Autophagy Protein Atg3 is Essential for Maintaining Mitochondrial Integrity and for Normal Intracellular Development of Toxoplasma gondii Tachyzoites 英文参考文献.docVIP

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Autophagy Protein Atg3 is Essential for Maintaining Mitochondrial Integrity and for Normal Intracellular Development of Toxoplasma gondii Tachyzoites 英文参考文献.doc

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Autophagy Protein Atg3 is Essential for Maintaining Mitochondrial Integrity and for Normal Intracellular Development of Toxoplasma gondii Tachyzoites 英文参考文献

AutophagyProteinAtg3isEssentialforMaintaining MitochondrialIntegrityandforNormalIntracellular DevelopmentofToxoplasmagondiiTachyzoites Se′bastienBesteiro1,2*,CarrieF.Brooks3,BorisStriepen3,Jean-Franc?oisDubremetz1 1UMR5235CNRS,Universite′sdeMontpellier2et1,DynamiquedesInteractionsMembranairesNormalesetPathologiques,Montpellier,France,2INSERM,Dynamique des Interactions Membranaires Normales et Pathologiques, Montpellier, France, 3Center for Tropical and Emerging Global Diseases, University of Georgia, Athens, Georgia,UnitedStatesofAmerica Abstract Autophagyisacellularprocessthatishighlyconservedamongeukaryotesandpermitsthedegradationofcellularmaterial. Autophagyisinvolvedinmultiplesurvival-promotingprocesses.Itnotonlyfacilitatesthemaintenanceofcellhomeostasis by degrading long-lived proteins and damaged organelles, but it also plays a role in cell differentiation and cell development. Equally important is its function for survival in stress-related conditions such as recycling of proteins and organelles during nutrient starvation. Protozoan parasites have complex life cycles and face dramatically changing environmentalconditions;whetherautophagyrepresentsacriticalcopingmechanismthroughoutthesechangesremains poorly documented. To investigate this in Toxoplasma gondii, we have used TgAtg8 as an autophagosome marker and showedthatautophagyandtheassociatedcellularmachineryarepresentandfunctionalintheparasite.InextracellularT. gondiitachyzoites,autophagosomeswereinducedinresponsetoaminoacidstarvation,buttheycouldalsobeobservedin cultureduringthenormalintracellulardevelopmentoftheparasites.Moreover,wegeneratedaconditionalT.gondiimutant lacking the orthologue of Atg3, a key autophagy protein. TgAtg3-depleted parasites were unable to regulate the conjugation of TgAtg8 to the autophagosomal membrane. The mutant parasites also exhibited a pronounced fragmentationoftheirmitochondrionandadrasticgrowthphenotype.Overall,ourresultsshowthatTgAtg3-dependent autophagymightberegula