Reference Report
| Reference | |||
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| 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 | ||
Data from Reference
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Aberrations (1)
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Alleles (26)
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Constructs (8)
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Genes (12)
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Insertions (2)
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Natural transposons (1)
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