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Vol. 11, Issue 9, 3177-3190, September 2000
Howard Hughes Medical Institute, Programs in Developmental Biology,
Neuroscience, and Genetics, Department of Anatomy and Department of
Biochemistry and Biophysics, The University of California, San
Francisco, California 94143
The Caenorhabditis elegans sax-1 gene regulates
several aspects of neuronal cell shape. sax-1 mutants
have expanded cell bodies and ectopic neurites in many classes of
neurons, suggesting that SAX-1 functions to restrict cell and neurite
growth. The ectopic neurites in sensory neurons of sax-1
mutants resemble the defects caused by decreased sensory activity.
However, the activity-dependent pathway, mediated in part by the UNC-43
calcium/calmodulin-dependent kinase II, functions in parallel with
SAX-1 to suppress neurite initiation. sax-1 encodes a
serine/threonine kinase in the Ndr family that is related to the Orb6
(Schizosaccharomyces pombe), Warts/Lats
(Drosophila), and COT-1 (Neurospora)
kinases that function in cell shape regulation. These kinases have
similarity to Rho kinases but lack consensus Rho-binding domains.
Dominant negative mutations in the C. elegans RhoA
GTPase cause neuronal cell shape defects similar to those of
sax-1 mutants, and genetic interactions between
rhoA and sax-1 suggest shared functions.
These results suggest that SAX-1/Ndr kinases are endogenous
inhibitors of neurite initiation and cell spreading.
Project
BIOTECH, University of Arizona, Tucson, AZ 85721.
Corresponding author. E-mail address:
cori{at}itsa.ucsf.edu.
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