title: Synaptotagmins 1 and 2 as mediators of rapid exocytosis at nerve terminals: the dyad hypothesis.
abstract: The dyad model was developed to explain the extremely rapid kinetics of synaptic vesicle exocytosis. In contrast to most hypotheses which invoke interactions among synaptotagmins, SNAREs and other regulatory molecules, the dyad model features a quartet of synaptotagmins arrayed at the synaptic vesicle-plasma membrane interface. Ca(2+)-triggered movements of these synaptotagmins initiate a sequence of events culminating in the fusion of the vesicular and plasma membranes. The relative simplicity of this model and its amenability to empirical testing provide a useful template for future investigations of the molecular events underlying the exocytotic cascade.
authors: Department of Molecular and Medical Pharmacology, UCLA David Geffen School of Medicine, Los Angeles, CA 90095, USA. cgundersen@mednet.ucla.edu
authors: Cameron B
authors: CB
authors: Gundersen
authors: Joy A
authors: JA
authors: Umbach
mesh_terms: D000818:Animals; D002462:Cell Membrane / Q000235:genetics / Q000378:metabolism*; D005089:Exocytosis / Q000502:physiology*; D051379:Mice; D008959:Models, Neurological; D013572:Synaptic Vesicles / Q000235:genetics / Q000378:metabolism*; D050863:Synaptotagmin I / Q000235:genetics / Q000378:metabolism*; D050861:Synaptotagmin II / Q000235:genetics / Q000378:metabolism*
chemical_list: D050863:Synaptotagmin I; D050861:Synaptotagmin II; C494311:Syt1 protein, mouse; C494263:Syt2 protein, mouse
keywords: C2 domains; Cysteine string proteins; Membrane fusion; Protein palmitoylation; SNAREs