|Title:||Control of cell fate determination by p21ras/Ras1, an essential component of torso signaling in Drosophila||Authors:||Lu, X.
|Keywords:||Drosophila; Kinase; Pattern formation; Ras; Signal transduction; Sos||Issue Date:||1993||Journal Volume:||7||Journal Issue:||4||Start page/Pages:||621-632||Source:||Genes and Development||Abstract:||
Determination of cell fate at the posterior termini of the Drosophila embryo is specified by the activation of the torso (tor) receptor tyrosine kinase. This signaling pathway is mediated by the serine/threonine kinase D-raf and a protein tyrosine phosphatase corkscrew (csw). We found that expression of an activated form of Ras1 during oogenesis resulted in embryos with tor gain-of-function phenotypes. To demonstrate that p21(ras)/Ras1 mediates tor signaling, we injected mammalian p21(ras) variants into early Drosophila embryos. We found that the injection of activated p21(v-ras) rescued the maternal-effect phenotypes of both tor and csw null mutations. These rescuing effects of p21(v-ras) are dependent on the presence of maternally derived D-raf activity. In addition, wild-type embryos show a terminal-class phenotype resembling csw when injected with p21(rasN17), a dominant-negative form of p21(ras). Furthermore, we have analyzed the maternal-effect phenotype of Son of sevenless (Sos), a positive regulator of Ras1, and showed that embryos derived from germ cells lacking Sos+ activity exhibit a terminal-class phenotype. Our study demonstrates that the Drosophila p21(ras) encoded by Ras1, is an intrinsic component of the tor signaling pathway, where it is both necessary and sufficient in specifying posterior terminal cell fates. p21(ras)/Ras1 operates upstream of the D-raf kinase in this signaling pathway.
|ISSN:||08909369||SDG/Keyword:||mutant protein; protein p21; protein serine threonine kinase; Ras protein; regulator protein; article; cell differentiation; embryo; enzyme activation; female; gene expression; microinjection; nonhuman; oocyte development; phenotype; priority journal; protein variant; regulator gene; signal transduction; Mammalia; Mammalia|
|Appears in Collections:||分子與細胞生物學研究所|
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