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

Détails

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Etat: Public
Version: Final published version
ID Serval
serval:BIB_B4A0AC3A2F16
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Munc18-1 mutations that strongly impair SNARE-complex binding support normal synaptic transmission.
Périodique
EMBO Journal
Auteur(s)
Meijer M., Burkhardt P., de Wit H., Toonen R.F., Fasshauer D., Verhage M.
ISSN
1460-2075 (Electronic)
ISSN-L
0261-4189
Statut éditorial
Publié
Date de publication
2012
Peer-reviewed
Oui
Volume
31
Numéro
9
Pages
2156-2168
Langue
anglais
Résumé
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.
Mots-clé
exocytosis, Munc18-1, SM proteins, SNARE complex, Syntaxin1a
Pubmed
Web of science
Open Access
Oui
Création de la notice
09/05/2012 12:47
Dernière modification de la notice
20/08/2019 15:23
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