Membrane resealing: synaptotagmin VII keeps running the show.
Ca2+ influx, an immediate consequence of plasma membrane disruption, triggers a resealing mechanism involving exocytosis. Although this has been known for about a decade, a better understanding of the organelles involved and of the molecular machinery controlling membrane repair has been slower to emerge. Recent studies have changed this picture, by identifying lysosomes as exocytotic vesicles involved in membrane resealing and the Ca2+-binding protein synaptotagmin VII as a regulator of this process. New evidence reinforces the role of the C2A and C2B domains of synaptotagmin VII in plasma membrane repair, highlighting the importance of this molecule as a powerful tool for future studies.
Andrews
Norma W
NW
Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06510, USA. norma.andrews@yale.edu
D016475:3T3 Cells / Q000378:metabolism / Q000648:ultrastructure; D000818:Animals; D002118:Calcium / Q000494:pharmacology / Q000502:physiology*; D020013:Calcium Signaling; D002462:Cell Membrane / Q000378:metabolism / Q000648:ultrastructure; D002463:Cell Membrane Permeability / Q000187:drug effects; D005057:Eukaryotic Cells / Q000378:metabolism / Q000648:ultrastructure; D005089:Exocytosis; D006801:Humans; D008247:Lysosomes / Q000502:physiology; D051379:Mice; D009498:Neurotoxins / Q000494:pharmacology; D017434:Protein Structure, Tertiary; D051381:Rats; D011993:Recombinant Fusion Proteins / Q000502:physiology; D050857:Synaptotagmins / Q000737:chemistry / Q000235:genetics / Q000276:immunology / Q000502:physiology*
D009498:Neurotoxins; D011993:Recombinant Fusion Proteins; D050857:Synaptotagmins; D002118:Calcium