Journal
SCIENCE
Volume 328, Issue 5979, Pages 760-763Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1187722
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Funding
- Korea Research Foundation [KRF-2008-313-C00365, KRF-C00142, KRF-C00180]
- Korean government [2009-0087691, R01-2008-00010920-0, 2007-D00243]
- National Institutes of Health [R01 GM051290]
- World Class University program in Korea [R31-2008-000-10105-0, R33-10163]
- National Research Foundation of Korea [2008-0059125, 핵C6A2508, 2008-313-C00365, 2008-331-C00142, 2007-313-D00243, CG035001, R31-2008-000-10105-0, R33-2008-000-10163-0, 2009-0087691, 314-2008-1-C00180] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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In neurons, synaptotagmin 1 (Syt1) is thought to mediate the fusion of synaptic vesicles with the plasma membrane when presynaptic Ca2+ levels rise. However, in vitro reconstitution experiments have failed to recapitulate key characteristics of Ca2+-triggered membrane fusion. Using an in vitro single-vesicle fusion assay, we found that membrane-anchored Syt1 enhanced Ca2+ sensitivity and fusion speed. This stimulatory activity of membrane-anchored Syt1 dropped as the Ca2+ level rose beyond physiological levels. Thus, Syt1 requires the membrane anchor to stimulate vesicle fusion at physiological Ca2+ levels and may function as a dynamic presynaptic Ca2+ sensor to control the probability of neurotransmitter release.
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