Two-way traffic on the road to plasma membrane repair.
Ca(2+) influx through plasma membrane wounds triggers a rapid-repair response that is essential for cell survival. Earlier studies showed that repair requires the exocytosis of intracellular vesicles. Exocytosis was thought to promote resealing by 'patching' the plasma membrane lesion or by facilitating bilayer restoration through reduction in membrane tension. However, cells also rapidly repair lesions created by pore-forming proteins, a form of injury that cannot be resealed solely by exocytosis. Recent studies indicate that, in cells injured by pores or mechanical abrasions, exocytosis is followed by lesion removal through endocytosis. Describing the relationship between wound-induced exocytosis and endocytosis has implications for the understanding of muscular degenerative diseases that are associated with defects in plasma membrane repair.
Section of Microbial Pathogenesis, Yale University School of Medicine, 295 Congress Street, New Haven, CT 06511, USA.
Vincent
V
Idone
Christina
C
Tam
Norma W
NW
Andrews
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling; D021941:Caveolae / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism* / Q000648:ultrastructure; D002966:Clathrin / Q000378:metabolism*; D004705:Endocytosis; D005089:Exocytosis; D006367:HeLa Cells; D006801:Humans; D007668:Kidney / Q000378:metabolism / Q000648:ultrastructure
D002966:Clathrin; D002118:Calcium