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Science 21 January 1994: Vol. 263. no. 5145, pp. 390 - 393 DOI: 10.1126/science.7904084
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Articles
Science, Vol 263, Issue 5145, 390-393
Copyright © 1994 by American Association for the Advancement of Science
Cell membrane resealing by a vesicular mechanism similar to neurotransmitter release
RA Steinhardt,
G Bi,
and
JM Alderton
Department of Molecular and Cell Biology, University of California, Berkeley 94720.
After injury to the cell membrane, rapid resealing of the membrane occurs with little loss of intracellular contents. This process has been studied by measurement of the rate of dye loss after membrane puncture in both the sea urchin embryo and 3T3 fibroblasts. Resealing of disrupted cell membranes requires external calcium that can be antagonized by magnesium. Block of multifunctional calcium/calmodulin kinase, which regulates exocytotic vesicle availability at synapses, and of kinesin, which is required for outward-directed transport of vesicles, inhibited membrane resealing. Resealing was also inhibited by botulinum neurotoxins B and A, suggesting that the two synaptosomal-associated proteins synaptobrevin and SNAP-25 also participate in resealing. This pattern of inhibition indicates that the calcium-dependent mechanisms for cell membrane resealing may involve vesicle delivery, docking, and fusion, similar to the exocytosis of neurotransmitters.
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