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Fig. 3 | Genome Biology

Fig. 3

From: Chromatin topology reorganization and transcription repression by PML-RARα in acute promyeloid leukemia

Fig. 3

PML-RARα selectively disrupt RNAPII transcriptome. a Scatter plots showing signal reduction of RNAPII occupancy at PML-RARα binding sites (left), RARα binding sites (middle), and other loci (right) in PR9+Zn cells. The red dots represent the data points of RNAPII binding intensity which was significantly higher in PR9 than in PR9+Zn cells. The gray dots denote the RNAPII data points without significant changes in binding intensity between PR9 and PR9+Zn cells. The numbers of corresponding sites and the percentages of RNAPII changes are shown in each plot. b Expression profiles of representative genes (n = 267) whose promoters both exhibited decreased RNAPII binding intensity and overlapped with PML-RARα binding in PR9, PR9+Zn, and PR9+Zn+ATRA cells. The blue dashed box highlights the genes that were repressed by PML-RARα. The yellow dashed box highlights the genes (n = 119) that were repressed by PML-RARα but rescued by ATRA treatment. Key genes known to be involved in leukemia biogenesis are indicated. c Gene Ontology (GO) enrichment analysis of genes (n = 280) whose promoters represent decreased RNAPII binding intensity (control vs. treatment) in the PML-RARα category that were characterized in a. The x-axis denotes the enrichment score of –log10 (FDR). d Screenshot of browser views of chromatin interaction loops and peaks for RARα (blue), RNAPII (red), and PML-RARα (purple) at the IRF2BP2 locus in PR9 and PR9+Zn cells. Strand-specific RNA-seq data in PR9 and PR9+Zn cells with a time course of ATRA treatment. The IRF2BP2 region is highlighted. e Line plot shows the mean expression level of IRF2BP2 over the time points of ZnOS4 and ATRA treatments

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