title: FOXO-independent suppression of programmed cell death by the PI3K/Akt signaling pathway in Drosophila.
abstract: Signaling through the PI3K/Akt/FOXO pathway plays an important role in vertebrates in protecting cells from programmed cell death. PI3K and Akt have been similarly shown to be involved in survival signaling in the invertebrate model organism Drosophila. However, it is not known whether PI3K and Akt execute this function by controlling a pro-apoptotic activity of Drosophila FOXO. In this study, we show that elevated signaling through PI3K and Akt can prevent developmentally controlled death in the salivary glands of the fruit fly. We further show that Drosophila FOXO is not required for normal salivary gland death and that the rescue of salivary gland death by PI3K occurs independent of FOXO. These results give support to the notion that FOXOs have acquired pro-apoptotic functions after separation of the vertebrate and invertebrate lineages.
authors.affiliation: Department of Biological Sciences, University of Arkansas, 601 Science Engineering, Fayetteville, AR 72701, USA.
authors.forename: Yanling
authors.initials: Y
authors.lastname: Liu
authors.forename: Michael
authors.initials: M
authors.lastname: Lehmann
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics; D004330:Drosophila / Q000201:enzymology / Q000235:genetics / Q000254:growth & development*; D029721:Drosophila Proteins / Q000235:genetics / Q000502:physiology*; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000502:physiology*; D009154:Mutation; D019869:Phosphatidylinositol 3-Kinases / Q000032:analysis / Q000502:physiology*; D051057:Proto-Oncogene Proteins c-akt / Q000032:analysis / Q000502:physiology*; D012469:Salivary Glands / Q000166:cytology / Q000201:enzymology / Q000254:growth & development*; D015398:Signal Transduction
chemical_list: D029721:Drosophila Proteins; C477334:FOXO protein, Drosophila; D051858:Forkhead Transcription Factors; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt