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MBC in Press, published online ahead of print October 26, 2005
Mol. Biol. Cell 10.1091/mbc.E05-05-0420

A more recent version of this article appeared on January 1, 2006
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Submitted on May 11, 2005
Revised on September 26, 2005
Accepted on October 19, 2005

Actin Is Required for Endocytosis at the Apical Surface of MDCK Cells where ARF6 and Clathrin Regulate the Actin Cytoskeleton

Tehila Hyman, Miri Shmuel, and Yoram Altschuler

Department of Pharmacology, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem-Ein Kerem Campus, Jerusalem 91120, Israel

Monitoring Editor: Jean Gruenberg

In epithelial cell lines, apical but not basolateral clathrin-mediated endocytosis has been shown to be affected by actin-disrupting drugs. Using electron and fluorescence microscopy, as well as biochemical assays, we show that the amount of actin dedicated to endocytosis is limiting at the apical surface of epithelia. In part, this contributes to the low basal rate of clathrin-dependent endocytosis observed at this epithelial surface. ARF6 in its GTP-bound state triggers the recruitment of actin from the cell cortex to the clathrin-coated pit to enable dynamin-dependent endocytosis. In addition, we show that perturbation of the apical endocytic system by expression of a clathrin heavy chain mutant results in the collapse of microvilli. This phenotype was completely reversed by the expression of an ARF6-GTP-locked mutant. These observations indicate that concomitant to actin recruitment, the apical clathrin endocytic system is deeply involved in the morphology of the apical plasma membrane.

Address correspondence to: Yoram Altschuler (yoram11{at}md.huji.ac.il)




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