IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v3y2012i1d10.1038_ncomms2212.html
   My bibliography  Save this article

The Hedgehog signalling pathway regulates autophagy

Author

Listed:
  • Maria Jimenez-Sanchez

    (Cambridge Institute for Medical Research, University of Cambridge, Addenbrooke’s Hospital)

  • Fiona M. Menzies

    (Cambridge Institute for Medical Research, University of Cambridge, Addenbrooke’s Hospital)

  • Yu-Yun Chang

    (Cell Biology and Development, University of Minnesota)

  • Nikol Simecek

    (Cambridge Institute for Medical Research, University of Cambridge, Addenbrooke’s Hospital)

  • Thomas P. Neufeld

    (Cell Biology and Development, University of Minnesota)

  • David C. Rubinsztein

    (Cambridge Institute for Medical Research, University of Cambridge, Addenbrooke’s Hospital)

Abstract

Autophagy is a highly conserved degradative process that removes damaged or unnecessary proteins and organelles, and recycles cytoplasmic contents during starvation. Autophagy is essential in physiological processes such as embryonic development but how autophagy is regulated by canonical developmental pathways is unclear. Here we show that the Hedgehog signalling pathway inhibits autophagosome synthesis, both in basal and in autophagy-induced conditions. This mechanism is conserved in mammalian cells and in Drosophila, and requires the orthologous transcription factors Gli2 and Ci, respectively. Furthermore, we identify that activation of the Hedgehog pathway reduces PERK levels, concomitant with a decrease in phosphorylation of the translation initiation factor eukaryotic initiation factor 2α, suggesting a novel target of this pathway and providing a possible link between Hedgehog signalling and autophagy.

Suggested Citation

  • Maria Jimenez-Sanchez & Fiona M. Menzies & Yu-Yun Chang & Nikol Simecek & Thomas P. Neufeld & David C. Rubinsztein, 2012. "The Hedgehog signalling pathway regulates autophagy," Nature Communications, Nature, vol. 3(1), pages 1-11, January.
    • Handle: RePEc:nat:natcom:v:3:y:2012:i:1:d:10.1038_ncomms2212
    DOI: 10.1038/ncomms2212
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms2212
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms2212?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
    ---><---

    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:3:y:2012:i:1:d:10.1038_ncomms2212. 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.