A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Reference Report

Reference
Citation Kurshan, P.T., Oztan, A., Schwarz, T.L. (2009). Presynaptic alpha(2)delta-3 is required for synaptic morphogenesis independent of its Ca(2+)-channel functions.  Nat. Neurosci. 12(11): 1415--1423. (Export to RIS)
FlyBase ID FBrf0209005
Publication Type Research paper
PubMed ID 19820706
PubMed Abstract Synaptogenesis involves the transformation of a growth cone into synaptic boutons specialized for transmitter release. In Drosophila embryos lacking the alpha(2)delta-3 subunit of presynaptic, voltage-dependent Ca(2+) channels, we found that motor neuron terminals failed to develop synaptic boutons and cytoskeletal abnormalities arose, including the loss of ankyrin2. Nevertheless, functional presynaptic specializations were present and apposed to clusters of postsynaptic glutamate receptors. The alpha(2)delta-3 protein has been thought to function strictly as an auxiliary subunit of the Ca(2+) channel, but the phenotype of alpha(2)delta-3 (also known as stj) mutations cannot be explained by a channel defect; embryos lacking the pore-forming alpha(1) subunit cacophony formed boutons. The synaptogenic function of alpha(2)delta-3 required only the alpha(2) peptide, whose expression sufficed to rescue bouton formation. Our results indicate that alpha(2)delta proteins have functions that are independent of their roles in the biophysics and localization of Ca(2+) channels and that synaptic architecture depends on these functions.
DOI 10.1038/nn.2417
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Publication Type Journal
Abbreviation Nat. Neurosci.
Title Nature Neuroscience
Publication Year 1998-
ISBN/ISSN 1097-6256
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