Cell Membrane Resealing by a Vesicular Mechanism Similar to Neurotransmitter Release

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...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1994-01, Vol.263 (5145), p.390-393
Main Authors: Steinhardt, Richard A., Bi, Guoqiang, Alderton, Janet M.
Format: Article
Language:English
Subjects:
3T3 Cells
Amino Acid Sequence
Animals
Antibodies
Biological and medical sciences
Botulinum Toxins - pharmacology
Calcium (Nutrient)
Calcium - metabolism
Calcium in the body
Calcium, Dietary
Calcium-Calmodulin-Dependent Protein Kinases - metabolism
Cell Division - drug effects
Cell Membrane - drug effects
Cell Membrane - physiology
Cell membranes
Cell membranes. Ionic channels. Membrane pores
Cell structures and functions
Eggs
Embryos
Exocytosis
Female
Fibroblasts
Fundamental and applied biological sciences. Psychology
Healing
Kinesin - physiology
Magnesium - pharmacology
Membrane Proteins - physiology
Mice
Molecular and cellular biology
Molecular Sequence Data
Nerve Tissue Proteins - physiology
Neurotransmitter Agents - metabolism
Oligopeptides - pharmacology
Ovum
Plasma membranes
R-SNARE Proteins
Salts
Sea Urchins
Swiss 3T3 cells
Synaptic Transmission
Synaptosomal-Associated Protein 25
Zygote
Zygotes
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Description
Summary: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.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.7904084