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Published online
doi:10.1083/jcb.200708010
The Journal of Cell Biology, Vol. 180, No. 5, 905-914
The Rockefeller University Press, 0021-9525 $30.00
© Idone et al.
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Repair of injured plasma membrane by rapid Ca2+-dependent endocytosis



Vincent Idone1, Christina Tam1, John W. Goss2, Derek Toomre2, Marc Pypaert2, and Norma W. Andrews1,2

1 Section of Microbial Pathogenesis and 2 Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06510

Correspondence to Norma W. Andrews: norma.andrews{at}yale.edu

Ca2+ influx through plasma membrane lesions triggers a rapid repair process that was previously shown to require the exocytosis of lysosomal organelles (Reddy, A., E. Caler, and N. Andrews. 2001. Cell. 106:157–169). However, how exocytosis leads to membrane resealing has remained obscure, particularly for stable lesions caused by pore-forming proteins. In this study, we show that Ca2+-dependent resealing after permeabilization with the bacterial toxin streptolysin O (SLO) requires endocytosis via a novel pathway that removes SLO-containing pores from the plasma membrane. We also find that endocytosis is similarly required to repair lesions formed in mechanically wounded cells. Inhibition of lesion endocytosis (by sterol depletion) inhibits repair, whereas enhancement of endocytosis through disruption of the actin cytoskeleton facilitates resealing. Thus, endocytosis promotes wound resealing by removing lesions from the plasma membrane. These findings provide an important new insight into how cells protect themselves not only from mechanical injury but also from microbial toxins and pore-forming proteins produced by the immune system.

Abbreviations used in this paper: MβCD, methyl–β-cyclodextrin; NRK, normal rat kidney; PI, propidium iodide; SLO, streptolysin O; TR, Texas red; WGA, wheat germ agglutinin.


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