Genetics, Vol. 156, 1069-1082, November 2000, Copyright © 2000

Calcium/Calmodulin-Dependent Protein Kinase II Regulates Caenorhabditis elegans Locomotion in Concert With a Go/Gq Signaling Network

Merrilee Robatzeka and James H. Thomasa
a Department of Genetics, University of Washington, Seattle, Washington 98195

Corresponding author: James H. Thomas, University of Washington, Department of Genetics, Box 357360, Seattle, WA 98195., jht{at}genetics.washington.edu (E-mail)

Communicating editor: P. ANDERSON

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 Ca2+/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 Go/Gq 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 Go/Gq pathways act in concert to regulate synaptic activity, perhaps through a direct interaction between CaMKII and Go.





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