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Wnt signalling tunes neurotransmitter release by directly targeting Synaptotagmin-1.


ABSTRACT: The functional assembly of the synaptic release machinery is well understood; however, how signalling factors modulate this process remains unknown. Recent studies suggest that Wnts play a role in presynaptic function. To examine the mechanisms involved, we investigated the interaction of release machinery proteins with Dishevelled-1 (Dvl1), a scaffold protein that determines the cellular locale of Wnt action. Here we show that Dvl1 directly interacts with Synaptotagmin-1 (Syt-1) and indirectly with the SNARE proteins SNAP25 and Syntaxin (Stx-1). Importantly, the interaction of Dvl1 with Syt-1, which is regulated by Wnts, modulates neurotransmitter release. Moreover, presynaptic terminals from Wnt signalling-deficient mice exhibit reduced release probability and are unable to sustain high-frequency release. Consistently, the readily releasable pool size and formation of SNARE complexes are reduced. Our studies demonstrate that Wnt signalling tunes neurotransmitter release and identify Syt-1 as a target for modulation by secreted signalling proteins.

SUBMITTER: Ciani L 

PROVIDER: S-EPMC4667432 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature

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Wnt signalling tunes neurotransmitter release by directly targeting Synaptotagmin-1.

Ciani Lorenza L   Marzo Aude A   Boyle Kieran K   Stamatakou Eleanna E   Lopes Douglas M DM   Anane Derek D   McLeod Faye F   Rosso Silvana B SB   Gibb Alasdair A   Salinas Patricia C PC  

Nature communications 20150924


The functional assembly of the synaptic release machinery is well understood; however, how signalling factors modulate this process remains unknown. Recent studies suggest that Wnts play a role in presynaptic function. To examine the mechanisms involved, we investigated the interaction of release machinery proteins with Dishevelled-1 (Dvl1), a scaffold protein that determines the cellular locale of Wnt action. Here we show that Dvl1 directly interacts with Synaptotagmin-1 (Syt-1) and indirectly  ...[more]

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