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3778 • The Journal of Neuroscience, March 14, 2012 • 32(11):3778–3785 Cellular/Molecular Synaptotagmin 1 Is Necessary for the Ca2 Dependence of Clathrin-Mediated Endocytosis 1 1 1 1 2 3 1 Li-Hua Yao, * Yan Rao, * Kelly Varga, Chun-Yang Wang, Peng Xiao, Manfred Lindau, and Liang-Wei Gong 1 2 Department of Biological Sciences, University of Illinois at Chicago, Chicago, Illinois 60607, School of Life Science, South China Normal University, Guangzhou GD 510631, China, and 3School of Applied and Engineering Physics, Cornell University, Ithaca, New York 14853 The role of Ca 2 in synaptic vesicle endocytosis remains uncertain due to the diversity in various preparations where several forms of endocytosis may contribute variably in different conditions. Although recent studies have demonstrated that Ca 2 is important for clathrin-mediated endocytosis (CME), the mechanistic role of Ca 2 in CME remains to be elucidated. By monitoring CME of single vesicles in mouse chromaffin cells with cell-attached capacitance measurements that offer millisecond time resolution, we demonstrate that the dynamics of vesicle fission during CME is Ca 2 dependent but becomes Ca 2 independent in synaptotagmin 1 (Syt1) knock-out cells. Our results thus suggest that Syt1 is necessary for the Ca 2 dependence of CME. Introduction and the changes of membrane capacitance in the other channel Neurotransmitter release is mediated by exocytosis of synaptic (Neher and Marty, 1982; Debus and Lindau, 2000). When the vesicles, and subsequent endocytosis is essential for supporting tubular membrane neck that connec