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Antagonism between G_oα and G_qα in Caenorhabditis elegans: the RGS protein EAT-16 is necessary for G_oα signaling and regulates G_qα activity

Hajdu-Cronin, Yvonne M. and Chen, Wen J. and Patikoglou, Georgia and Koelle, Michael R. and Sternberg, Paul W. (1999) Antagonism between G_oα and G_qα in Caenorhabditis elegans: the RGS protein EAT-16 is necessary for G_oα signaling and regulates G_qα activity. Genes and Development, 13 (14). pp. 1780-1793. ISSN 0890-9369. PMCID PMC316886.

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To elucidate the cellular role of the heterotrimeric G protein G_o, we have taken a molecular genetic approach inCaenorhabditis elegans. We screened for suppressors of activated GOA-1 (G_oα) that do not simply decrease its expression and found mutations in only two genes, sag-1 andeat-16. Animals defective in either gene display a hyperactive phenotype similar to that of goa-1 loss-of-function mutants. Double-mutant analysis indicates that both sag-1 andeat-16act downstream of, or parallel to, Goα and negatively regulate EGL-30 (G_qα) signaling. eat-16encodes a regulator of G protein signaling (RGS) most similar to the mammalian RGS7 and RGS9 proteins and can inhibit endogenous mammalian G_q/G_(11) in COS-7 cells. Animals defective in both sag-1 and eat-16 are inviable, but reducing function in egl-30 restores viability, indicating that the lethality of the eat-16; sag-1 double mutant is due to excessive G_qα activity. Analysis of these mutations indicates that the G_o and G_q pathways function antagonistically in C. elegans, and that G_oα negatively regulates the G_q pathway, possibly via EAT-16 or SAG-1. We propose that a major cellular role of G_o is to antagonize signaling by G_q.

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URLURL TypeDescription CentralArticle
Sternberg, Paul W.0000-0002-7699-0173
Alternate Title:Antagonism between Goα and Gqα in Caenorhabditis elegans: the RGS protein EAT-16 is necessary for Goα signaling and regulates Gqα activity
Additional Information:© 1999 by Cold Spring Harbor Laboratory Press. Received April 26, 1999; revised version accepted June 2, 1999. We thank Jane Mendel for the locomotion assay conditions; Hou-Pu Chou and Chieh Chang for writing software used to record locomotion data; John DeModena for technical assistance; Yuji Kohara for cDNA; Andrew Fire, Joohong Ahnn, Geraldine Seydoux, and Siqun Xu for GFP vectors; Merrilee Robatzek and James Thomas for sa609 andsa735; Bo Yu, Jennifer Gu, and Valeria Mancino for assistance with COS-7 cell assays; Lorna Brundage, Carol Bastiani, Stephen Nurrish, Laurant Ségalat, Joshua Kaplan, Ron Ellis, and Jo Anne Powell-Coffman for sharing strains and communicating unpublished results; and Lorna Brundage, L. René Garcia, Jane Mendel, Carol Bastiani, Maureen Barr, Nadeem Moghal, Henry Lester, Mel Simon, and members of our laboratories for stimulating discussions and critical reading of this manuscript. Some of the strains used in this study were provided by the Caenorhabditis Genetics Center. This project is supported by HHMI, with which P.W.S. is an investigator. The publication costs of this article were defrayed in part by payment of page charges. This article must therefore be hereby marked ‘advertisement’ in accordance with 18 USC section 1734 solely to indicate this fact.
Funding AgencyGrant Number
Howard Hughes Medical Institute (HHMI)UNSPECIFIED
Subject Keywords:C. elegans; G_o protein; G_q protein; RGS protein; signaling; regulation
Issue or Number:14
PubMed Central ID:PMC316886
Record Number:CaltechAUTHORS:20190514-115053085
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Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:95490
Deposited By: Tony Diaz
Deposited On:14 May 2019 20:31
Last Modified:03 Oct 2019 21:13

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