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The SWI/SNF chromatin remodelling complex is required for maintenance of lineage specific enhancers

Author

Listed:
  • Burak H. Alver

    (Harvard Medical School)

  • Kimberly H. Kim

    (Dana-Farber Cancer Institute
    Children's Hospital
    Harvard Medical School
    Present address: Department of Oncology Target Discovery, Pfizer, Pearl River, New York 10965, USA)

  • Ping Lu

    (Dana-Farber Cancer Institute
    Children's Hospital
    Harvard Medical School)

  • Xiaofeng Wang

    (Dana-Farber Cancer Institute
    Children's Hospital
    Harvard Medical School)

  • Haley E. Manchester

    (Dana-Farber Cancer Institute
    Children's Hospital
    Harvard Medical School)

  • Weishan Wang

    (Dana-Farber Cancer Institute
    Children's Hospital
    Harvard Medical School)

  • Jeffrey R. Haswell

    (Dana-Farber Cancer Institute
    Children's Hospital
    Harvard Medical School)

  • Peter J. Park

    (Harvard Medical School)

  • Charles W. M. Roberts

    (Dana-Farber Cancer Institute
    Children's Hospital
    Harvard Medical School
    St. Jude Children's Research Hospital)

Abstract

Genes encoding subunits of SWI/SNF (BAF) chromatin remodelling complexes are collectively altered in over 20% of human malignancies, but the mechanisms by which these complexes alter chromatin to modulate transcription and cell fate are poorly understood. Utilizing mouse embryonic fibroblast and cancer cell line models, here we show via ChIP-seq and biochemical assays that SWI/SNF complexes are preferentially targeted to distal lineage specific enhancers and interact with p300 to modulate histone H3 lysine 27 acetylation. We identify a greater requirement for SWI/SNF at typical enhancers than at most super-enhancers and at enhancers in untranscribed regions than in transcribed regions. Our data further demonstrate that SWI/SNF-dependent distal enhancers are essential for controlling expression of genes linked to developmental processes. Our findings thus establish SWI/SNF complexes as regulators of the enhancer landscape and provide insight into the roles of SWI/SNF in cellular fate control.

Suggested Citation

  • Burak H. Alver & Kimberly H. Kim & Ping Lu & Xiaofeng Wang & Haley E. Manchester & Weishan Wang & Jeffrey R. Haswell & Peter J. Park & Charles W. M. Roberts, 2017. "The SWI/SNF chromatin remodelling complex is required for maintenance of lineage specific enhancers," Nature Communications, Nature, vol. 8(1), pages 1-10, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14648
    DOI: 10.1038/ncomms14648
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    Cited by:

    1. Cheng Zeng & Jiwei Chen & Emmalee W. Cooke & Arijita Subuddhi & Eliana T. Roodman & Fei Xavier Chen & Kaixiang Cao, 2023. "Demethylase-independent roles of LSD1 in regulating enhancers and cell fate transition," Nature Communications, Nature, vol. 14(1), pages 1-15, December.
    2. Gang Ren & Wai Lim Ku & Guangzhe Ge & Jackson A. Hoffman & Jee Youn Kang & Qingsong Tang & Kairong Cui & Yong He & Yukun Guan & Bin Gao & Chengyu Liu & Trevor K. Archer & Keji Zhao, 2024. "Acute depletion of BRG1 reveals its primary function as an activator of transcription," Nature Communications, Nature, vol. 15(1), pages 1-16, December.
    3. Jan-Renier Moonen & James Chappell & Minyi Shi & Tsutomu Shinohara & Dan Li & Maxwell R. Mumbach & Fan Zhang & Ramesh V. Nair & Joseph Nasser & Daniel H. Mai & Shalina Taylor & Lingli Wang & Ross J. M, 2022. "KLF4 recruits SWI/SNF to increase chromatin accessibility and reprogram the endothelial enhancer landscape under laminar shear stress," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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