Open AccessCalcium/Calmodulin-Dependent Protein Kinase II Regulates Caenorhabditis elegans Locomotion in Concert With a Go/Gq Signaling Network
Author(s) -
Merrilee Robatzek,
James H. Thomas
Publication year - 2000
Publication title -
genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.792
H-Index - 246
eISSN - 1943-2631
pISSN - 0016-6731
DOI - 10.1093/genetics/156.3.1069
Subject(s) - caenorhabditis elegans , biology , diacylglycerol kinase , calmodulin , microbiology and biotechnology , mutant , genetic screen , phenotype , gq alpha subunit , mutation , protein kinase a , genetics , gene , signal transduction , phosphorylation , protein kinase c , neuroscience , g protein , biochemistry , enzyme
Caenorhabditis elegans locomotion is a complex behavior generated by a defined set of motor neurons and interneurons. Genetic analysis shows that UNC-43, the C. elegans Ca(2+)/calmodulin protein kinase II (CaMKII), controls locomotion rate. Elevated UNC-43 activity, from a gain-of-function mutation, causes severely lethargic locomotion, presumably by inappropriate phosphorylation of targets. In a genetic screen for suppressors of this phenotype, we identified multiple alleles of four genes in a G(o)/G(q) G-protein signaling network, which has been shown to regulate synaptic activity via diacylglycerol. Mutations in goa-1, dgk-1, eat-16, or eat-11 strongly or completely suppressed unc-43(gf) lethargy, but affected other mutants with reduced locomotion only weakly. We conclude that CaMKII and G(o)/G(q) pathways act in concert to regulate synaptic activity, perhaps through a direct interaction between CaMKII and G(o).