IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v10y2019i1d10.1038_s41467-019-08949-w.html
   My bibliography  Save this article

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
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-019-08949-w
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/s41467-019-08949-w?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Jie Zhang & Gongcheng Hu & Yuli Lu & Huawei Ren & Yin Huang & Yulin Wen & Binrui Ji & Diyang Wang & Haidong Wang & Huisheng Liu & Ning Ma & Lingling Zhang & Guangjin Pan & Yibo Qu & Hua Wang & Wei Zha, 2024. "CTCF mutation at R567 causes developmental disorders via 3D genome rearrangement and abnormal neurodevelopment," Nature Communications, Nature, vol. 15(1), pages 1-21, December.
    2. 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.
    3. 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.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-08949-w. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.