Replication and Recombination Factors Contributing to Recombination-Dependent Bypass of DNA Lesions by Template Switch 英文参考文献.docVIP

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Replication and Recombination Factors Contributing to Recombination-Dependent Bypass of DNA Lesions by Template Switch 英文参考文献.doc

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Replication and Recombination Factors Contributing to Recombination-Dependent Bypass of DNA Lesions by Template Switch 英文参考文献

ReplicationandRecombinationFactorsContributingto Recombination-DependentBypassofDNALesionsby TemplateSwitch FabioVanoli1.¤,MarcoFumasoni1,2.,BarnabasSzakal1,LaurentMaloisel3,DanaBranzei1* 1FondazioneIFOM,IstitutoFIRCdiOncologiaMolecolare,Milan,Italy,2Universita`degliStudidiMilano,Milan,Italy,3CEA,DSV,iRCM,SIGRR,LRGM,andCNRS,UMR217, Fontenay-aux-Roses,France Abstract Damagetolerancemechanismsmediatingdamage-bypassandgap-fillingarecrucialforgenomeintegrity.Amajordamage tolerance pathway involves recombination and is referred to as template switch. Template switch intermediates were visualizedby2DgelelectrophoresisintheproximityofreplicationforksasX-shapedstructuresinvolvingsisterchromatid junctions.ThehomologousrecombinationfactorRad51isrequiredfortheformation/stabilizationoftheseintermediates, butitsmodeofactionremainstobeinvestigated.Byusingacombinationofgeneticandphysicalapproaches,weshow thatthehomologousrecombinationfactorsRad55andRad57,butnotRad59,arerequiredfortheformationoftemplate switch intermediates. The replication-proficient but recombination-defective rfa1-t11 mutant is normal in triggering a checkpoint response following DNA damage but is impaired in X-structure formation. The Exo1 nuclease also has stimulatoryrolesinthisprocess.Thecheckpointkinase,Rad53,isrequiredforX-moleculeformationandphosphorylates Rad55robustlyinresponsetoDNAdamage.AlthoughRad55phosphorylationisthoughttoactivaterecombinationalrepair under conditions of genotoxic stress, we find that Rad55 phosphomutants do not affect the efficiency of X-molecule formation.WealsoexaminedtheDNApolymeraseimplicatedintheDNAsynthesisstepoftemplateswitch.Deficienciesin translesionsynthesispolymerasesdonotaffectX-moleculeformation,whereasDNApolymerased,requiredalsoforbulk DNAsynthesis,playsanimportantrole.Ourdataindicatethatasubsetofhomologousrecombinationfactors,togetherwith DNApolymerased,promotetheformationoftemplateswitchintermediatesthatarethenpreferentiallydissolvedbythe actionoftheSgs1helicaseinas