Med5(Nut1) and Med17(Srb4) Are Direct Targets of Mediator Histone H4 Tail Interactions 英文参考文献.docVIP

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Med5(Nut1) and Med17(Srb4) Are Direct Targets of Mediator Histone H4 Tail Interactions 英文参考文献.doc

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Med5(Nut1) and Med17(Srb4) Are Direct Targets of Mediator Histone H4 Tail Interactions 英文参考文献

Med5(Nut1)andMed17(Srb4)AreDirectTargetsof MediatorHistoneH4TailInteractions ZhongleLiu,LawrenceC.Myers* DepartmentofBiochemistry,DartmouthMedicalSchool,Hanover,NewHampshire,UnitedStatesofAmerica Abstract The Mediator complex transmits activation signals from DNA bound transcription factors to the core transcription machinery.Inadditiontoitscanonicalroleintranscriptionalactivation,recentstudieshavedemonstratedthatS.cerevisiae Mediatorcaninteractdirectlywithnucleosomes,andtheirhistonetails.MutationsinMediatorsubunitshaveshownthat Mediatorandcertainchromatinstructuresmutuallyimpacteachotherstructurallyandfunctionallyinvivo.Wehavetakena UV photo cross-linking approach to further delineate the molecular basis of Mediator chromatin interactions and help determine whether the impact of certain Mediator mutants on chromatin is direct. Specifically, by using histone tail peptides substituted with an amino acid analog that is a UV activatible crosslinker, we have identified specific subunits within Mediator that participate in histone tail interactions. Using Mediator purified from mutant yeast strains we have evaluatedtheimpactofthesesubunitsonhistonetailbinding.ThisanalysishasidentifiedtheMed5subunitofMediatoras a target for histone tail interactions and suggests that the previously observed effect of med5 mutations on telomeric heterochromatinandsilencingisdirect. Citation:LiuZ,MyersLC(2012)Med5(Nut1)andMed17(Srb4)AreDirectTargetsofMediatorHistoneH4TailInteractions.PLoSONE7(6):e38416.doi:10.1371/ journal.pone.0038416 Editor:MaryBryk,TexasAMUniversity,UnitedStatesofAmerica ReceivedMarch23,2012;AcceptedMay9,2012;PublishedJune5,2012 Copyright: ? 2012 Liu, Myers. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited. Funding:ThisworkwassupportedbyNationalInstituteofGeneralMedicalSciencesgrantR01GM62483(LCM).The