ranked by increasing H3K9K14ac signals. SEs associated with genes critical in myeloid differentiation are highlighted in red. c Venn diagram of the numbers of unique and common SEs in PR9- and ZnSO4-treated PR9 cells based on differential analysis of H3K9K14ac signals. d Boxplots for normalized data signal intensity of RNAPII binding and loops at SE sites in PR9 and PR9+Zn (+Zn) cells (left), and the RARα binding and looping in PR9 cells and PML-RARα binding and looping in PR9+Zn (+Zn) cells at SE sites (right). **p < 0.001, by Kolmogorov-Smirnov test. e An example of chromatin interactions at the IRF2BPL locus identified by ChIA-PET of RARα (blue) and RNAPII (red) in PR9 cells, and PML-RARα (purple) and RNAPII (red) in PR9+Zn cells. Each ChIA-PET data are shown in tracks of loops (up) and peaks (below). f At the same location as in e, two SEs (highlighted) were identified with clusters of multiple H3K9K14ac peaks in PR9 cells. The H3K9K14ac peak signals were notably reduced in PR9+Zn cells. Similarly, the ChIP-seq signals for P300 and IRF1obserevd in PR9 cells were also reduced in PR9+Zn cells. Also, the expression of IRF2BPL as measured by RNA-seq data (RPKM) in PR9 cells was reduced by more than twofold in PR9+Zn cells