Two Neuronal G Proteins are Involved in Chemosensation of the Caenorhabditis elegans Dauer-Inducing Pheromone
Abstract
Caenorhabditis elegans uses chemosensation to determine its course of development. Young larvae can arrest as dauer larvae in response to increasing population density, which they measure by a nematode-excreted pheromone, and decreasing food supply. Dauer larvae can resume development in response to a decrease in pheromone and increase in food concentration. We show here that two novel G protein alpha subunits (GPA-2 and GPA-3) show promoter activity in subsets of chemosensory neurons and are involved in the decision to form dauer larvae primarily through the response to dauer pheromone. Dominant activating mutations in these G proteins result in constitutive, pheromone-independent dauer formation, whereas inactivation results in reduced sensitivity to pheromone, and, under certain conditions, an alteration in the response to food. Interactions between gpa-2, gpa-3 and other genes controlling dauer formation suggest that these G proteins may act in parallel to regulate the neuronal decision making that precedes dauer formation.
Additional Information
© 1997 by the Genetics Society of America. Manuscript received August 8, 1996; Accepted for publication December 2, 1996. We thank Betsy Malone and Jim Thomas for help and advice on the pheromone response assays and for sending us the strain JT6130, and Andy Fire for providing us with the lacZ and GFP expression vectors. We thank Cori Bargmann and Ikue More for additional phenotypic analysis of deletion mutants, Henri Van Luenen for help in preparing the manuscript and Rik Korswagen, Lorna Brundage and Dave Sonnenborn for critical reading of the manuscript. Some of the swains were provided by the Caenorhabditis Genetic Center. This work was supported by a Pioneer grant from the Netherlands Organization for Scientific Research (NWO) to R.H.A.P. and from the Human Frontiers in Science Program (HFSP) to R.H.A.P. and P.W.S., an investigator with the Howard Hughes Medical Institute. The transposon mutant library from which the Tcl mutants were isolated is currently supported by grant 5 RO1 RR10082 from the National Institutes of Health National Center for Research Resources.Attached Files
Published - ge1453715.pdf
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Additional details
- PMCID
- PMC1207856
- Eprint ID
- 95510
- Resolver ID
- CaltechAUTHORS:20190515-104420137
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek (NWO)
- Human Frontier Science Program
- Howard Hughes Medical Institute (HHMI)
- NIH
- 5 RO1 RR10082
- Created
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2019-05-16Created from EPrint's datestamp field
- Updated
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2019-10-03Created from EPrint's last_modified field