IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v15y2024i1d10.1038_s41467-024-45283-2.html
   My bibliography  Save this article

Rescue of mitochondrial import failure by intercellular organellar transfer

Author

Listed:
  • Hope I. Needs

    (University of Bristol)

  • Emily Glover

    (University of Bristol)

  • Gonçalo C. Pereira

    (University of Bristol
    Nanna Therapeutics, Merrifield Centre)

  • Alina Witt

    (Universität Bielefeld)

  • Wolfgang Hübner

    (Universität Bielefeld)

  • Mark P. Dodding

    (University of Bristol)

  • Jeremy M. Henley

    (University of Bristol)

  • Ian Collinson

    (University of Bristol)

Abstract

Mitochondria are the powerhouses of eukaryotic cells, composed mostly of nuclear-encoded proteins imported from the cytosol. Thus, problems with the import machinery will disrupt their regenerative capacity and the cell’s energy supplies – particularly troublesome for energy-demanding cells of nervous tissue and muscle. Unsurprisingly then, import breakdown is implicated in disease. Here, we explore the consequences of import failure in mammalian cells; wherein, blocking the import machinery impacts mitochondrial ultra-structure and dynamics, but, surprisingly, does not affect import. Our data are consistent with a response involving intercellular mitochondrial transport via tunnelling nanotubes to import healthy mitochondria and jettison those with blocked import sites. These observations support the existence of a widespread mechanism for the rescue of mitochondrial dysfunction.

Suggested Citation

  • Hope I. Needs & Emily Glover & Gonçalo C. Pereira & Alina Witt & Wolfgang Hübner & Mark P. Dodding & Jeremy M. Henley & Ian Collinson, 2024. "Rescue of mitochondrial import failure by intercellular organellar transfer," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
  • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-45283-2
    DOI: 10.1038/s41467-024-45283-2
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-024-45283-2
    File Function: Abstract
    Download Restriction: no

    File URL: https://libkey.io/10.1038/s41467-024-45283-2?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
    ---><---

    References listed on IDEAS

    as
    1. Lidia Wrobel & Ulrike Topf & Piotr Bragoszewski & Sebastian Wiese & Malgorzata E. Sztolsztener & Silke Oeljeklaus & Aksana Varabyova & Maciej Lirski & Piotr Chroscicki & Seweryn Mroczek & Elzbieta Jan, 2015. "Mistargeted mitochondrial proteins activate a proteostatic response in the cytosol," Nature, Nature, vol. 524(7566), pages 485-488, August.
    2. Xiaowen Wang & Xin Jie Chen, 2015. "A cytosolic network suppressing mitochondria-mediated proteostatic stress and cell death," Nature, Nature, vol. 524(7566), pages 481-484, August.
    Full references (including those not matched with items on IDEAS)

    Most related items

    These are the items that most often cite the same works as this one and are cited by the same works as this one.
    1. Eirini Lionaki & Ilias Gkikas & Ioanna Daskalaki & Maria-Konstantina Ioannidi & Maria I. Klapa & Nektarios Tavernarakis, 2022. "Mitochondrial protein import determines lifespan through metabolic reprogramming and de novo serine biosynthesis," Nature Communications, Nature, vol. 13(1), pages 1-16, December.
    2. Evelyn Fessler & Luisa Krumwiede & Lucas T. Jae, 2022. "DELE1 tracks perturbed protein import and processing in human mitochondria," Nature Communications, Nature, vol. 13(1), pages 1-15, December.
    3. Minji Kim & Remigiusz A. Serwa & Lukasz Samluk & Ida Suppanz & Agata Kodroń & Tomasz M. Stępkowski & Praveenraj Elancheliyan & Biniyam Tsegaye & Silke Oeljeklaus & Michal Wasilewski & Bettina Warschei, 2023. "Immunoproteasome-specific subunit PSMB9 induction is required to regulate cellular proteostasis upon mitochondrial dysfunction," Nature Communications, Nature, vol. 14(1), pages 1-23, December.
    4. Caroline E. Dewar & Silke Oeljeklaus & Jan Mani & Wignand W. D. Mühlhäuser & Corinne Känel & Johannes Zimmermann & Torsten Ochsenreiter & Bettina Warscheid & André Schneider, 2022. "Mistargeting of aggregation prone mitochondrial proteins activates a nucleus-mediated posttranscriptional quality control pathway in trypanosomes," Nature Communications, Nature, vol. 13(1), pages 1-17, 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:15:y:2024:i:1:d:10.1038_s41467-024-45283-2. 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.

    If CitEc recognized a bibliographic reference but did not link an item in RePEc to it, you can help with 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.