Journal
CELL
Volume 138, Issue 5, Pages 947-960Publisher
CELL PRESS
DOI: 10.1016/j.cell.2009.06.033
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Funding
- National Institute of Neurological Disease [F30NS056520]
- Baylor College of Medicine Intellectual and Developmental Disabilities Research Center
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Synaptic vesicle (SV) exo- and endocytosis are tightly coupled to sustain neurotransmission in presynaptic terminals, and both are regulated by Ca2+. Ca2+ influx triggered by voltage-gated Ca2+ channels is necessary for SV fusion. However, extracellular Ca2+ has also been shown to be required for endocytosis. The intracellular Ca2+ levels (<1 mu M) that trigger endocytosis are typically much lower than those (>10 mu M) needed to induce exocytosis, and endocytosis is inhibited when the Ca2+ level exceeds 1 mu M. Here, we identify and characterize a transmembrane protein associated with SVs that, upon SV fusion, localizes at periactive zones. Loss of Flower results in impaired intracellular resting Ca2+ levels and impaired endocytosis. Flower multimerizes and is able to form a channel to control Ca2+ influx. We propose that Flower functions as a Ca2+ channel to regulate synaptic endocytosis and hence couples exo- with endocytosis.
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