Alternative Epigenetic Chromatin States of Polycomb Target Genes 英文参考文献.docVIP

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Alternative Epigenetic Chromatin States of Polycomb Target Genes 英文参考文献.doc

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Alternative Epigenetic Chromatin States of Polycomb Target Genes 英文参考文献

AlternativeEpigeneticChromatinStatesofPolycomb TargetGenes YuriB.Schwartz1.,TatyanaG.Kahn1.,PerStenberg2,3,KatsuhitoOhno1,RichardBourgon4 ,Vincenzo Pirrotta1* 1Department of Molecular Biology and Biochemistry, Rutgers University, Nelson Laboratories, Piscataway, New Jersey, United States of America, 2Department of MolecularBiology,Umea?University,Umea?,Sweden,3ComputationalLifeScienceCluster,Umea?University,Umea?,Sweden,4EuropeanBioinformaticsInstitute,Wellcome TrustGenomeCampus,Hinxton,Cambridge,UnitedKingdom Abstract Polycomb(PcG)regulationhasbeenthoughttoproducestablelong-termgenesilencing.GenomicanalysesinDrosophila and mammals, however, have shown that it targets many genes, which can switch state during development. Genetic evidenceindicatesthatcriticalfortheactivestateofPcGtargetgenesarethehistonemethyltransferasesTrithorax(TRX) andASH1.HereweanalyzetherepertoireofalternativestatesinwhichPcGtargetgenesarefoundindifferentDrosophila celllinesandtheroleofPcGproteinsTRXandASH1incontrollingthesestates.Usingextensivegenome-widechromatin immunoprecipitation analysis, RNAi knockdowns, and quantitative RT–PCR, we show that, in addition to the known repressedstate,PcGtargetscanresideinatranscriptionallyactivestatecharacterizedbyformationofanextendeddomain enriched in ASH1, the N-terminal, but not C-terminal moiety of TRX and H3K27ac. ASH1/TRX N-ter domains and transcription are not incompatible with repressive marks, sometimes resulting in a ‘‘balanced’’ state modulated by both repressors and activators. Often however, loss of PcG repression results instead in a ‘‘void’’ state, lacking transcription, H3K27ac,orbindingofTRXorASH1.WeconcludethatPcGrepressionisdynamic,notstatic,andthatthepropensityofa targetgenetoswitchstatesdependsonrelativelevelsofPcG,TRX,andactivators.N-terTRXplaysaremarkablerolethat antagonizes PcG repression and preempts H3K27 methylation by acetylation. This role is distinct from that usually attributedtoTRX/MLLproteinsatthepromoter.Theseresultsha