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dc.contributor.authorGracheva, Elena O.
dc.contributor.authorBurdina, Anna O.
dc.contributor.authorHolgado, Andrea M.
dc.contributor.authorBerthelot-Grosjean, Martine
dc.contributor.authorAckley, Brian D.
dc.contributor.authorHadwiger, Gayla
dc.contributor.authorNonet, Michael L.
dc.contributor.authorWeimer, Robby M.
dc.contributor.authorRichmond, Janet E.
dc.date.accessioned2014-10-06T18:40:50Z
dc.date.available2014-10-06T18:40:50Z
dc.date.issued2006-07-25
dc.identifier.citationGracheva, 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
dc.identifier.issn1544-9173
dc.identifier.urihttp://hdl.handle.net/1808/15184
dc.descriptionThis is the publisher's version, also available electronically from http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0040261.
dc.description.abstractCaenorhabditis 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.
dc.publisherPublic Library of Science
dc.titleTomosyn Inhibits Synaptic Vesicle Priming in Caenorhabditis elegans
dc.typeArticle
kusw.kuauthorAckley, Brian D.
kusw.kudepartmentMolecular Biosciences
kusw.oastatusfullparticipation
dc.identifier.doi10.1371/journal.pbio.0040261
kusw.oaversionScholarly/refereed, publisher version
kusw.oapolicyThis item meets KU Open Access policy criteria.
dc.rights.accessrightsopenAccess


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