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Nat Neurosci. 2003 Oct;6(10):1023-30. Epub 2003 Sep 14.

Defects in synaptic vesicle docking in unc-18 mutants.

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  • 1Department of Biology, University of Utah, 257 South 1400 East, Salt Lake City, Utah 84112-0840, USA.

Abstract

Sec1-related proteins function in most, if not all, membrane trafficking pathways in eukaryotic cells. The Sec1-related protein required in neurons for synaptic vesicle exocytosis is UNC-18. Several models for UNC-18 function during vesicle exocytosis are under consideration. We have tested these models by characterizing unc-18 mutants of the nematode Caenorhabditis elegans. In the absence of UNC-18, the size of the readily releasable pool is severely reduced. Our results show that the near absence of fusion-competent vesicles is not caused by a reduction in syntaxin levels, by a mislocalization of syntaxin, by a defect in fusion or by a failure to open syntaxin during priming. Rather, we found a reduction of docked vesicles at the active zone in unc-18 mutants, suggesting that UNC-18 functions, directly or indirectly, as a facilitator of vesicle docking.

PMID:
12973353
[PubMed - indexed for MEDLINE]
PMCID:
PMC3874415
Free PMC Article

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