Dicty News Electronic Edition Volume 17, number 3 August 3, 2001 Please submit abstracts of your papers as soon as they have been accepted for publication by sending them to dicty@northwestern.edu. Back issues of Dicty-News, the Dicty Reference database and other useful information is available at DictyBase--http://dictybase.org. ============== Abstracts ============== RasC is required for optimal activation of adenylyl cyclase and Akt/PKB during aggregation. Chinten James Lim, George B. Spiegelman, and Gerald Weeks. Department of Microbiology and Immunology, Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, V6T 1Z3 Canada. EMBO J., in press. ABSTRACT Disruption of Dictyostelium rasC, encoding a Ras subfamily protein, generated cells incapable of aggregation. While rasC expression is enriched in a cell type specific manner during post-aggregative development, the defect in rasC- cells is restricted to aggregation and fully corrected by application of exogenous cAMP pulses. cAMP is not produced in rasC- cells stimulated by 2'-deoxy-cAMP, but is produced in response to GTPgS in cell lysates, indicating that G-protein coupled cAMP receptor activation of adenylyl cyclase is regulated by RasC. However, cAMP induced ERK2 phosphorylation is unaffected in rasC- cells, indicating RasC is not an upstream activator of the MAPK required for cAMP relay. rasC- cells also exhibit reduced chemotaxis to cAMP during early development and delayed response to periodic cAMP stimuli produced by wildtype cells in chimeric mixtures. Furthermore, cAMP induced Akt/PKB phosphorylation through a PI3K dependent pathway is dramatically reduced in rasC- cells, suggesting that G-protein coupled serpentine receptor activation of PI3K is regulated by RasC. Cells lacking the RasGEF, AleA, exhibit similar defects as rasC- cells, suggesting that AleA may activate RasC. ----------------------------------------------------------------------------- [End Dicty News, volume 17, number 3]