New PDF release: analysis of diverse signal transduction pathways using the

By Celine Moorman

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N. OLSON and C. S. RUBIN, 1998 Structure, expression, and properties of an atypical protein kinase C (PKC3) from Caenorhabditis elegans. J Biol Chem 273: 1130-1143. , and M. HA N , 1994 Suppression of activated Let-60 ras protein defines a role of Caenorhabditis elegans Sur-1 MAP kinase in vulval differentiation. Genes Dev 8: 147-159. , N. TAVERNARAKIS and M. DRISCOLL, 2001 Necrotic cell death in C. elegans requires the function of calreticulin and regulators of Ca2+ release from the endoplasmic reticulum.

2001). Loss of function of goa-1 results in increased locomotion rates (Mendel et al. 1995; Segalat et al. 1995), whereas reduction of function of egl-30 results in decreased locomotion rates (Brundage et al. 1996). These G-protein pathways regulate diacylglycerol levels in an antagonistic manner (Lackner et al. 1999; Miller et al. 1999), either stimulating or inhibiting acetylcholine release through the diacylglycerol-binding protein, UNC-13. Our results show that there is yet another G-protein signaling cascade involved in locomotion: G␣s signals to the adenylyl cyclase SGS-1 to regulate locomotion.

The sgs-1 gene is ubiquitously expressed in the nervous system and muscle cells of C. elegans (Berger et al. 1998; Korswagen et al. 1998). A second adenylyl cyclase gene in C. elegans, acy-2, shows a more restricted expression pattern (Korswagen et al. 1998). This gene is not involved in G␣sinduced neuronal degeneration, but probably has an essential function together with G␣s in the canal-associated neurons of C. elegans (Korswagen et al. 1998). Over the last decade, great effort has been undertaken to understand the catalytic mechanism of adenylyl cyclase and its regulation.

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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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