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Nucleolar Protein Trafficking in Response to HIV-1 Tat Rewiring the Nucleolus 英文参考文献
NucleolarProteinTraffickinginResponsetoHIV-1Tat:
RewiringtheNucleolus
MohamedAliJarboui1,CarloBidoia1,ElenaWoods1,BarbaraRoe1,KieranWynne2,GiulianoElia2,
WilliamW.Hall1,VirginieW.Gautier1*
1CentreforResearchinInfectiousDiseases(CRID),SchoolofMedicineandMedicalScience(SMMS),UniversityCollegeDublin(UCD),Dublin,Ireland,2MassSpectrometry
Resource(MSR),ConwayInstituteforBiomolecularandBiomedicalResearch,UniversityCollegeDublin(UCD),Dublin,Ireland
Abstract
Thetrans-activatorTatproteinisaviralregulatoryproteinessentialforHIV-1replication.Tattraffickstothenucleoplasm
andthenucleolus.Thenucleolus,ahighlydynamicandstructuredmembrane-lesssub-nuclearcompartment,isthesiteof
rRNAandribosomebiogenesisandisinvolvedinnumerouscellularfunctionsincludingtranscriptionalregulation,cellcycle
controlandviralinfection.Importantly,transientnucleolartraffickingofbothTatandHIV-1viraltranscriptsarecriticalin
HIV-1replication,however,therole(s)ofthenucleolusinHIV-1replicationremainsunclear.Tobetterunderstandhowthe
interactionofTatwiththenucleolarmachinerycontributestoHIV-1pathogenesis,weinvestigatedthequantitativechanges
in the composition of the nucleolar proteome of Jurkat T-cells stably expressing HIV-1 Tat fused to a TAP tag. Using an
organellarproteomicapproachbasedonmassspectrometry,coupledwithStableIsotopeLabellinginCellculture(SILAC),
wequantified520proteins,including49proteinsshowingsignificantchangesinabundanceinJurkatT-cellnucleolusupon
Tat expression. Numerous proteins exhibiting afold change werewell characterised Tat interactors and/or known tobe
critical for HIV-1 replication. This suggests that the spatial control and subcellular compartimentaliation of these cellular
cofactors by Tat provide an additional layer of control for regulating cellular machinery involved in HIV-1 pathogenesis.
PathwayanalysisandnetworkreconstructionrevealedthatTatexpressionspecificallyresultedinthenucleolarenrichment
ofproteinscollectivelyparticipatinginribosomalbiogenesis,proteinhomeostasis,metaboli
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