Recycling of E-Cadherin: a potential mechanism for regulating cadherin dynamics

Le, T. L., Yap, A. S. and Stow, J. L. (1999) Recycling of E-Cadherin: a potential mechanism for regulating cadherin dynamics. The Journal of Cell Biology, 146 1: 219-232. doi:10.1083/jcb.146.1.219

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Author Le, T. L.
Yap, A. S.
Stow, J. L.
Title Recycling of E-Cadherin: a potential mechanism for regulating cadherin dynamics
Journal name The Journal of Cell Biology   Check publisher's open access policy
ISSN 0021-9525
Publication date 1999-07-12
Sub-type Article (original research)
DOI 10.1083/jcb.146.1.219
Open Access Status File (Publisher version)
Volume 146
Issue 1
Start page 219
End page 232
Total pages 14
Place of publication New York, NY, United States
Publisher The Rockefeller University Press
Collection year 1999
Language eng
Abstract E-Cadherin plays critical roles in many aspects of cell adhesion, epithelial development, and the establishment and maintenance of epithelial polarity. The fate of E-cadherin once it is delivered to the basolateral cell surface, and the mechanisms which govern its participation in adherens junctions, are not well understood. Using surface biotinylation and recycling assays, we observed that some of the cell surface E-cadherin is actively internalized and is then recycled back to the plasma membrane. The pool of E-cadherin undergoing endocytosis and recycling was markedly increased in cells without stable cell-cell contacts, i.e., in preconfluent cells and after cell contacts were disrupted by depletion of extracellular Ca2+, suggesting that endocytic trafficking of E-cadherin is regulated by cell-cell contact. The reformation of cell junctions after replacement of Ca2+ was then found to be inhibited when recycling of endocytosed E-cadherin was disrupted by bafilomycin treatment. The endocytosis and recycling of E-cadherin and of the transferrin receptor were similarly inhibited by potassium depletion and by bafilomycin treatment, and both proteins were accumulated in intracellular compartments by an 18 degrees C temperature block, suggesting that endocytosis may occur via a clathrin-mediated pathway. We conclude that a pool of surface E-cadherin is constantly trafficked through an endocytic, recycling pathway and that this may provide a mechanism for regulating the availability of E-cadherin for junction formation in development, tissue remodeling, and tumorigenesis.
Keyword Cell Biology
Epithelial Junctions
Epithelial Morphogenesis
Clathrin-coated Vesicles
Adhesion Molecule Uvomorulin
Cell-cell Adhesion
Mouse Intestinal Epithelium
Canine Kidney-cells
Mediated Adhesion
Membrane Domains
Apical Membrane
Q-Index Code C1

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Chemistry and Molecular Biosciences
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Citation counts: TR Web of Science Citation Count  Cited 398 times in Thomson Reuters Web of Science Article | Citations
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Created: Tue, 10 Jun 2008, 15:22:27 EST