Munc18-1 mutations that strongly impair SNARE-complex binding support normal synaptic transmission |
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Authors: | Meijer Marieke Burkhardt Pawel de Wit Heidi Toonen Ruud F Fasshauer Dirk Verhage Matthijs |
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Affiliation: | Department of Functional Genomics and Department of Clinical Genetics, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, VU University Amsterdam, The Netherlands. |
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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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Keywords: | exocytosis Munc18‐1 SM proteins SNARE complex Syntaxin1a |
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