TY - JOUR T1 - Orchestration of Stepwise Synaptic Growth by K<sup>+</sup> and Ca<sup>2+</sup> Channels in <em>Drosophila</em> JF - The Journal of Neuroscience JO - J. Neurosci. SP - 15821 LP - 15833 DO - 10.1523/JNEUROSCI.3448-10.2010 VL - 30 IS - 47 AU - Jihye Lee AU - Chun-Fang Wu Y1 - 2010/11/24 UR - http://www.jneurosci.org/content/30/47/15821.abstract N2 - 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. ER -