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Enhancer hubs and loop collisions identified from single-allele topologies.

Author information

Affiliations

  • 1. Center for Molecular Medicine, University Medical Center, Utrecht University, Utrecht, the Netherlands.
      Authors
    • Allahyar A 1
    • Straver R 1
    • Renkens IJ 1
    • Kloosterman WP 1
    • de Ridder J 1
    (5 authors)
  • 2. Oncode Institute, Hubrecht Institute-KNAW and University Medical Center Utrecht, Utrecht, the Netherlands.
      Authors
    • Vermeulen C 2
    • Bouwman BAM 2
    • Krijger PHL 2
    • Verstegen MJAM 2
    • Geeven G 2
    • van Kranenburg M 2
    • Pieterse M 2
    • de Laat W 2
    (8 authors)
  • 3. Division of Gene Regulation, Netherlands Cancer Institute, Amsterdam, the Netherlands.
      Authors
    • Haarhuis JHI 3
    • Rowland BD 3
    (2 authors)
  • 4. Division of Cell Biology, Netherlands Cancer Institute, Amsterdam, the Netherlands.
      Authors
    • Jalink K 4
    (1 author)
  • 5. Oncode Institute and Division of Gene Regulation, Netherlands Cancer Institute, Amsterdam, the Netherlands.
      Authors
    • Teunissen H 5
    • de Wit E 5
    (2 authors)

ORCIDs linked to this article

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Nature Genetics, 09 Jul 2018, 50(8):1151-1160
https://doi.org/10.1038/s41588-018-0161-5 PMID: 29988121 

This article is based on a previously available preprint.

Abstract 

Chromatin folding contributes to the regulation of genomic processes such as gene activity. Existing conformation capture methods characterize genome topology through analysis of pairwise chromatin contacts in populations of cells but cannot discern whether individual interactions occur simultaneously or competitively. Here we present multi-contact 4C (MC-4C), which applies Nanopore sequencing to study multi-way DNA conformations of individual alleles. MC-4C distinguishes cooperative from random and competing interactions and identifies previously missed structures in subpopulations of cells. We show that individual elements of the β-globin superenhancer can aggregate into an enhancer hub that can simultaneously accommodate two genes. Neighboring chromatin domain loops can form rosette-like structures through collision of their CTCF-bound anchors, as seen most prominently in cells lacking the cohesin-unloading factor WAPL. Here, massive collision of CTCF-anchored chromatin loops is believed to reflect 'cohesin traffic jams'. Single-allele topology studies thus help us understand the mechanisms underlying genome folding and functioning.

Full text links 

Read article at publisher's site: https://doi.org/10.1038/s41588-018-0161-5

Read article for free, from open access legal sources, via Unpaywall: https://www.biorxiv.org/content/biorxiv/early/2017/10/20/206094.full.pdfUnpaywall

References 

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NIH HHS (1)