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PubMed · 12062020

Dynactin is necessary for synapse stabilization.

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

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ActinsAnimalsAnimals, Genetically ModifiedCell DifferentiationCentral Nervous SystemCytoskeletal ProteinsDrosophilaDrosophila ProteinsDynactin ComplexFemaleGene Expression Regulation, DevelopmentalMaleMicrotubule-Associated ProteinsMotor NeuronsMutationNeuromuscular JunctionNeuronal PlasticityPresynaptic TerminalsRNATransgenesJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.

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Benjamin A Eaton, Richard D Fetter, Graeme W Davis. 2002-05-30. Dynactin is necessary for synapse stabilization.. https://doi.org/10.1016/s0896-6273(02)00721-3

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