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Original Article

^a Laboratory of Cellular and Molecular Biophysics, National Institute of Child Health and Human Development
^b Computational Bioscience and Engineering Laboratory, Center for Information Technology, National Institutes of Health, Bethesda, MD 20892
^c Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, GA 30912
Laboratory of Cellular and Molecular Biophysics, National Institute of Child Health and Human Development, National Institutes of Health, Building 10, Room 10D14, 10 Center Drive MSC 1855, Bethesda, MD 20892-1855.(301) 594-0813

psblank{at}helix.nih.gov

Although the relationship between exocytosis and calcium is fundamental both to synaptic and nonneuronal secretory function, analysis is problematic because of the temporal and spatial properties of calcium, and the fact that vesicle transport, priming, retrieval, and recycling are coupled. By analyzing the kinetics of sea urchin egg secretory vesicle exocytosis in vitro, the final steps of exocytosis are resolved. These steps are modeled as a three-state system: activated, committed, and fused, where interstate transitions are given by the probabilities that an active fusion complex commits () and that a committed fusion complex results in fusion, p. The number of committed complexes per vesicle docking site is Poisson distributed with mean n. Experimentally, p and n increase with increasing calcium, whereas and the pn ratio remain constant, reducing the kinetic description to only one calcium-dependent, controlling variable, n. On average, the calcium dependence of the maximum rate (R_max) and the time to reach R_max (T_peak) are described by the calcium dependence of n. Thus, the nonlinear relationship between the free calcium concentration and the rate of exocytosis can be explained solely by the calcium dependence of the distribution of fusion complexes at vesicle docking sites.

Key Words: cytoplasmic vesicles • membrane fusion • sea urchins • secretion • neurosecretion

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