Tomosyn Inhibits Synaptic Vesicle Priming in Caenorhabditis elegans
Gracheva, Elena O.
Burdina, Anna O.
Holgado, Andrea M.
Ackley, Brian D.
Nonet, Michael L.
Weimer, Robby M.
Richmond, Janet E.
Public Library of Science
Scholarly/refereed, publisher version
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Caenorhabditis elegans TOM-1 is orthologous to vertebrate tomosyn, a cytosolic syntaxin-binding protein implicated in the modulation of both constitutive and regulated exocytosis. To investigate how TOM-1 regulates exocytosis of synaptic vesicles in vivo, we analyzed C. elegans tom-1 mutants. Our electrophysiological analysis indicates that evoked postsynaptic responses at tom-1 mutant synapses are prolonged leading to a two-fold increase in total charge transfer. The enhanced response in tom-1 mutants is not associated with any detectable changes in postsynaptic response kinetics, neuronal outgrowth, or synaptogenesis. However, at the ultrastructural level, we observe a concomitant increase in the number of plasma membrane-contacting vesicles in tom-1 mutant synapses, a phenotype reversed by neuronal expression of TOM-1. Priming defective unc-13 mutants show a dramatic reduction in plasma membrane-contacting vesicles, suggesting these vesicles largely represent the primed vesicle pool at the C. elegans neuromuscular junction. Consistent with this conclusion, hyperosmotic responses in tom-1 mutants are enhanced, indicating the primed vesicle pool is enhanced. Furthermore, the synaptic defects of unc-13 mutants are partially suppressed in tom-1 unc-13 double mutants. These data indicate that in the intact nervous system, TOM-1 negatively regulates synaptic vesicle priming.
This is the publisher's version, also available electronically from http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0040261.
Gracheva, Elena O. et al. (2006). "Tomosyn Inhibits Synaptic Vesicle Priming in Caenorhabditis elegans." PLOS Biology, 4(8):e261. http://www.dx.doi.org/10.1371/journal.pbio.0040261
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