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First published online 23 May 2006
doi: 10.1242/jcs.02973

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Wingless signaling modulates cadherin-mediated cell adhesion in Drosophila imaginal disc cells

¹ Howard Hughes Medical Institute and Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA
² Abteilung Stammzellbiologie, DFG Research Center for Molecular Physiology of the Brain (CMPB), Georg-August-Universität Göttingen, Justus-von-Liebig-Weg 11, 37077 Göttingen, Germany
³ Department of Biological Sciences and Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA

^* Author for correspondence (e-mail: awodarz{at}gwdg.de)

Accepted 8 March 2006

Armadillo, the Drosophila homolog of ß-catenin, plays a crucial role in both the Wingless signal transduction pathway and cadherin-mediated cell-cell adhesion, raising the possibility that Wg signaling affects cell adhesion. Here, we use a tissue culture system that allows conditional activation of the Wingless signaling pathway and modulation of E-cadherin expression levels. We show that activation of the Wingless signaling pathway leads to the accumulation of hypophosphorylated Armadillo in the cytoplasm and in cellular processes, and to a concomitant reduction of membrane-associated Armadillo. Activation of the Wingless pathway causes a loss of E-cadherin from the cell surface, reduced cell adhesion and increased spreading of the cells on the substratum. After the initial loss of E-cadherin from the cell surface, E-cadherin gene expression is increased by Wingless. We suggest that Wingless signaling causes changes in Armadillo levels and subcellular localization that result in a transient reduction of cadherin-mediated cell adhesion, thus facilitating cell shape changes, division and movement of cells in epithelial tissues.

Key words: Wingless, Wnt, Cadherin, Catenin, Cell adhesion

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