Fig. 1

Mapping of 3D epigenome organizations in myeloid cells with inducible PML-RARα. a Schematic of experimental designs using an inducible system. PR9 cells contain an inducible construct of the fusion gene PML-RARα. Upon ZnSO4 induction, the fusion gene will be activated, and the PML-RARα protein is expressed and interacts with the myeloid genome. Both PR9 and PR9+Zn cells were analyzed by ChIA-PET, ChIP-seq, and RNA-seq to map the 3D epigenomes. b 2D chromatin contact maps of the PML and RARα ChIA-PET data from PR9 (top) and PR9+Zn (bottom) cells. To be noted, PML ChIA-PET did not produce meaningful data, while the RARα ChIA-PET generated abundant data mapping RARα-mediated chromatin interactions in PR9 cells (top). However, both PML and RARα experiments in PR9+Zn cells produced equal amounts of data with the same patterns, indicating the detection of chromatin interactions mediated by the fusion protein PML-RARα. The boxed segments were zoomed in for details in e. c 2D chromatin contact maps of the CTCF ChIA-PET data from PR9 (top) and PR9+Zn (bottom) cells. d 2D chromatin contact maps of the RNAPII ChIA-PET data from PR9 (top) and PR9+Zn (bottom) cells. e Screenshots of browser views displaying a genomic segment at CEBPB loci in chr20, exemplifying the chromatin interactions detected by ChIA-PET using PML, RARα, CTCF, and RNAPII antibodies in PR9 (left) and PR9+Zn (right) cells. As shown, the CTCF data (green) exhibited the same patterns and intensity in both PR9 and PR9+Zn cells; no PML data (pink) in PR9 cells, but extensive data in PR9+Zn cells; weak RARα signals in PR9 but strong and abundant (purple) in PR9+Zn; strong RNAPII (red) binding at the CEBPB gene locus and interaction loops to enhancer sites in PR9 cells, but absent in PR9+Zn cells. The RNA-seq data showing that CEBPB is expressed in PR9 cells (RPKM = 3.43), but reduced by twofold in PR9+Zn cells (RPKM = 1.28)