Role of Tetanus Neurotoxin Insensitive Vesicle-Associated Membrane Protein (TI-VAMP) in Vesicular Transport Mediating Neurite Outgrowth

How vesicular transport participates in neurite outgrowth is still poorly understood. Neurite outgrowth is not sensitive to tetanus neurotoxin thus does not involve synaptobrevin-mediated vesicular transport to the plasma membrane of neurons. Tetanus neurotoxin-insensitive vesicle-associated membran...

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Bibliographic Details
Published in:The Journal of cell biology 2000-05, Vol.149 (4), p.889-899
Main Authors: Martinez-Arca, Sonia, Alberts, Philipp, Zahraoui, Ahmed, Louvard, Daniel, Galli, Thierry
Format: Article
Language:English
Subjects:
Animals
Antibodies
Biological Transport - drug effects
Botulinum Toxins - pharmacology
Cell Differentiation
Cell membranes
Cells
Cellular biology
Endothelial cells
Epithelial cells
Exocytosis - drug effects
HeLa cells
Intracellular Membranes - metabolism
Membrane Proteins - metabolism
Membranes
Metalloendopeptidases - pharmacology
Nerve Tissue Proteins - metabolism
Neurites
Neurology
Neurons
Neurons - cytology
Original
PC12 Cells
Protein Binding
Proteins
R SNARE proteins
Rats
SNARE Proteins
Staurosporine - pharmacology
Synaptosomal-Associated Protein 25
Tetanus Toxin - pharmacology
Vesicular Transport Proteins
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Summary:How vesicular transport participates in neurite outgrowth is still poorly understood. Neurite outgrowth is not sensitive to tetanus neurotoxin thus does not involve synaptobrevin-mediated vesicular transport to the plasma membrane of neurons. Tetanus neurotoxin-insensitive vesicle-associated membrane protein (TI-VAMP) is a vesicle-SNARE (soluble N-ethylmaleimide-sensitive fusion protein [NSF] attachment protein [SNAP] receptor), involved in transport to the apical plasma membrane in epithelial cells, a tetanus neurotoxin-resistant pathway. Here we show that TI-VAMP is essential for vesicular transport-mediating neurite outgrowth in staurosporine-differentiated PC12 cells. The NH2-terminal domain, which precedes the SNARE motif of TI-VAMP, inhibits the association of TI-VAMP with synaptosome-associated protein of 25 kD (SNAP25). Expression of this domain inhibits neurite outgrowth as potently as Botulinum neurotoxin E, which cleaves SNAP25. In contrast, expression of the NH2-terminal deletion mutant of TI-VAMP increases SNARE complex formation and strongly stimulates neurite outgrowth. These results provide the first functional evidence for the role of TI-VAMP in neurite outgrowth and point to its NH2-terminal domain as a key regulator in this process.
ISSN:0021-9525
1540-8140
DOI:10.1083/jcb.149.4.889