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.
journal_name
Neuronjournal_title
Neuronauthors
Eaton BA,Fetter RD,Davis GWdoi
10.1016/s0896-6273(02)00721-3subject
Has Abstractpub_date
2002-05-30 00:00:00pages
729-41issue
5eissn
0896-6273issn
1097-4199pii
S0896627302007213journal_volume
34pub_type
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