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dc.contributor.authorStevens, Robin Jean
dc.contributor.authorAkbergenova, Yulia
dc.contributor.authorJorquera, Ramon
dc.contributor.authorLittleton, J. Troy
dc.date.accessioned2013-08-01T19:27:00Z
dc.date.available2013-08-01T19:27:00Z
dc.date.issued2012-12
dc.date.submitted2012-10
dc.identifier.issn0270-6474
dc.identifier.issn1529-2401
dc.identifier.urihttp://hdl.handle.net/1721.1/79760
dc.description.abstractSustained neuronal communication relies on the coordinated activity of multiple proteins that regulate synaptic vesicle biogenesis and cycling within the presynaptic terminal. Synaptogyrin and synaptophysin are conserved MARVEL domain-containing transmembrane proteins that are among the most abundant synaptic vesicle constituents, although their role in the synaptic vesicle cycle has remained elusive. To further investigate the function of these proteins, we generated and characterized a synaptogyrin (gyr)-null mutant in Drosophila, whose genome encodes a single synaptogyrin isoform and lacks a synaptophysin homolog. We demonstrate that Drosophila synaptogyrin plays a modulatory role in synaptic vesicle biogenesis at larval neuromuscular junctions. Drosophila lacking synaptogyrin are viable and fertile and have no overt deficits in motor function. However, ultrastructural analysis of gyr larvae revealed increased synaptic vesicle diameter and enhanced variability in the size of synaptic vesicles. In addition, the resolution of endocytic cisternae into synaptic vesicles in response to strong stimulation is defective in gyr mutants. Electrophysiological analysis demonstrated an increase in quantal size and a concomitant decrease in quantal content, suggesting functional consequences for transmission caused by the loss of synaptogyrin. Furthermore, high-frequency stimulation resulted in increased facilitation and a delay in recovery from synaptic depression, indicating that synaptic vesicle exo-endocytosis is abnormally regulated during intense stimulation conditions. These results suggest that synaptogyrin modulates the synaptic vesicle exo-endocytic cycle and is required for the proper biogenesis of synaptic vesicles at nerve terminals.en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (NIH grant NS40296)en_US
dc.description.sponsorshipPew Charitable Trusts (Pew Latin American Fellows Program in the Biomedical Sciences)en_US
dc.language.isoen_US
dc.publisherSociety for Neuroscienceen_US
dc.relation.isversionofhttp://dx.doi.org/10.1523/jneurosci.2668-12.2012en_US
dc.rightsArticle is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.en_US
dc.sourceSFNen_US
dc.titleAbnormal Synaptic Vesicle Biogenesis in Drosophila Synaptogyrin Mutantsen_US
dc.typeArticleen_US
dc.identifier.citationStevens, R. J., Y. Akbergenova, R. A. Jorquera, and J. T. Littleton. “Abnormal Synaptic Vesicle Biogenesis in Drosophila Synaptogyrin Mutants.” Journal of Neuroscience 32, no. 50 (December 12, 2012): 18054-18067.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Brain and Cognitive Sciencesen_US
dc.contributor.departmentPicower Institute for Learning and Memoryen_US
dc.contributor.mitauthorStevens, Robin Jeanen_US
dc.contributor.mitauthorAkbergenova, Yuliaen_US
dc.contributor.mitauthorJorquera, Ramonen_US
dc.contributor.mitauthorLittleton, J. Troyen_US
dc.relation.journalJournal of Neuroscienceen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsStevens, R. J.; Akbergenova, Y.; Jorquera, R. A.; Littleton, J. T.en_US
dc.identifier.orcidhttps://orcid.org/0000-0001-5576-2887
dspace.mitauthor.errortrue
mit.licensePUBLISHER_POLICYen_US
mit.metadata.statusComplete


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