ETS-4 Is a Transcriptional Regulator of Life Span in Caenorhabditis elegans 英文参考文献.docVIP

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ETS-4 Is a Transcriptional Regulator of Life Span in Caenorhabditis elegans 英文参考文献.doc

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ETS-4 Is a Transcriptional Regulator of Life Span in Caenorhabditis elegans 英文参考文献

ETS-4IsaTranscriptionalRegulatorofLifeSpanin Caenorhabditiselegans BargaviThyagarajan1¤a,AdamG.Blaszczak1¤b,KatherineJ.Chandler1,JenniferL.Watts2,W.Evan Johnson1,3,BarbaraJ.Graves1* 1HuntsmanCancerInstitute,DepartmentofOncologicalSciences,UniversityofUtah,SaltLakeCity,Utah,UnitedStatesofAmerica,2SchoolofMolecularBiosciences, WashingtonStateUniversity,Pullman,Washington,UnitedStatesofAmerica,3DepartmentofStatistics,BrighamYoungUniversity,Provo,Utah,UnitedStatesofAmerica Abstract Aging is a complex phenotype responsive to a plethora of environmental inputs; yet only a limited number of transcriptionalregulatorsareknowntoinfluencelifespan.Howthedownstreamexpressionprogramsmediatedbythese factors (or others) are coordinated into common or distinct set of aging effectors is an addressable question in model organisms, such as C. elegans. Here, we establish the transcription factor ETS-4, an ortholog of vertebrate SPDEF, as a longevity determinant. Adult worms with ets-4 mutations had a significant extension of mean life span. Restoring ETS-4 activity in the intestine, but not neurons, of ets-4 mutant worms rescued life span to wild-type levels. Using RNAi, we demonstratedthatets-4isrequiredpost-developmentallytoregulateadultlifespan;thusuncouplingtheroleofETS-4in aging from potential functions in worm intestinal development. Seventy ETS-4-regulated genes, identified by gene expressionprofilingoftwodistinctets-4allelesandanalyzedbybioinformatics,wereenrichedforknownlongevityeffectors thatfunctioninlipidtransport,lipidmetabolism,andinnateimmunity.Putativetargetgeneswereenrichedforonesthat change expression during normal aging, the majority of which are controlled by the GATA factors. Also, some ETS-4- regulated genes function downstream of the FOXO factor, DAF-16 and the insulin/IGF-1 signaling pathway. However, epistasisandphenotypicanalysesindicatethatets-4functionedinparalleltotheinsulin/IGF-1receptor,daf-2andakt-1/2 kinases. Furthermore, ets-4 required daf-16 to modul