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Originally published as Genetics Published Articles Ahead of Print on October 16, 2004.
Genetics, Vol. 169, 651-670, February 2005, Copyright © 2005
doi:10.1534/genetics.104.031286
Convergent, RIC-8-Dependent G
Signaling Pathways in the Caenorhabditis elegans Synaptic Signaling Network
Nicole K. Reynolds, Michael A. Schade and Kenneth G. Miller1
Program in Molecular, Cell and Developmental Biology, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104
1 Corresponding author: Program in Molecular and Cell Biology, Oklahoma Medical Research Foundation, 825 NE 13th St., Oklahoma City, OK 73104.
E-mail: millerk{at}omrf.ouhsc.edu
We used gain-of-function and null synaptic signaling network mutants to investigate the relationship of the G
q and Gs pathways to synaptic vesicle priming and to each other. Genetic epistasis studies using Gq gain-of-function and null mutations, along with a mutation that blocks synaptic vesicle priming and the synaptic vesicle priming stimulator phorbol ester, suggest that the Gq pathway generates the core, obligatory signals for synaptic vesicle priming. In contrast, the Gs pathway is not required for the core priming function, because steady-state levels of neurotransmitter release are not significantly altered in animals lacking a neuronal Gs pathway, even though these animals are strongly paralyzed as a result of functional (nondevelopmental) defects. However, our genetic analysis indicates that these two functionally distinct pathways converge and that they do so downstream of DAG production. Further linking the two pathways, our epistasis analysis of a ric-8 null mutant suggests that RIC-8 (a receptor-independent G guanine nucleotide exchange factor) is required to maintain both the Gq vesicle priming pathway and the neuronal Gs pathway in a functional state. We propose that the neuronal Gs pathway transduces critical positional information onto the core Gq pathway to stabilize the priming of selected synapses that are optimal for locomotion.
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