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Crump, Nicholas T; Smith, Alastair L; Godfrey, Laura; Dopico-Fernandez, Ana M; Denny, Nicholas; Harman, Joe R; Hamley, Joseph C; Jackson, Nicole E; Chahrour, Catherine; Riva, Simone; Rice, Siobhan; Kim, Jaehoon; Basrur, Venkatesha; Fermin, Damian; Elenitoba-Johnson, Kojo; Roeder, Robert G; Allis, C David; Roberts, Irene; Roy, Anindita; Geng, Huimin; Davies, James O J; Milne, Thomas A
Nature communications, 08/2023, Volume: 14, Issue: 1Journal Article
Aberrant enhancer activation is a key mechanism driving oncogene expression in many cancers. While much is known about the regulation of larger chromosome domains in eukaryotes, the details of enhancer-promoter interactions remain poorly understood. Recent work suggests co-activators like BRD4 and Mediator have little impact on enhancer-promoter interactions. In leukemias controlled by the MLL-AF4 fusion protein, we use the ultra-high resolution technique Micro-Capture-C (MCC) to show that MLL-AF4 binding promotes broad, high-density regions of enhancer-promoter interactions at a subset of key targets. These enhancers are enriched for transcription elongation factors like PAF1C and FACT, and the loss of these factors abolishes enhancer-promoter contact. This work not only provides an additional model for how MLL-AF4 is able to drive high levels of transcription at key genes in leukemia but also suggests a more general model linking enhancer-promoter crosstalk and transcription elongation.
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