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A cytoplasmic role of Wnt/β-catenin transcriptional cofactors Bcl9, Bcl9l, and Pygopus in tooth enamel formation.
Institute of Molecular Life Sciences, University of Zurich, 8057 Zurich, Switzerland.
Orofacial Development and Regeneration, Institute of Oral Biology, Center of Dental Medicine, University of Zurich, 8032 Zurich, Switzerland.
Orofacial Development and Regeneration, Institute of Oral Biology, Center of Dental Medicine, University of Zurich, 8032 Zurich, Switzerland.
Institute of Molecular Life Sciences, University of Zurich, 8057 Zurich, Switzerland.
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2017 (English)In: Science Signaling, ISSN 1945-0877, E-ISSN 1937-9145, Vol. 10, no 465, article id eaah4598Article in journal (Refereed) Published
Abstract [en]

Wnt-stimulated β-catenin transcriptional regulation is necessary for the development of most organs, including teeth. Bcl9 and Bcl9l are tissue-specific transcriptional cofactors that cooperate with β-catenin. In the nucleus, Bcl9 and Bcl9l simultaneously bind β-catenin and the transcriptional activator Pygo2 to promote the transcription of a subset of Wnt target genes. We showed that Bcl9 and Bcl9l function in the cytoplasm during tooth enamel formation in a manner that is independent of Wnt-stimulated β-catenin-dependent transcription. Bcl9, Bcl9l, and Pygo2 localized mainly to the cytoplasm of the epithelial-derived ameloblasts, the cells responsible for enamel production. In ameloblasts, Bcl9 interacted with proteins involved in enamel formation and proteins involved in exocytosis and vesicular trafficking. Conditional deletion of both Bcl9 and Bcl9l or both Pygo1 and Pygo2 in mice produced teeth with defective enamel that was bright white and deficient in iron, which is reminiscent of human tooth enamel pathologies. Overall, our data revealed that these proteins, originally defined through their function as β-catenin transcriptional cofactors, function in odontogenesis through a previously uncharacterized cytoplasmic mechanism, revealing that they have roles beyond that of transcriptional cofactors.

Place, publisher, year, edition, pages
2017. Vol. 10, no 465, article id eaah4598
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Clinical Medicine
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URN: urn:nbn:se:liu:diva-145418DOI: 10.1126/scisignal.aah4598PubMedID: 28174279OAI: oai:DiVA.org:liu-145418DiVA, id: diva2:1187026
Available from: 2018-03-02 Created: 2018-03-02 Last updated: 2018-03-09

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CiteExportLink to record
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  • apa
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