IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v502y2013i7470d10.1038_nature12639.html
   My bibliography  Save this article

Functional interaction between autophagy and ciliogenesis

Author

Listed:
  • Olatz Pampliega

    (Albert Einstein College of Medicine)

  • Idil Orhon

    (INSERM U845
    Paris-Descartes University, 75014 Paris, France
    INSERM U984; 92296 Châtenay-Malabry, France
    University Paris-Sud 11)

  • Bindi Patel

    (Albert Einstein College of Medicine)

  • Sunandini Sridhar

    (Albert Einstein College of Medicine)

  • Antonio Díaz-Carretero

    (Albert Einstein College of Medicine)

  • Isabelle Beau

    (INSERM U984; 92296 Châtenay-Malabry, France
    University Paris-Sud 11)

  • Patrice Codogno

    (INSERM U845
    Paris-Descartes University, 75014 Paris, France
    INSERM U984; 92296 Châtenay-Malabry, France
    University Paris-Sud 11)

  • Birgit H. Satir

    (Albert Einstein College of Medicine)

  • Peter Satir

    (Albert Einstein College of Medicine)

  • Ana Maria Cuervo

    (Albert Einstein College of Medicine
    Albert Einstein College of Medicine
    Institute for Aging Studies, Albert Einstein College of Medicine)

Abstract

Nutrient deprivation is a stimulus shared by both autophagy and the formation of primary cilia. The recently discovered role of primary cilia in nutrient sensing and signalling motivated us to explore the possible functional interactions between this signalling hub and autophagy. Here we show that part of the molecular machinery involved in ciliogenesis also participates in the early steps of the autophagic process. Signalling from the cilia, such as that from the Hedgehog pathway, induces autophagy by acting directly on essential autophagy-related proteins strategically located in the base of the cilium by ciliary trafficking proteins. Whereas abrogation of ciliogenesis partially inhibits autophagy, blockage of autophagy enhances primary cilia growth and cilia-associated signalling during normal nutritional conditions. We propose that basal autophagy regulates ciliary growth through the degradation of proteins required for intraflagellar transport. Compromised ability to activate the autophagic response may underlie some common ciliopathies.

Suggested Citation

  • Olatz Pampliega & Idil Orhon & Bindi Patel & Sunandini Sridhar & Antonio Díaz-Carretero & Isabelle Beau & Patrice Codogno & Birgit H. Satir & Peter Satir & Ana Maria Cuervo, 2013. "Functional interaction between autophagy and ciliogenesis," Nature, Nature, vol. 502(7470), pages 194-200, October.
  • Handle: RePEc:nat:nature:v:502:y:2013:i:7470:d:10.1038_nature12639
    DOI: 10.1038/nature12639
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/nature12639
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.

    File URL: https://libkey.io/10.1038/nature12639?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
    ---><---

    As the access to this document is restricted, you may want to search for a different version of it.

    Citations

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


    Cited by:

    1. Aurore Claude-Taupin & Pierre Isnard & Alessia Bagattin & Nicolas Kuperwasser & Federica Roccio & Biagina Ruscica & Nicolas Goudin & Meriem Garfa-Traoré & Alice Regnier & Lisa Turinsky & Martine Burti, 2023. "The AMPK-Sirtuin 1-YAP axis is regulated by fluid flow intensity and controls autophagy flux in kidney epithelial cells," Nature Communications, Nature, vol. 14(1), pages 1-20, 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:nature:v:502:y:2013:i:7470:d:10.1038_nature12639. 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.