ArticleeLife2024
A genome-wide nucleosome-resolution map of promoter-centered interactions in human cells corroborates the enhancer-promoter looping model.
Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Quantitative Control of Transposable Elements: From Genome Plasticity to Immune Regulatory Circuits.Cell biochemistry and function · 2026Review
- Polymorphic 3D genome architecture mediated by transposable elements.bioRxiv : the preprint server for biology · 2026Article
- Deciphering histone mark-specific fine-scale chromatin organization at high resolution with Micro-C-ChIP.Nature communications · 2025Article
- Transcriptional programs of cell identity and p53-induced stress responses are associated with distinctive features of spatial genome organization.Nucleic acids research · 2025Article
- Long G4-rich enhancers target promoters via a G4 DNA-based mechanism.Nucleic acids research · 2025Article
- Long non-coding RNAs direct the SWI/SNF complex to cell type-specific enhancers.Nature communications · 2025Article
- Article
- The BAF complex enhances transcription through interaction with H3K56ac in the histone globular domain.Nature communications · 2024Article
- Enhancer Function in the 3D Genome.Genes · 2023Review
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Authors and funding
4 authors.
Funding
Abstract
The enhancer-promoter looping model, in which enhancers activate their target genes via physical contact, has long dominated the field of gene regulation. However, the ubiquity of this model has been questioned due to evidence of alternative mechanisms and the lack of its systematic validation, primarily owing to the absence of suitable experimental techniques. In this study, we present a new MNase-based proximity ligation method called MChIP-C, allowing for the measurement of protein-mediated chromatin interactions at single-nucleosome resolution on a genome-wide scale. By applying MChIP-C to study H3K4me3 promoter-centered interactions in K562 cells, we found that it had greatly improved resolution and sensitivity compared to restriction endonuclease-based C-methods. This allowed us to identify EP300 histone acetyltransferase and the SWI/SNF remodeling complex as potential candidates for establishing and/or maintaining enhancer-promoter interactions. Finally, leveraging data from published CRISPRi screens, we found that most functionally verified enhancers do physically interact with their cognate promoters, supporting the enhancer-promoter looping model.
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Registered trials
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