The aryl hydrocarbon receptor controls cyclin O to promote epithelial multiciliogenesis

Matteo Villa, Stefania Crotta, Kevin S. Dingwell, Elizabeth M. A. Hirst, Manolis Gialitakis, Helena Ahlfors, James C. Smith, Brigitta Stockinger and Andreas Wack ()
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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

Nature Communications, 2016, vol. 7, issue 1, 1-11

Abstract: 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.

Date: 2016
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DOI: 10.1038/ncomms12652

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