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Int. J. Mol. Sci. 2017, 18(7), 1582; doi:10.3390/ijms18071582

A Membrane-Fusion Model That Exploits a β-to-α Transition in the Hydrophobic Domains of Syntaxin 1A and Synaptobrevin 2

Department of Molecular & Medical Pharmacology, David Geffen UCLA School of Medicine, Los Angeles, CA 90095, USA
Received: 11 June 2017 / Revised: 14 July 2017 / Accepted: 18 July 2017 / Published: 21 July 2017
(This article belongs to the Special Issue Membrane Fusion)
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Abstract

Parallel zippering of the SNARE domains of syntaxin 1A/B, SNAP-25, and VAMP/synaptobrevin 2 is widely regarded as supplying the driving force for exocytotic events at nerve terminals and elsewhere. However, in spite of intensive research, no consensus has been reached concerning the molecular mechanism by which these SNARE proteins catalyze membrane fusion. As an alternative to SNARE-based models, a scenario was developed in which synaptotagmin 1 (or, 2) can serve as a template to guide lipid movements that underlie fast, synchronous exocytosis at nerve terminals. This “dyad model” advanced a novel proposal concerning the membrane disposition of the palmitoylated, cysteine-rich region of these synaptotagmins. Unexpectedly, it now emerges that a similar principle can be exploited to reveal how the hydrophobic, carboxyl-terminal domains of syntaxin 1A and synaptobrevin 2 can perturb membrane structure at the interface between a docked synaptic vesicle and the plasma membrane. These “β-to-α transition” models will be compared and contrasted with other proposals for how macromolecules are thought to intervene to drive membrane fusion. View Full-Text
Keywords: synaptic vesicle; exocytosis; SNARE proteins; secondary-structure transitions; regulated secretion synaptic vesicle; exocytosis; SNARE proteins; secondary-structure transitions; regulated secretion
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Gundersen, C.B. A Membrane-Fusion Model That Exploits a β-to-α Transition in the Hydrophobic Domains of Syntaxin 1A and Synaptobrevin 2. Int. J. Mol. Sci. 2017, 18, 1582.

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