By Celine Moorman
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Extra resources for analysis of diverse signal transduction pathways using the genetic model system caenorhabditis elegans celine moorman
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.
analysis of diverse signal transduction pathways using the genetic model system caenorhabditis elegans celine moorman by Celine Moorman