IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v8y2017i1d10.1038_ncomms15754.html
   My bibliography  Save this article

Constriction of the mitochondrial inner compartment is a priming event for mitochondrial division

Author

Listed:
  • Bongki Cho

    (Korea University College of Medicine
    Daegu Gyeongbuk Institute of Science and Technology)

  • Hyo Min Cho

    (Korea University College of Medicine)

  • Youhwa Jo

    (Korea University College of Medicine)

  • Hee Dae Kim

    (Seoul National University)

  • Myungjae Song

    (Yonsei University College of Medicine)

  • Cheil Moon

    (Daegu Gyeongbuk Institute of Science and Technology)

  • Hyongbum Kim

    (Yonsei University College of Medicine)

  • Kyungjin Kim

    (Daegu Gyeongbuk Institute of Science and Technology
    Korea Brain Research Institute)

  • Hiromi Sesaki

    (Johns Hopkins University School of Medicine)

  • Im Joo Rhyu

    (Korea University College of Medicine)

  • Hyun Kim

    (Korea University College of Medicine)

  • Woong Sun

    (Korea University College of Medicine)

Abstract

Mitochondrial division is critical for the maintenance and regulation of mitochondrial function, quality and distribution. This process is controlled by cytosolic actin-based constriction machinery and dynamin-related protein 1 (Drp1) on mitochondrial outer membrane (OMM). Although mitochondrial physiology, including oxidative phosphorylation, is also important for efficient mitochondrial division, morphological alterations of the mitochondrial inner-membrane (IMM) have not been clearly elucidated. Here we report spontaneous and repetitive constriction of mitochondrial inner compartment (CoMIC) associated with subsequent division in neurons. Although CoMIC is potentiated by inhibition of Drp1 and occurs at the potential division spots contacting the endoplasmic reticulum, it appears on IMM independently of OMM. Intra-mitochondrial influx of Ca2+ induces and potentiates CoMIC, and leads to K+-mediated mitochondrial bulging and depolarization. Synergistically, optic atrophy 1 (Opa1) also regulates CoMIC via controlling Mic60-mediated OMM–IMM tethering. Therefore, we propose that CoMIC is a priming event for efficient mitochondrial division.

Suggested Citation

  • Bongki Cho & Hyo Min Cho & Youhwa Jo & Hee Dae Kim & Myungjae Song & Cheil Moon & Hyongbum Kim & Kyungjin Kim & Hiromi Sesaki & Im Joo Rhyu & Hyun Kim & Woong Sun, 2017. "Constriction of the mitochondrial inner compartment is a priming event for mitochondrial division," Nature Communications, Nature, vol. 8(1), pages 1-17, August.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15754
    DOI: 10.1038/ncomms15754
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms15754
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms15754?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. Daniel M. Virga & Stevie Hamilton & Bertha Osei & Abigail Morgan & Parker Kneis & Emiliano Zamponi & Natalie J. Park & Victoria L. Hewitt & David Zhang & Kevin C. Gonzalez & Fiona M. Russell & D. Grah, 2024. "Activity-dependent compartmentalization of dendritic mitochondria morphology through local regulation of fusion-fission balance in neurons in vivo," Nature Communications, Nature, vol. 15(1), pages 1-21, December.
    2. Erminia Donnarumma & Michael Kohlhaas & Elodie Vimont & Etienne Kornobis & Thibault Chaze & Quentin Giai Gianetto & Mariette Matondo & Maryse Moya-Nilges & Christoph Maack & Timothy Wai, 2022. "Mitochondrial Fission Process 1 controls inner membrane integrity and protects against heart failure," Nature Communications, Nature, vol. 13(1), pages 1-24, 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:8:y:2017:i:1:d:10.1038_ncomms15754. 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.