A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Reference Report

Reference
Citation Lee, J., Wu, C.F. (2010). Orchestration of stepwise synaptic growth by k+ and Ca2+ channels in Drosophila.  J. Neurosci. 30(47): 15821--15833. (Export to RIS)
FlyBase ID FBrf0212405
Publication Type Research paper
PubMed ID 21106821
PubMed 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 Ca(2+)-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 Ca(2+) channels, Dmca1D, and PSD-95-like scaffold protein, Discs large, are required for satellite budding induced by slowpoke and seizure mutations. Pre-synaptic cacophony Ca(2+) 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 Ca(2+)/CaM-dependent adenylyl cyclase, demonstrating a convergence of K(+) channels of different functional categories in regulation of excitability-dependent Ca(2+) influx for triggering cAMP-mediated growth plasticity.
DOI 10.1523/JNEUROSCI.3448-10.2010
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Language of Publication English
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Publication Type Journal
Abbreviation J. Neurosci.
Title Journal of Neuroscience
Publication Year 1981-
ISBN/ISSN 0270-6474 1529-2401
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