Special Issue Research Article
GSK3β affects apical–basal polarity and cell–cell adhesion by regulating aPKC levels
Version of Record online: 6 MAY 2009
Copyright © 2009 Wiley-Liss, Inc.
Special Issue: Special Issue on WNT Signaling in Development and Disease
Volume 239, Issue 1, pages 115–125, January 2010
How to Cite
Colosimo, P. F., Liu, X., Kaplan, N. A. and Tolwinski, N. S. (2010), GSK3β affects apical–basal polarity and cell–cell adhesion by regulating aPKC levels. Dev. Dyn., 239: 115–125. doi: 10.1002/dvdy.21963
- Issue online: 15 DEC 2009
- Version of Record online: 6 MAY 2009
- Manuscript Accepted: 24 MAR 2009
- Frank A. Howard Fellows Program at the Sloan-Kettering Institute
- atypical PKC
The dynamic rearrangement of cell–cell contacts is required for the establishment of functional epithelial cell sheets. However, the signaling pathways and cellular mechanisms that initiate and maintain this polarity are not well understood. We show that loss of the Wnt signaling component GSK3β results in increased levels of aPKC and leads to defects in apical–basal polarity. We find that GSK3β directly phosphorylates aPKC, which likely promotes its ubiquitin-mediated proteosomal degradation. aPKC increases the levels of Armadillo and stabilizes adherens junctions. These results suggest that the Wnt pathway component GSK3β regulates the polarity determinant aPKC, which in turn affects cell–cell contacts during the development of polarized tissues. Developmental Dynamics 239:115–125, 2010. © 2009 Wiley-Liss, Inc.