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J Physiol Volume 585, Number 3, 705-709, December 15, 2007 DOI: 10.1113/jphysiol.2007.138321
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SYMPOSIUM REPORT

Tomosyn negatively regulates both synaptic transmitter and neuropeptide release at the C. elegans neuromuscular junction

 Elena O. Gracheva1, Anna O. Burdina1, Denis Touroutine1, Martine Berthelot-Grosjean1, Hetal Parekh1 and Janet E. Richmond1

1 Department of Biological Sciences, University of Illinois at Chicago, Chicago, IL, USA

The SNARE proteins, syntaxin, SNAP-25 and synaptobrevin form a tertiary complex essential for vesicle fusion. Proteins that influence SNARE complex assembly are therefore likely to be important regulators of fusion events. In this study we have focused on tomosyn, a highly conserved, neuronally enriched, syntaxin-binding protein that has been implicated in the regulation of vesicle exocytosis. To directly test the role of tomosyn in neurosecretion we analysed loss-of-function mutants in the single Caenorhabditis elegans tomosyn gene, tom-1. These mutants exhibit enhanced synaptic transmission based on electrophysiological analysis of neuromuscular junction activity. This phenotype is the result of increased synaptic vesicle priming. In addition, we present evidence that tom-1 mutants also exhibit enhanced peptide release from dense core vesicles. These results indicate that tomosyn negatively regulates secretion for both vesicle types, possibly through a common mechanism, interfering with SNARE complex formation, thereby inhibiting vesicle fusion.

(Received 8 June 2007; accepted after revision 6 July 2007; first published online 12 July 2007)
Corresponding author J. E. Richmond: Department of Biological Sciences, University of Illinois at Chicago, Chicago, IL, USA. Email: jer{at}uic.edu

This report was presented at a symposium on Signals and SNAREs regulating vesicle exocytosis, which took place at the Life Sciences 2007 meeting, 9–12 July 2007, Glasgow, UK.




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