Postsynaptic regulation of synaptic plasticity by synaptotagmin 4 requires both C2 domains

Cynthia F. Barber, Ramon A. Jorquera, Jan E. Melom, J. Troy Littleton

Resultado de la investigación: Contribución a una revistaArtículorevisión exhaustiva

34 Citas (Scopus)

Resumen

Ca2+ influx into synaptic compartments during activity is a key mediator of neuronal plasticity. Although the role of presynaptic Ca 2+ in triggering vesicle fusion though the Ca2+ sensor synaptotagmin 1 (Syt 1) is established, molecular mechanisms that underlie responses to postsynaptic Ca2+ influx remain unclear. In this study, we demonstrate that fusion-competent Syt 4 vesicles localize postsynaptically at both neuromuscular junctions (NMJs) and central nervous system synapses in Drosophila melanogaster. Syt 4 messenger RNA and protein expression are strongly regulated by neuronal activity, whereas altered levels of postsynaptic Syt 4 modify synaptic growth and presynaptic release properties. Syt 4 is required for known forms of activity-dependent structural plasticity at NMJs. Synaptic proliferation and retrograde signaling mediated by Syt 4 requires functional C2A and C2B Ca2+-binding sites, as well as serine 284, an evolutionarily conserved substitution for a key Ca2+-binding aspartic acid found in other synaptotagmins. These data suggest that Syt 4 regulates activity-dependent release of postsynaptic retrograde signals that promote synaptic plasticity, similar to the role of Syt 1 as a Ca2+ sensor for presynaptic vesicle fusion.

Idioma originalInglés
Páginas (desde-hasta)295-310
Número de páginas16
PublicaciónJournal of Cell Biology
Volumen187
N.º2
DOI
EstadoPublicada - 19 oct 2009
Publicado de forma externa

Áreas temáticas de ASJC Scopus

  • Biología celular

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