AI Article Synopsis
- Munc18-1 is a crucial protein for synaptic transmission, but its exact role in fusion machinery versus fusion complex assembly is debated.
- * Researchers found that specific mutations in Munc18-1 that affected its ability to bind Syntaxin1a and SNARE complexes still allowed normal neuronal functions, including vesicle docking and synaptic plasticity.
- * These findings suggest that Munc18-1 primarily functions in the early stages of SNARE-complex assembly rather than being essential for the maintenance of assembled complexes during synaptic transmission.
Article 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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3343470 | PMC |
| http://dx.doi.org/10.1038/emboj.2012.72 | DOI Listing |
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