Synaptic transmission regulated by a presynaptic MALS/Liprin-alpha protein complex.
Neurotransmission requires proper organization of synaptic vesicle pools and rapid release of vesicle contents upon presynaptic depolarization. Genetic studies have begun to reveal a critical role for scaffolding proteins in such processes. Mutations in genes encoding components of the highly conserved MALS/CASK/Mint-1 complex cause presynaptic defects. In all three mutants, neurotransmitter release is reduced in a manner consistent with aberrant vesicle cycling to the readily releasable pool. Recently, liprin-alpha proteins, which define active zone size and morphology, were found to associate with MALS/CASK, suggesting that this complex links the presynaptic release machinery to the active zone, thereby regulating neurotransmitter release.
Olsen
Olav
O
Departments of Physiology and Cellular & Molecular Pharmacology, University of California-San Francisco, 600 16th Street, San Francisco, CA, USA.
Moore
Kimberly A
KA
Nicoll
Roger A
RA
Bredt
David S
DS
D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism; D000818:Animals; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000378:metabolism*; D051528:Guanylate Kinases; D006801:Humans; D008565:Membrane Proteins / Q000378:metabolism*; D008954:Models, Biological; D009419:Nerve Tissue Proteins / Q000378:metabolism; D017729:Presynaptic Terminals / Q000378:metabolism / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology*
C079091:APBA1 protein, human; D048868:Adaptor Proteins, Signal Transducing; D008565:Membrane Proteins; D009419:Nerve Tissue Proteins; C106868:CASK kinases; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D051528:Guanylate Kinases