Diverse behavioural defects caused by mutations in Caenorhabditis elegans unc-43 CaM Kinase II

David J. Reiner, Elizabeth M. Newton, Hong Tian and James H. Thomas ()
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David J. Reiner: University of Washington
Elizabeth M. Newton: University of Washington
Hong Tian: University of Washington
James H. Thomas: University of Washington

Nature, 1999, vol. 402, issue 6758, 199-203

Abstract: Abstract Calcium/calmodulin-dependent serine/threonine kinase type II (CaMKII) is one of the most abundant proteins in the mammalian brain, where it is thought to regulate synaptic plasticity and other processes1,2,3. Activation of the multisubunit kinase4 by calcium is effectively cooperative and can persist long after transient calcium rises1,5,6. Despite extensive biochemical characterization of CaMKII and identification of numerous in vitro kinase targets1, little is known about its function in vivo. Here we report that unc-43 encodes the only Caenorhabditis elegans CaMKII. A gain-of-function unc-43 mutation reduces locomotory activity, alters excitation of three muscle types and lengthens the period of the motor output of a behavioural clock. Null unc-43 mutations cause phenotypes generally opposite to those of the gain-of-function mutation. Mutations in the unc-103 potassium channel gene suppress a gain-of-function phenotype of unc-43 in one tissue without affecting other tissues; thus, UNC-103 may be a tissue-specific target of CaMKII in vivo.

Date: 1999
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DOI: 10.1038/46072

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