Functional Interactions between the eruptedtsg101 Growth Suppressor Gene and the DaPKC and rbf1 Genes in Drosophila Imaginal Disc Tumors 英文参考文献.docVIP

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Functional Interactions between the eruptedtsg101 Growth Suppressor Gene and the DaPKC and rbf1 Genes in Drosophila Imaginal Disc Tumors 英文参考文献.doc

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Functional Interactions between the eruptedtsg101 Growth Suppressor Gene and the DaPKC and rbf1 Genes in Drosophila Imaginal Disc Tumors 英文参考文献

FunctionalInteractionsbetweentheerupted/tsg101 GrowthSuppressorGeneandtheDaPKCandrbf1Genes inDrosophilaImaginalDiscTumors M.MelissaGilbert,BrianS.Robinson,KennethH.Moberg* DepartmentofCellBiology,EmoryUniversitySchoolofMedicine,Atlanta,Georgia,UnitedStatesofAmerica Abstract Background: The Drosophila gene erupted (ept) encodes the fly homolog of human Tumor Susceptibility Gene-101 (TSG101),whichfunctionsaspartoftheconservedESCRT-1complextofacilitatethemovementofcargoesthroughthe endolysosomalpathway.Lossofeptorothergenesthatencodecomponentsoftheendocyticmachinery(e.g.synatxin7/ avalanche,rab5,andvps25)producesdisorganizedovergrowthofimaginaldisctissue.Excesscelldivisionispostulatedto beaprimarycauseofthese‘neoplastic’phenotypes,buttheautonomouseffectofthesemutationsoncellcyclecontrolhas notbeenexamined. Principal Findings: Here we show that disc cells lacking ept function display an altered cell cycle profile indicative of deregulatedprogressionthroughtheG1-to-Sphasetransitionandexpressreducedlevelsofthetumorsuppressorortholog and G1/S inhibitor Rbf1. Genetic reductions of the Drosophila aPKC kinase (DaPKC), which has been shown to promote tumorgrowthinotherflytumormodels,preventboththeeptneoplasticphenotypeandthereductioninRbf1levelsthat otherwiseoccursinclonesofeptmutantcells;thiseffectiscoincidentwithchangesinlocalizationofNotchandCrumbs, two proteins whose sorting is altered in ept mutant cells. The effect on Rbf1 can also be blocked by removal of the c- secretasecomponentpresenilin,suggestingthatcleavageofac-secretasetargetinfluencesRbf1levelsineptmutantcells. Expressionofexogenousrbf1completelyablateseptmutanteyetissuesbutonlymildlyaffectsthedevelopmentofdiscs composedofcellswithwildtypeept. Conclusions:Together,thesedatashowthatlossofeptaltersnuclearcellcyclecontrolindevelopingimaginaldiscsand identifytheDaPKC,presenilin,andrbf1genesasmodifiersofmolecularandcellularphenotypesthatresultfromlossofept. Citation: GilbertMM,RobinsonBS, MobergKH(2009)FunctionalI