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Membrane repair (p. 873)

Plasma membrane disruption is more common than one might think: around 20% of muscle cells can suffer lesions during exercise, and wounding also affects irreplaceable cells, such as neurons. Small holes in the plasma membrane might `self-seal' because of the inherent thermodynamic properties of lipids. Large holes, by contrast, require a dynamic cellular mechanism. Paul McNeil discusses our understanding of this resealing mechanism. Some forty years ago, external Ca<sup>2+</sup> was found to be required for resealing. More recent work in sea urchin eggs has revealed that Ca<sup>2+</sup> influx stimulates fusion of internal vesicles to form abnormally large vesicles that `patch up' the plasma membrane by exocytosis. Analysis of surface markers from wounded cells indicates that these vesicles are in fact lysosomes. Because these organelles lie below the cell cortex, Ca²⁺-dependent depolymerization of cortical actin is a crucial step in resealing. The cytoskeleton might also have a positive role in resealing, however, providing tracks for delivery of vesicles to the disruption site.

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Related articles in JCS:

Repairing a torn cell surface: make way, lysosomes to the rescue

Paul L. McNeil
JCS 2002 115: 873-879. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?