IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v7y2016i1d10.1038_ncomms12652.html
   My bibliography  Save this article

The aryl hydrocarbon receptor controls cyclin O to promote epithelial multiciliogenesis

Author

Listed:
  • Matteo Villa

    (Laboratory of AhRimmunity, The Francis Crick Institute, Mill Hill Laboratory)

  • Stefania Crotta

    (Laboratory of Immunoregulation, The Francis Crick Institute, Mill Hill Laboratory)

  • Kevin S. Dingwell

    (Laboratory of Developmental Biology, The Francis Crick Institute, Mill Hill Laboratory)

  • Elizabeth M. A. Hirst

    (EM Technology Platform, The Francis Crick Institute, Mill Hill Laboratory)

  • Manolis Gialitakis

    (Laboratory of AhRimmunity, The Francis Crick Institute, Mill Hill Laboratory)

  • Helena Ahlfors

    (Lymphocyte Signalling and Development, The Babraham Institute)

  • James C. Smith

    (Laboratory of Developmental Biology, The Francis Crick Institute, Mill Hill Laboratory)

  • Brigitta Stockinger

    (Laboratory of AhRimmunity, The Francis Crick Institute, Mill Hill Laboratory)

  • Andreas Wack

    (Laboratory of Immunoregulation, The Francis Crick Institute, Mill Hill Laboratory)

Abstract

Epithelia function as barriers against environmental insults and express the transcription factor aryl hydrocarbon receptor (AhR). However, AhR function in these tissues is unknown. Here we show that AhR regulates multiciliogenesis in both murine airway epithelia and in Xenopus laevis epidermis. In air-exposed airway epithelia, induction of factors required for multiciliogenesis, including cyclin O (Ccno) and Multicilin (Mcidas), is AhR dependent, and air exposure induces AhR binding to the Ccno promoter. Submersion and hypoxic conditions impede AhR-dependent Ccno induction. This is mediated by the persistence of Notch signalling, as Notch blockade renders multiciliogenesis and Ccno induction by AhR independent from air exposure. In contrast to Ccno induction, air exposure does not induce the canonical AhR target cytochrome P450 1a1 (Cyp1a1). Inversely, exposure to AhR ligands induces Cyp1a1 but not Ccno and impeded ciliogenesis. These data indicate that AhR involvement in detoxification of environmental pollutants may impede its physiological role, resulting in respiratory pathology.

Suggested Citation

  • Matteo Villa & Stefania Crotta & Kevin S. Dingwell & Elizabeth M. A. Hirst & Manolis Gialitakis & Helena Ahlfors & James C. Smith & Brigitta Stockinger & Andreas Wack, 2016. "The aryl hydrocarbon receptor controls cyclin O to promote epithelial multiciliogenesis," Nature Communications, Nature, vol. 7(1), pages 1-11, November.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12652
    DOI: 10.1038/ncomms12652
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms12652
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms12652?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. Stefania Crotta & Matteo Villa & Jack Major & Katja Finsterbusch & Miriam Llorian & Peter Carmeliet & Joerg Buescher & Andreas Wack, 2023. "Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation," 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:7:y:2016:i:1:d:10.1038_ncomms12652. 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.