Orchestration of Stepwise Synaptic Growth by K[superscript +] and Ca[superscript 2+] Channels in Drosophila
Name
Wu-2010-Orchestration of Stepwise Synaptic.pdf
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Author(s)
Lee, Jihye
Wu, Chun-Fang
Alternative Title
Orchestration of Stepwise Synaptic Growth by K+ and Ca2+ Channels in Drosophila
Date Issued
September 2010
Journal
Journal of Neuroscience
Publisher
Society for Neuroscience
Citation
Lee, Jihye and Chun-Fang Wu. "Orchestration of Stepwise Synaptic Growth by K[superscript +] and Ca[superscript 2+] Channels in Drosophila."Journal of Neuroscience, 24 November 2010, 30(47): 15821-15833
Version
Final published version
Abstract
Synapse formation is tightly associated with neuronal excitability. We found striking synaptic overgrowth caused by Drosophila K+-channel mutations of the seizure and slowpoke genes, encoding Erg and Ca2+-activated large-conductance (BK) channels, respectively. These mutants display two distinct patterns of “satellite” budding from larval motor terminus synaptic boutons. Double-mutant analysis indicates that BK and Erg K+ channels interact with separate sets of synaptic proteins to affect distinct growth steps. Post-synaptic L-type Ca2+ channels, Dmca1D, and PSD-95-like scaffold protein, Discs large, are required for satellite budding induced by slowpoke and seizure mutations. Pre-synaptic cacophony Ca2+ channels and the NCAM-like adhesion molecule, Fasciclin II, take part in a maturation step that is partially arrested by seizure mutations. Importantly, slowpoke and seizure satellites were both suppressed by rutabaga mutations that disrupt Ca2+/CaM-dependent adenylyl cyclase, demonstrating a convergence of K+ channels of different functional categories in regulation of excitability-dependent Ca2+ influx for triggering cAMP-mediated growth plasticity.
MIT Department
Picower Institute for Learning and Memory
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DOI of Published Version
https://doi.org/10.1523/jneurosci.3448-10.2010
