| Proteasome inhibition induces developmentally deregulated programs of apoptotic and autophagic cell death during Drosophila melanogaster oogenesis. | |
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MedLine Citation:
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PMID: 20819072 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Ubiquitin/proteasome-mediated degradation of eukaryotic proteins is critically implicated in a number of signalling pathways and cellular processes. To specifically impair proteasome activities, in vitro developing Drosophila melanogaster egg chambers were exposed to the MG132 or epoxomicin proteasome inhibitors, while a GAL4/UAS binary genetic system was employed to generate double transgenic flies overexpressing β2 and β6 conditional mutant proteasome subunits in a cell type-specific manner. MG132 and epoxomicin administration resulted in severe deregulation of in vitro developing egg chambers, which was tightly associated with precocious induction of nurse cell-specific apoptotic and autophagic death programmes, featured by actin cytoskeleton disorganization, nuclear chromatin condensation, DRICE caspase activation and autophagosome accumulation. In vivo targeted overexpression of β2 and β6 conditional mutants, specifically in the nurse cell compartment, led to a notable up-regulation of sporadic apoptosis potency during early and mid-oogenesis 'checkpoints', thus reasonably justifying the observed reduction in eclosion efficiency. Furthermore, in response to the intracellular abundance of β2 and β6 conditional mutant forms, specifically in numerous tissues of third instar larval stage, the developmental course was arrested, and lethal phenotypes were obtained at this particular embryonic period, with the double transgenic heterozygote embryos being unable to further proceed to complete maturation to adult flies. Our data demonstrate that physiological proteasome function is required to ensure normal oogenesis and embryogenesis in D. melanogaster, since targeted and cell type-dependent proteasome inactivation initiates developmentally deregulated apoptotic and autophagic mechanisms. |
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Authors:
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Panagiotis D Velentzas; Athanassios D Velentzas; Vassiliki E Mpakou; Issidora S Papassideri; Dimitrios J Stravopodis; Lukas H Margaritis |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Cell biology international Volume: 35 ISSN: 1095-8355 ISO Abbreviation: Cell Biol. Int. Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-12-01 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9307129 Medline TA: Cell Biol Int Country: England |
Other Details:
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Languages: eng Pagination: 15-27 Citation Subset: IM |
Affiliation:
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Faculty of Biology, Department of Cell Biology and Biophysics, University of Athens, Panepistimiopolis 157 84, Athens, Greece. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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