Article abstract
Nature Neuroscience 10, 1300 - 1307 (2007)
Published online: 23 September 2007 | doi:10.1038/nn1981
Epidermal growth factor signaling induces behavioral quiescence in Caenorhabditis elegans
Cheryl Van Buskirk1 & Paul W Sternberg1
Abstract
The epidermal growth factor receptor (EGFR)/ErbB receptor tyrosine kinases regulate several aspects of development, including the development of the mammalian nervous system. ErbB signaling also has physiological effects on neuronal function, with influences on synaptic plasticity and daily cycles of activity. However, little is known about the effectors of EGFR activation in neurons. Here we show that EGF signaling has a nondevelopmental effect on behavior in Caenorhabditis elegans. Ectopic expression of the EGF-like ligand LIN-3 at any stage induces a reversible cessation of feeding and locomotion. These effects are mediated by neuronal EGFR (also called LET-23) and phospholipase C–
(PLC-), diacylglycerol-binding proteins, and regulators of synaptic vesicle release. Activation of EGFR within a single neuron, ALA, is sufficient to induce a quiescent state. This pathway modulates the cessation of pharyngeal pumping and locomotion that normally occurs during the lethargus period that precedes larval molting. Our results reveal an evolutionarily conserved role for EGF signaling in the regulation of behavioral quiescence.
- Howard Hughes Medical Institute, Division of Biology 156-29, California Institute of Technology, 1200 E. California Blvd. Pasadena, California 91125, USA.
Correspondence to: Paul W Sternberg1 e-mail: pws@caltech.edu
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