期刊
JOURNAL OF CELL BIOLOGY
卷 181, 期 1, 页码 157-170出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200712152
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- Howard Hughes Medical Institute Funding Source: Medline
- NICHD NIH HHS [P30 HD024064] Funding Source: Medline
- NINDS NIH HHS [F30 NS056520, F30NS056520] Funding Source: Medline
In a screen to identify genes involved in synaptic function, we isolated mutations in Drosophila melanogaster straightjacket (stj), an alpha 2 delta subunit of the voltage-gated calcium channel. stj mutant photoreceptors develop normal synaptic connections but display reduced on-off transients in electroretinogram recordings, indicating a failure to evoke postsynaptic responses and, thus, a defect in neurotransmission. stj is expressed in neurons but excluded from glia. Mutants exhibit endogenous seizure-like activity, indicating altered neuronal excitability. However, at the synaptic level, stj larval neuromuscular junctions exhibit approximately fourfold reduction in synaptic release compared with controls stemming from a reduced release probability at these synapses. These defects likely stem from destabilization of Cacophony (Cac), the primary presynaptic alpha(1) subunit in D. melanogaster. Interestingly, neuronal overexpression of cac partially rescues the viability and physiological defects in stj mutants, indicating a role for the alpha 2 delta Ca2+ channel subunit in mediating the proper localization of an alpha(1) subunit at synapses.
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