Fig. 8: RNA Pol2 clusters collapse, migrating to promoters with CpG islands.

a Schematic patterns describing the various types of RNA Pol2 cluster collapse. In these instances, RNA Pol2 migrates from enhancers and promoters without CpG islands and collects at promoters with CpG islands across MYOD1, SOX8, FGFR4 and PIPOX. b 3D contact maps of SOX8 and MYOD1 showing AQuA-CPM RNA Pol2 contacts. After 6 h dCBP1 treatment, there is an observed loss of long-range contacts with a gain of short-range contacts at a central location. c Schematic map of RNA Pol2 migration between promoters and enhancers with and without CpG island. The RNA Pol2 contacts between enhancers lacking CpG islands were mainly lost, whereas the contacts between the promoters having CpG islands were highly gained. The enhancers lacking CpG islands gained contacts to CpG containing promoters. d Aggregate Peak Analysis (APA) plots for RNA Pol2 HiChIP in RH4 cells edited to express PAX3-FOXO1-FKBP12(F36V) treated with DMSO (left), dTAG-47 (center), and the delta of dTAG-47 compared to DMSO (right). AQuA CPM is represented as bins of +/− 1 kilobases at Pol2 anchors, e Depiction of the super-cluster disruption model. CBP/p300 entangled with P3F acetylates enhancers to seed RNA Pol2 clustering and dynamic interaction with P3F target genes, which is disrupted when the CBP/p300-P3F driven RNA Pol2 super-clustering is lost.