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ZNF143 provides sequence specificity to secure chromatin interactions at gene promoters

Author

Listed:
  • Swneke D. Bailey

    (The Princess Margaret Cancer Centre—University Health Network
    University of Toronto)

  • Xiaoyang Zhang

    (Norris Cotton Cancer Center, Dartmouth Medical School
    Present address: Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA)

  • Kinjal Desai

    (Norris Cotton Cancer Center, Dartmouth Medical School)

  • Malika Aid

    (Bioinformatics and Computational Genomics Laboratory, Institut de Recherches Cliniques de Montréal (IRCM))

  • Olivia Corradin

    (Case Western Reserve University)

  • Richard Cowper-Sal·lari

    (The Princess Margaret Cancer Centre—University Health Network
    Present address: The Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02139, USA)

  • Batool Akhtar-Zaidi

    (Case Western Reserve University
    Case Comprehensive Cancer Center, Case Western Reserve University
    Present address: Massachusetts Institute of Technology (MIT), Cambridge, Massachusetts 02142, USA)

  • Peter C. Scacheri

    (Case Western Reserve University
    Case Comprehensive Cancer Center, Case Western Reserve University)

  • Benjamin Haibe-Kains

    (The Princess Margaret Cancer Centre—University Health Network
    University of Toronto
    Bioinformatics and Computational Genomics Laboratory, Institut de Recherches Cliniques de Montréal (IRCM))

  • Mathieu Lupien

    (The Princess Margaret Cancer Centre—University Health Network
    University of Toronto
    Ontario Institute for Cancer Research)

Abstract

Chromatin interactions connect distal regulatory elements to target gene promoters guiding stimulus- and lineage-specific transcription. Few factors securing chromatin interactions have so far been identified. Here, by integrating chromatin interaction maps with the large collection of transcription factor-binding profiles provided by the ENCODE project, we demonstrate that the zinc-finger protein ZNF143 preferentially occupies anchors of chromatin interactions connecting promoters with distal regulatory elements. It binds directly to promoters and associates with lineage-specific chromatin interactions and gene expression. Silencing ZNF143 or modulating its DNA-binding affinity using single-nucleotide polymorphisms (SNPs) as a surrogate of site-directed mutagenesis reveals the sequence dependency of chromatin interactions at gene promoters. We also find that chromatin interactions alone do not regulate gene expression. Together, our results identify ZNF143 as a novel chromatin-looping factor that contributes to the architectural foundation of the genome by providing sequence specificity at promoters connected with distal regulatory elements.

Suggested Citation

  • Swneke D. Bailey & Xiaoyang Zhang & Kinjal Desai & Malika Aid & Olivia Corradin & Richard Cowper-Sal·lari & Batool Akhtar-Zaidi & Peter C. Scacheri & Benjamin Haibe-Kains & Mathieu Lupien, 2015. "ZNF143 provides sequence specificity to secure chromatin interactions at gene promoters," Nature Communications, Nature, vol. 6(1), pages 1-10, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7186
    DOI: 10.1038/ncomms7186
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    Cited by:

    1. Qiliang Ding & Matthew M. Edwards & Ning Wang & Xiang Zhu & Alexa N. Bracci & Michelle L. Hulke & Ya Hu & Yao Tong & Joyce Hsiao & Christine J. Charvet & Sulagna Ghosh & Robert E. Handsaker & Kevin Eg, 2021. "The genetic architecture of DNA replication timing in human pluripotent stem cells," Nature Communications, Nature, vol. 12(1), pages 1-18, December.
    2. Shuzhen Kuang & Katherine S. Pollard, 2024. "Exploring the roles of RNAs in chromatin architecture using deep learning," Nature Communications, Nature, vol. 15(1), pages 1-14, December.

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