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Herzmark, J. M. Nakamoto, C. van Dop and H. R. Bourne, 1994 Rapid GDP release from Gs␣ in patients with gain and loss of endocrine function. Nature 371: 164–168. , J. Chang, E. Gensch, A. Rudner and R. Tabtiang, 1993 A C. elegans mutant that lives twice as long as wild type. Nature 366: 461–464. Korswagen, H. , J. H. Park, Y. Ohshima and R. H. Plasterk, 1997 An activating mutation in a Caenorhabditis elegans Gs protein induces neural degeneration. Genes Dev. 11: 1493–1503. Korswagen, H. , A. M.

Elegans. Science 267: 1652–1655. Miller, K. , A. Alfonso, M. Nguyen, J. A. Crowell, C. D. , 1996 A genetic selection for Caenorhabditis elegans synaptic transmission mutants. Proc. Natl. Acad. Sci. USA 93: 12593– 12598. Miller, K. , M. D. Emerson and J. B. Rand, 1999 Go␣ and diacylglycerol kinase negatively regulate the Gq␣ pathway in C. elegans. Neuron 24: 323–333. , L. Segalat and J. M. Kaplan, 1999 Serotonin inhibition of synaptic transmission: G␣o decreases the abundance of UNC-13 at release sites.

Ten animals for each genotype were scored for 2 min and each animal was scored twice. Statistics were calculated by using directed Student’s t-tests. Movement levels were determined by measuring thrashing levels. One thrash is defined as one change in direction of bending at the mid-body (Miller et al. 1996). Animals were synchronized using NaOCl bleaching and were raised at 20Њ for 96 hr after synchronization using NaOCl. An animal was placed in microtiter plates with 50 ␮l M9 and allowed to recover for 2 min.

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analysis of diverse signal transduction pathways using the genetic model system caenorhabditis elegans celine moorman by Celine Moorman


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