Epidermal growth factor signaling induces behavioral quiescence in Caenorhabditis elegans
- Creators
- Van Buskirk, Cheryl
-
Sternberg, Paul W.
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-γ (PLC-γ), 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.
Additional Information
© 2007 Nature Publishing Group; Received 9 July; accepted 17 August; published online 23 September 2007. We thank the Caenorhabditis Genetics Center for providing strains, S. Kim (Stanford University School of Medicine) for anti-LET-23 antibody, J. DeModena for antibody staining, S. Xu (Univ. Michigan) for the plc-3(sy698) allele, S. Mitani (Tokyo Women's Medical University School of Medicine) for the plc-3(tm1340) allele, N. Moghal, M. Kato, and S. Xu for critical reading of the manuscript, and C.J. Cronin for help with the automated tracking system and locomotion data analysis. This work was supported by a California Breast Cancer Research Program fellowship to C.V.B., by a US National Institute on Drug Abuse grant (DA018341) to P.W.S., and by the Howard Hughes Medical Institute, with which C.V.B. is an Associate and P.W.S. is an Investigator. Author Contributions: C.V.B. designed and conducted the experiments and wrote the manuscript; P.W.S. supervised the project.Additional details
- Eprint ID
- 55862
- Resolver ID
- CaltechAUTHORS:20150317-140501183
- California Breast Cancer Research Program
- DA018341
- National Institute on Drug Abuse (NIDA)
- Howard Hughes Medical Institute (HHMI)
- Created
-
2015-03-17Created from EPrint's datestamp field
- Updated
-
2021-11-10Created from EPrint's last_modified field