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J. Cell Biol.,
Volume 142, Number 5, September 7, 1998 1325-1335
Department of Cell Biology, Emory University School of Medicine, Atlanta, Georgia 30322-3030
G protein-coupled receptors trigger the reorganization of the actin cytoskeleton in many cell
types, but the steps in this signal transduction cascade
are poorly understood. During Dictyostelium development, extracellular cAMP functions as a chemoattractant and morphogenetic signal that is transduced via a
family of G protein-coupled receptors, the cARs. In a
strain where the cAR2 receptor gene is disrupted by
homologous recombination, the developmental program arrests before tip formation. In a genetic screen
for suppressors of this phenotype, a gene encoding a
protein related to the Wiskott-Aldrich Syndrome protein was discovered. Loss of this protein, which we call
SCAR (suppressor of cAR), restores tip formation and
most later development to cAR2
strains, and causes a
multiple-tip phenotype in a cAR2+ strain as well as
leading to the production of extremely small cells in
suspension culture. SCARcells have reduced levels of
F-actin staining during vegetative growth, and abnormal cell morphology and actin distribution during chemotaxis. Uncharacterized homologues of SCAR
have also been identified in humans, mouse, Caenorhabditis elegans, and Drosophila. These data suggest that SCAR may be a conserved negative regulator of G protein-coupled signaling, and that it plays an important role in regulating the actin cytoskeleton.
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