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Resources » Paper

Dong M-Q et al. (1998) East Coast Worm Meeting "Three G Protein Inhibitors Stimulate Egg Laying in C. elegans"

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00011223

    Dong M-Q, & Koelle MR (1998). Three G Protein Inhibitors Stimulate Egg Laying in C. elegans presented in East Coast Worm Meeting. Unpublished information; cite only with author permission.

    RGS proteins (regulators of G protein signaling) inhibit G proteins signaling by directly converting active G proteins (GTP-bound) into their inactive GDP-bound forms. Eleven genes with RGS homology have been identified in the C. elegans genome. We found that only three of them, egl-10, C05B5.7, and F16H9.1, stimulate egg laying when they are overexpressed, suggesting that these three genes may somehow function together to control egg laying. EGL-10 has previously been shown to inhibit GOA-1, a G protein alpha subunit, which in turn inhibits egg laying1. Our current interest is in understanding the roles of C05B5.7 and F16H9.1 in the regulation of egg laying, and in understanding the relationship among the three RGS genes and goa-1. We have obtained cDNAs for C05B5.7 and F16H9.1, which encode the most similar pair of RGS proteins in C. elegans (77% identity in the RGS domain and 64% identity overall). We examined the expression patterns of C05B5.7 and F16H9.1 by injecting promoter::GFP constructs into worms. Expression of C05B5.7::GFP was found in most or all neurons, resembling the expression patterns of both egl-10 and goa-1. F16H9.1::GFP was expressed in a large subset of neurons and in the uterine muscles. We are analyzing a C05B5.7 knock-out strain obtained for us by NemaPharm. So far we have not found any egg-laying defects in the C05B5.7 single mutant. However, preliminary data suggest that the C05B5.7 mutation enhances the egg-laying defect of n480, a weak egl-10 allele. We also found that overexpression of C05B5.7 from an integrated transgene array rescued the egg-laying defect of an egl-10 null mutant. We are trying to obtain F16H9.1 mutants to complete our studies. As C05B5.7 and F16H9.1 may be functionally redundant, given the close similarity in their protein sequences and expression patterns, we may need to knock out both genes to understand their functions. Biochemical analysis of the three RGS proteins are in progress. Our short-term goal is to examine whether and how well C05B5.7 and F16H9.1 proteins stimulate the GTPase activity of GOA-1 in vitro as compared to EGL-10. This may help explain why there are multiple RGS genes involved in the signaling pathway that regulates egg laying. 1. Koelle, M.R. and Horvitz, H.R. (1996) Cell 84, 115-125

    Affiliation:
    - Dept. of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT 06536


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