Munc18-1 mutations that strongly impair SNARE-complex binding support normal synaptic transmission.

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State: Public
Version: Final published version
Serval ID
serval:BIB_B4A0AC3A2F16
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Munc18-1 mutations that strongly impair SNARE-complex binding support normal synaptic transmission.
Journal
EMBO Journal
Author(s)
Meijer M., Burkhardt P., de Wit H., Toonen R.F., Fasshauer D., Verhage M.
ISSN
1460-2075 (Electronic)
ISSN-L
0261-4189
Publication state
Published
Issued date
2012
Peer-reviewed
Oui
Volume
31
Number
9
Pages
2156-2168
Language
english
Abstract
Synaptic transmission depends critically on the Sec1p/Munc18 protein Munc18-1, but it is unclear whether Munc18-1 primarily operates as a integral part of the fusion machinery or has a more upstream role in fusion complex assembly. Here, we show that point mutations in Munc18-1 that interfere with binding to the free Syntaxin1a N-terminus and strongly impair binding to assembled SNARE complexes all support normal docking, priming and fusion of synaptic vesicles, and normal synaptic plasticity in munc18-1 null mutant neurons. These data support a prevailing role of Munc18-1 before/during SNARE-complex assembly, while its continued association to assembled SNARE complexes is dispensable for synaptic transmission.
Keywords
exocytosis, Munc18-1, SM proteins, SNARE complex, Syntaxin1a
Pubmed
Web of science
Open Access
Yes
Create date
09/05/2012 12:47
Last modification date
20/08/2019 15:23
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