Absence of Ataxin-3 Leads to Enhanced Stress Response in C. elegans 英文参考文献.docVIP

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Absence of Ataxin-3 Leads to Enhanced Stress Response in C. elegans 英文参考文献.doc

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Absence of Ataxin-3 Leads to Enhanced Stress Response in C. elegans 英文参考文献

AbsenceofAtaxin-3LeadstoEnhancedStressResponse inC.elegans AnaJoa?oRodrigues1.,AndreiaNeves-Carvalho1.,AndreiaTeixeira-Castro1,AnneRokka2 ,Garry Corthals2,ElsaLogarinho1,3,Patr?′ciaMaciel1* 1LifeandHealthSciencesResearchInstitute(ICVS),SchoolofHealthSciences,UniversityofMinho,Braga,Portugal,2TurkuCentreforBiotechnology,UniversityofTurku andAboAkademiUniversity,Turku,Finland,3InstitutodeBiologiaMoleculareCelular(IBMC),Porto,Portugal Abstract Ataxin-3, the protein involved in Machado-Joseph disease, is able to bind ubiquitylated substrates and act as a deubiquitylating enzyme in vitro, and it has been involved in the modulation of protein degradation by the ubiquitin- proteasomepathway.C.elegansandmouseataxin-3knockoutmodelsareviableandwithoutanyobviousphenotypeina basalconditionhowevertheirphenotypeinstresssituationshasneverbeendescribed. Consideringtheroleofataxin-3in theproteindegradationpathway,weanalyzedtheeffectsofheatshock,aknownproteinhomeostasisstressor,inC.elegans ataxin-3 (ATX-3) knockout animals. We found that ATX-3 mutants have an exacerbated stress response and survive significantly better than wild type animals when subjected to a noxious heat shock stimulus. This increased thermotolerance of mutants was further enhanced by pre-exposure to a mild heat shock. At a molecular level, ATX-3 mutantshaveadistincttranscriptomicandproteomicprofilewithseveralmolecularchaperonesabnormallyup-regulated duringheatshockandrecovery,consistentwiththeobservedresistancephenotype. TheimprovedthermotoleranceinATX- 3mutantsisindependentofheatshockfactor1,themaestrooftheheatshockresponse,butfullydependentonDAF-16,a criticalstressresponsivetranscriptionfactorinvolvedinlongevityandstressresistance.Wealsoshowthattheincreased thermotoleranceofATX-3mutantsismainlyduetoHSP-16.2,C12C8.1andF44E5.5giventhattheknockdownoftheseheat shock proteins using RNA interference causes the phenotype to revert. This report suggests that the absence of ATX-3 activatestheDAF-16pathwayle