Sustained Wnt/β-catenin signalling causes neuroepithelial aberrations through the accumulation of aPKC at the apical pole

Antonio Herrera, Murielle Saade, Anghara Menendez, Elisa Marti and Sebastian Pons ()
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Antonio Herrera: Instituto de Investigaciones Biomédicas de Barcelona, CSIC-IDIBAPS
Murielle Saade: Instituto de Biología Molecular de Barcelona, CSIC, Parc Científic de Barcelona
Anghara Menendez: Instituto de Investigaciones Biomédicas de Barcelona, CSIC-IDIBAPS
Elisa Marti: Instituto de Biología Molecular de Barcelona, CSIC, Parc Científic de Barcelona
Sebastian Pons: Instituto de Investigaciones Biomédicas de Barcelona, CSIC-IDIBAPS

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: Abstract β-Catenin mediates the canonical Wnt pathway by stimulating Tcf-dependent transcription and also associates to N-cadherin at the apical complex (AC) of neuroblasts. Here, we show that while β-catenin activity is required to form the AC and to maintain the cell polarity, oncogenic mutations that render stable forms of β-catenin (sβ-catenin) maintain the stemness of neuroblasts, inhibiting their differentiation and provoking aberrant growth. In examining the transcriptional and structural roles of β-catenin, we find that while β-catenin/Tcf transcriptional activity induces atypical protein kinase C (aPKC) expression, an alternative effect of β-catenin restricts aPKC to the apical pole of neuroepithelial cells. In agreement, we show that a constitutively active form of aPKC reproduces the neuroepithelial aberrations induced by β-catenin. Therefore, we conclude that β-catenin controls the cell fate and polarity of the neuroblasts through the expression and localization of aPKC.

Date: 2014
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5168

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DOI: 10.1038/ncomms5168

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