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Activation of Protein Kinase A-Independent Pathways by Gsα in Drosophila
William J. Wolfgang, Ian J. H. Roberts, Frank Quan, Cahir O'Kane and Michael Forte
Proceedings of the National Academy of Sciences of the United States of America
Vol. 93, No. 25 (Dec. 10, 1996), pp. 14542-14547
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/41120
Page Count: 6
You can always find the topics here!Topics: Epithelial cells, Blisters, Phenotypes, Drosophila, Genetics, Genetic mutation, Cultured cells, Somatic cells, Cells, Integrins
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One of the best-described transmembrane signal transduction mechanisms is based on receptor activation of the α subunit of the heterotrimeric G protein Gs, leading to stimulation of adenylyl cyclase and the production of cAMP. Intracellular cAMP is then thought to mediate its effects largely, if not entirely, by activation of protein kinase A and the subsequent phosphorylation of substrates which in turn control diverse cellular phenomena. In this report we demonstrate, by two different methods, that reduction or elimination of protein kinase A activity had no effect on phenotypes generated by activation of Gsα pathways in Drosophila wing epithelial cells. These genetic studies show that the Gsα pathway mediates its primary effects by a novel pathway in differentiating wing epithelial cells. This novel pathway may in part be responsible for some of the complex, cell-specific responses observed following activation of this pathway in different cell types.
Proceedings of the National Academy of Sciences of the United States of America © 1996 National Academy of Sciences