Dynactin is necessary for synapse stabilization

Benjamin A. Eaton, Richard D. Fetter, Graeme W. Davis

Research output: Contribution to journalArticle

194 Scopus citations

Abstract

We present evidence that synapse retraction occurs during normal synaptic growth at the Drosophila neuromuscular junction (NMJ). An RNAi-based screen to identify the molecular mechanisms that regulate synapse retraction identified Arp-1/centractin, a subunit of the dynactin complex. Arp-1 dsRNA enhances synapse retraction, and this effect is phenocopied by a mutation in P150/Glued, also a dynactin component. The Glued protein is enriched within the presynaptic nerve terminal, and presynaptic expression of a dominant-negative Glued transgene enhances retraction. Retraction is associated with a local disruption of the synaptic microtubule cytoskeleton. Electrophysiological, ultrastructural, and immunohistochemical data support a model in which presynaptic retraction precedes disassembly of the postsynaptic apparatus. Our data suggests that dynactin functions locally within the presynaptic arbor to promote synapse stability.

Original languageEnglish (US)
Pages (from-to)729-741
Number of pages13
JournalNeuron
Volume34
Issue number5
DOIs
StatePublished - May 30 2002
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)

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