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An alternative CTCF isoform antagonizes canonical CTCF occupancy and changes chromatin architecture to promote apoptosis

Author

Listed:
  • Jiao Li

    (Guangzhou Medical University
    Chinese Academy of Sciences
    Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

  • Kaimeng Huang

    (Guangzhou Medical University
    Chinese Academy of Sciences
    Chinese Academy of Sciences)

  • Gongcheng Hu

    (Guangzhou Medical University
    Chinese Academy of Sciences
    Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

  • Isaac A. Babarinde

    (Southern University of Science and Technology)

  • Yaoyi Li

    (Guangzhou Medical University
    Chinese Academy of Sciences
    Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

  • Xiaotao Dong

    (Guangzhou Medical University
    Chinese Academy of Sciences
    Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

  • Yu-Sheng Chen

    (Chinese Academy of Sciences)

  • Liping Shang

    (Guangzhou Medical University)

  • Wenjing Guo

    (Guangzhou Medical University)

  • Junwei Wang

    (Guangzhou Medical University)

  • Zhaoming Chen

    (Guangzhou Medical University
    Chinese Academy of Sciences)

  • Andrew P. Hutchins

    (Southern University of Science and Technology)

  • Yun-Gui Yang

    (University of Chinese Academy of Sciences
    Chinese Academy of Sciences)

  • Hongjie Yao

    (Guangzhou Medical University
    Chinese Academy of Sciences
    Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

Abstract

CTCF plays key roles in gene regulation, chromatin insulation, imprinting, X chromosome inactivation and organizing the higher-order chromatin architecture of mammalian genomes. Previous studies have mainly focused on the roles of the canonical CTCF isoform. Here, we explore the functions of an alternatively spliced human CTCF isoform in which exons 3 and 4 are skipped, producing a shorter isoform (CTCF-s). Functionally, we find that CTCF-s competes with the genome binding of canonical CTCF and binds a similar DNA sequence. CTCF-s binding disrupts CTCF/cohesin binding, alters CTCF-mediated chromatin looping and promotes the activation of IFI6 that leads to apoptosis. This effect is caused by an abnormal long-range interaction at the IFI6 enhancer and promoter. Taken together, this study reveals a non-canonical function for CTCF-s that antagonizes the genomic binding of canonical CTCF and cohesin, and that modulates chromatin looping and causes apoptosis by stimulating IFI6 expression.

Suggested Citation

  • Jiao Li & Kaimeng Huang & Gongcheng Hu & Isaac A. Babarinde & Yaoyi Li & Xiaotao Dong & Yu-Sheng Chen & Liping Shang & Wenjing Guo & Junwei Wang & Zhaoming Chen & Andrew P. Hutchins & Yun-Gui Yang & H, 2019. "An alternative CTCF isoform antagonizes canonical CTCF occupancy and changes chromatin architecture to promote apoptosis," Nature Communications, Nature, vol. 10(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-08949-w
    DOI: 10.1038/s41467-019-08949-w
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    Cited by:

    1. Yanjiang Liu & Gongcheng Hu & Shengxiong Yang & Mingze Yao & Zicong Liu & Chenghong Yan & Yulin Wen & Wangfang Ping & Juehan Wang & Yawei Song & Xiaotao Dong & Guangjin Pan & Hongjie Yao, 2023. "Functional dissection of PRC1 subunits RYBP and YAF2 during neural differentiation of embryonic stem cells," Nature Communications, Nature, vol. 14(1), pages 1-14, December.
    2. Zhao Wei & Song Wang & Yaning Xu & Wenzheng Wang & Fraser Soares & Musaddeque Ahmed & Ping Su & Tingting Wang & Elias Orouji & Xin Xu & Yong Zeng & Sujun Chen & Xiaoyu Liu & Tianwei Jia & Zhaojian Liu, 2023. "MYC reshapes CTCF-mediated chromatin architecture in prostate cancer," Nature Communications, Nature, vol. 14(1), pages 1-15, December.

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