NDLI: The trans-SNARE-regulating function of Munc18-1 is essential to synaptic exocytosis.

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The trans-SNARE-regulating function of Munc18-1 is essential to synaptic exocytosis.

Content Provider	Semantic Scholar
Author	Shen, Chong Rathore, Shailendra S. Yu, Haijia Gulbranson, Daniel Richard Hua, Rui Zhang, Chen Schoppa, Nathan E. Shen, Jingshi
Copyright Year	2015
Abstract	The fusion of neurotransmitter-filled synaptic vesicles with the plasma membrane requires two classes of molecules-SNAP receptor (SNARE) and Sec1/Munc18 (SM) protein. Reconstitution studies suggest that the SM protein Munc18-1 promotes the zippering of trans-SNARE complexes and accelerates the kinetics of SNARE-dependent membrane fusion. However, the physiological role of this trans-SNARE-regulating function in synaptic exocytosis remains to be established. Here we first demonstrate that two mutations in the vesicle-anchored v-SNARE selectively impair the ability of Munc18-1 to promote trans-SNARE zippering, whereas other known Munc18-1/SNARE-binding modes are unaffected. In cultured neurons, these v-SNARE mutations strongly inhibit spontaneous as well as evoked neurotransmitter release, providing genetic evidence for the trans-SNARE-regulating function of Munc18-1 in synaptic exocytosis. Finally, we show that the trans-SNARE-regulating function of Munc18-1 is compromised by a mutation associated with Ohtahara Syndrome, a severe form of epilepsy.
Starting Page	8852
Ending Page	8852
Page Count	1
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://or.nsfc.gov.cn/bitstream/00001903-5/234171/1/1000014040129.pdf
PubMed reference number	26572858v1
Alternate Webpage(s)	https://doi.org/10.1038/ncomms9852
DOI	10.1038/ncomms9852
Journal	Nature communications
Volume Number	6
Language	English
Access Restriction	Open
Subject Keyword	Class Cri-du-Chat Syndrome Epilepsy Fill Membrane Fusion Mutation Neurotransmitters Plasma membrane SNAP receptor Synaptic Vesicles Vesicle (morphologic abnormality) neurotransmitter release synaptic vesicle exocytosis
Content Type	Text
Resource Type	Article

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