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Epidermal growth factor signaling induces behavioral quiescence in Caenorhabditis elegans

Van Buskirk, Cheryl and Sternberg, Paul W. (2007) Epidermal growth factor signaling induces behavioral quiescence in Caenorhabditis elegans. Nature Neuroscience, 10 (10). pp. 1300-1307. ISSN 1097-6256. doi:10.1038/nn1981. https://resolver.caltech.edu/CaltechAUTHORS:20150317-140501183

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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.


Item Type:Article
Related URLs:
URLURL TypeDescription
http://dx.doi.org/10.1038/nn1981 DOIArticle
http://www.nature.com/neuro/journal/v10/n10/full/nn1981.htmlPublisherArticle
ORCID:
AuthorORCID
Sternberg, Paul W.0000-0002-7699-0173
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.
Funders:
Funding AgencyGrant Number
California Breast Cancer Research ProgramUNSPECIFIED
National Institute on Drug Abuse (NIDA)DA018341
Howard Hughes Medical Institute (HHMI)UNSPECIFIED
Issue or Number:10
DOI:10.1038/nn1981
Record Number:CaltechAUTHORS:20150317-140501183
Persistent URL:https://resolver.caltech.edu/CaltechAUTHORS:20150317-140501183
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:55862
Collection:CaltechAUTHORS
Deposited By: Tony Diaz
Deposited On:17 Mar 2015 21:39
Last Modified:10 Nov 2021 20:51

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