Docking of secretory vesicles is syntaxin dependent

Secretory vesicles dock at the plasma membrane before they undergo fusion. Molecular docking mechanisms are poorly defined but believed to be independent of SNARE proteins. Here, we challenged this hypothesis by acute deletion of the target SNARE, syntaxin, in vertebrate neurons and neuroendocrine c...

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Bibliographic Details
Published in:PloS one 2006-12, Vol.1 (1), p.e126
Main Authors: de Wit, Heidi, Cornelisse, L Niels, Toonen, Ruud F G, Verhage, Matthijs
Format: Article
Language:English
Subjects:
Actin
Animals
Bassoon music
Botulinum Toxins - genetics
Caenorhabditis elegans
Cell Biology
Cells, Cultured
Chromaffin cells
Chromaffin Cells - physiology
Chromaffin Cells - ultrastructure
Clonal deletion
Cortex
Defects
Gene Expression
Gene Targeting
Genomics
Green Fluorescent Proteins - genetics
Membrane fusion
Membrane Fusion - physiology
Mice
Microscopy, Electron, Transmission
Molecular docking
Munc18 Proteins - physiology
Muscle proteins
Neuroendocrine system
Neuroscience
Plasma
Proteins
Qa-SNARE Proteins - deficiency
Qa-SNARE Proteins - genetics
Qa-SNARE Proteins - physiology
Reduction
Secretory vesicles
Secretory Vesicles - physiology
Secretory Vesicles - ultrastructure
SNAP receptors
Studies
Synapses
Syntaxin
Vesicles
Yeast
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Summary:Secretory vesicles dock at the plasma membrane before they undergo fusion. Molecular docking mechanisms are poorly defined but believed to be independent of SNARE proteins. Here, we challenged this hypothesis by acute deletion of the target SNARE, syntaxin, in vertebrate neurons and neuroendocrine cells. Deletion resulted in fusion arrest in both systems. No docking defects were observed in synapses, in line with previous observations. However, a drastic reduction in morphologically docked secretory vesicles was observed in chromaffin cells. Syntaxin-deficient chromaffin cells showed a small reduction in total and plasma membrane staining for the docking factor Munc18-1, which appears insufficient to explain the drastic reduction in docking. The sub-membrane cortical actin network was unaffected by syntaxin deletion. These observations expose a docking role for syntaxin in the neuroendocrine system. Additional layers of regulation may have evolved to make syntaxin redundant for docking in highly specialized systems like synaptic active zones.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0000126