@article {cite-key,
	title = {Wingless signaling modulates cadherin-mediated cell adhesion in Drosophila imaginal disc cells.},
	journal = {J Cell Sci},
	volume = {119},
	number = {Pt 12},
	year = {2006},
	month = {Jun},
	pages = {2425{\textendash}2434},
	address = {Howard Hughes Medical Institute and Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA. awodarz@gwdg.de},
	abstract = {Armadillo, the Drosophila homolog of beta-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.},
	issn = {0021-9533 (Print); 0021-9533 (Linking)},
	doi = {10.1242/jcs.02973},
	author = {Wodarz, Andreas and Stewart, Daniel B and Nelson, W James and Nusse, Roel}
}
