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J. Cell Biol., Volume 146, Number 1, July 12, 1999 219-232
Copyright © 1999 by The Rockefeller University Press.

Recycling of E-Cadherin: A Potential Mechanism for Regulating Cadherin Dynamics

Tam Luan Lea,b, Alpha S. Yapa,c, and Jennifer L. Stowa,b
a Centre for Molecular and Cellular Biology, The University of Queensland, Brisbane, 4072 Queensland, Australia
b Department of Biochemistry, The University of Queensland, Brisbane, 4072 Queensland, Australia
c Department of Physiology and Pharmacology, The University of Queensland, Brisbane, 4072 Queensland, Australia

Correspondence to: Jennifer L. Stow, Centre for Molecular & Cellular Biology, University of Queensland, Brisbane, 4072 QLD, Australia., j.stow{at}cmcb.uq.edu.au (E-mail), 61 7 3365 4985 (phone), 61 7 3365 4388 (fax)

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°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.

Key Words: epithelial junctions, endocytosis, epithelial morphogenesis, clathrin-coated vesicles, biotinylation


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