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Morey, M., Corominas, M., Serras, F. (2003). DIAP1 suppresses ROS-induced apoptosis caused by impairment of the selD/sps1 homolog in Drosophila.  J. Cell Sci. 116(22): 4597--4604.
FlyBase ID
FBrf0167775
Publication Type
Research paper
Abstract

The cellular antioxidant defense systems neutralize the cytotoxic by-products referred to as reactive oxygen species (ROS). Among them, selenoproteins have important antioxidant and detoxification functions. The interference in selenoprotein biosynthesis results in accumulation of ROS and consequently in a toxic intracellular environment. The resulting ROS imbalance can trigger apoptosis to eliminate the deleterious cells. In Drosophila, a null mutation in the selD gene (homologous to the human selenophosphate synthetase type 1) causes an impairment of selenoprotein biosynthesis, a ROS burst and lethality. We propose this mutation (known as selDptuf) as a tool to understand the link between ROS accumulation and cell death. To this aim we have analyzed the mechanism by which selDptuf mutant cells become apoptotic in Drosophila imaginal discs. The apoptotic effect of selDptuf does not require the activity of the Ras/MAPK-dependent proapoptotic gene hid, but results in stabilization of the tumor suppressor protein Dmp53 and transcription of the Drosophila pro-apoptotic gene reaper (rpr). We also provide genetic evidence that the initiator caspase DRONC is activated and that the effector caspase DRICE is processed to commit selDptuf mutant cells to death. Moreover, the ectopic expression of the inhibitor of apoptosis DIAP1 rescues the cellular viability of selDptuf mutant cells. These observations indicate that selDptuf ROS-induced apoptosis in Drosophila is mainly driven by the caspase-dependent Dmp53/Rpr pathway.

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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    J. Cell Sci.
    Title
    Journal of Cell Science
    Publication Year
    1966-
    ISBN/ISSN
    0021-9533
    Data From Reference
    Genes (14)