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Resources » Paper

Koelle MR (1997) International C. elegans Meeting "THREE OF THE 11 RGS PROTEINS IN C. ELEGANS REGULATE G PROTEIN SIGNALING IN THE EGG-LAYING SYSTEM"

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00022450

    Koelle MR (1997). THREE OF THE 11 RGS PROTEINS IN C. ELEGANS REGULATE G PROTEIN SIGNALING IN THE EGG-LAYING SYSTEM presented in International C. elegans Meeting. Unpublished information; cite only with author permission.

    The recently identified family of RGS proteins inhibit signaling by heterotrimeric G proteins (1). RGS proteins bind to G protein alpha subunits and accelerate their GTPase activity, thereby driving G proteins toward their inactive GDP-bound form (2). In C. elegans, the prototypical RGS protein EGL-10 regulates neurotransmission through the G protein GOA-1: loss-of-function egl-10 mutants are egg-laying defective due to increased GOA-1 signaling (3). We would like to know why there are so many RGS proteins: we found that mammals have at least 17 RGS homologs, and the C. elegans genome sequence predicts 10 RGS proteins besides EGL-10. To begin to address this issue we separately overexpressed each C. elegans RGS gene in transgenic worms by microinjecting genomic DNA for each gene into wild-type worms to form multicopy transgenes. Based on our results with egl-10 and also on studies of RGS genes in yeast and Aspergillus nidulans, we expect that overexpressing an RGS gene in this manner will generally block signaling by the G protein(s) that the RGS protein normally partially inhibits. We assayed egg-laying behavior in our transgenic strains to see if the G protein signaling pathways that control the frequency of this behavior were affected. Overexpression of eight of the RGS genes had no effect on egg laying. Overexpressing either of two RGS genes, egl-10 or C05B5.7, strongly increased the frequency of egg laying and of several other behaviors in the same manner as GOA-1 loss-of-function mutations. These two RGS genes thus both appear to inhibit the G protein GOA-1. Overexpressing an RGS homolog on cosmid C16C2 mildly inhibited egg laying, suggesting that this RGS gene might inhibit the G protein EGL-30, whose activity increases the frequency of egg laying. We are investigating the logic by which three RGS proteins function together to control one behavior. 1. Koelle MR. (1997). Current Opinion in Cell Biol., in press. 2. Berman DM, Wilkie TM, and Gilman AG. (1996). Cell 86:445-452. 3. Koelle MR and Horvitz HR. (1996). Cell 84: 115-15.

    Affiliation:
    - Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT 06520, USA


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