JCB logo
Accuri Cytometers
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published online March 3, 2008
doi:10.1083/jcb.200708010
The Journal of Cell Biology, Vol. 180, No. 5, 905-914
The Rockefeller University Press, 0021-9525 $30.00
© 2008 Idone et al.
This Article
Right arrow Full Text
Right arrow PDF (Full Text)
Right arrow PPT slides of all figures
Right arrow Supplemental Material Index
Right arrow Related biobytes podcast
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Google Scholar
Right arrow Articles by Idone, V.
Right arrow Articles by Andrews, N. W.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Idone, V.
Right arrow Articles by Andrews, N. W.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*CALCIUM COMPOUNDS
*CALCIUM, ELEMENTAL
Related Collections
Right arrowRelated In this Issue article
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Report

 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.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

Related In this Issue article

Cells' puncture repair kit
Mitch Leslie
J. Cell Biol. 2008 180: 847. [Full Text] [PDF]



This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents