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Defects in synaptic vesicle docking in unc-18 mutants

2003; Nature Portfolio; Volume: 6; Issue: 10 Linguagem: Inglês

10.1038/nn1118

1546-1726

Robby M. Weimer, Janet E. Richmond, Warren S. Davis, Gayla Hadwiger, Michael L. Nonet, Erik M. Jørgensen,

Photoreceptor and optogenetics research

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.