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Journal Article

Examining Synaptotagmin 1 Function in Dense Core Vesicle Exocytosis under Direct Control of Ca2+

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Soerensen,  J. B.
Research Group of Molecular Mechanisms of the Exocytosis, MPI for biophysical chemistry, Max Planck Society;

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Neher,  E.
Department of Membrane Biophysics, MPI for biophysical chemistry, Max Planck Society;

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Citation

Soerensen, J. B., Fernández-Chacón, R., Südhof, T. C., & Neher, E. (2003). Examining Synaptotagmin 1 Function in Dense Core Vesicle Exocytosis under Direct Control of Ca2+. Journal of General Physiology, 122(3), 265-276. doi:10.1085/jgp.200308855.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0012-F047-A
Abstract
We tested the long-standing hypothesis that synaptotagmin 1 is the Ca2+ sensor for fast neurosecretion by analyzing the intracellular Ca2+ dependence of large dense-core vesicle exocytosis in a mouse strain carrying a mutated synaptotagmin C2A domain. The mutation (R233Q) causes a twofold increase in the KD of Ca2+-dependent phospholipid binding to the double C2A-C2B domain of synaptotagmin. Using photolysis of caged calcium and capacitance measurements we found that secretion from mutant cells had lower secretory rates, longer secretory delays, and a higher intracellular Ca2+-threshold for secretion due to a twofold increase in the apparent KD of the Ca2+ sensor for fast exocytosis. Single amperometric fusion events were unchanged. We conclude that Ca2+-dependent phospholipid binding to synaptotagmin 1 mirrors the intracellular Ca2+ dependence of exocytosis.