ArticleNature cell biology2026
Lineage-determining transcription factors constrain cohesin to drive multi-enhancer oncogene regulation.
Article in Nature cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Single-allele chromatin tracing reveals cytokine-dependent super-enhancer repositioning in CD4Immunity · 2026Article
- Applying the Poincaré Disc Method to Analyze the Hierarchical Structure of TADs in Hi-C Data.Genes · 2026Article
- Transcription factors as drivers of 3D enhancer-promoter interactions.Current opinion in structural biology · 2026Review
- Cohesin bridging as a physical principle of enhancer-promoter communication.bioRxiv : the preprint server for biology · 2026Article
- The role of cohesin loading at enhancers in the flux of loop extrusion and long-range transcriptional control.bioRxiv : the preprint server for biology · 2026Article
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10 authors.
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Abstract
Multiple enhancers, often separated by vast genomic distances, regulate key genes. However, how the folding of individual chromatin fibres enables cell-type-restricted multi-enhancer regulation remains unclear. Here, using acute protein degradation and time-resolved chromatin conformation capture in mantle cell lymphoma, we found that the B cell-lineage-determining factor EBF1 organizes multiple enhancers around sparsely distributed genes essential for B cell identity and oncogenesis. Time-resolved sub-diffraction optical tracing of more than 100,000 chromatin fibres further revealed diverse topological conformations that facilitate multi-enhancer interactions. Mechanistically, we discovered that enhancer positioning at local topological centres is required for promoter engagement, with EBF1 acting as a permeable barrier to loop-extruding cohesin at enhancers. Extending these findings to T cell leukaemia, we show that lineage-determining transcription factors such as EBF1 and TCF1 radially position enhancers within gene loci to enable multi-enhancer regulation of key oncogenes at the single-allele level.
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