Excess Single-Stranded DNA Inhibits Meiotic Double-Strand Break Repair 英文参考文献.docVIP

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Excess Single-Stranded DNA Inhibits Meiotic Double-Strand Break Repair 英文参考文献.doc

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Excess Single-Stranded DNA Inhibits Meiotic Double-Strand Break Repair 英文参考文献

ExcessSingle-StrandedDNAInhibitsMeiotic Double-StrandBreakRepair Rebecca Johnson1[¤a,Vale′rie Borde2[,Matthew J.Neale1[¤b,Anna Bishop-Bailey1,Matthew North1¤c, Sheila Harris1¤d,Alain Nicolas2,Alastair S.H.Goldman1* 1DepartmentofMolecularBiologyandBiotechnology,UniversityofSheffield,Sheffield,UnitedKingdom,2InstitutCurie,CentredeRecherche,RecombinaisonetInstabilite GenetiqueUMR7147CNRSUniversite′ P.etM.Curie,Paris,France During meiosis, self-inflicted DNA double-strand breaks (DSBs) are created by the protein Spo11 and repaired by homologous recombination leading to gene conversions and crossovers. Crossover formation is vital for the segregationofhomologouschromosomesduringthefirstmeioticdivisionandrequirestheRecAorthologue,Dmc1.We analyzedrepairduringmeiosisofsite-specificDSBscreatedbyanothernuclease,VMA1-derivedendonuclease(VDE),in cells lacking Dmc1 strand-exchange protein. Turnover and resection of the VDE-DSBs was assessed in two different reporter cassettes that can repair using flanking direct repeat sequences, thereby obviating the need for a Dmc1- dependent DNA strand invasion step. Access of the single-strand binding complex replication protein A, which is normallyusedinallmodesofDSBrepair,wascheckedinchromatinimmunoprecipitationexperiments,usingantibody against Rfa1. Repair of the VDE-DSBs was severely inhibited in dmc1D cells, a defect that was associated with a reduction in the long tract resection required to initiate single-strand annealing between the flanking repeat sequences. Mutants that either reduce Spo11-DSB formation or abolish resection at Spo11-DSBs rescued the repair block. We also found that a replication protein A component, Rfa1, does not accumulate to expected levels at unrepairedsingle-strandedDNA(ssDNA)indmc1Dcells.TherequirementofDmc1forVDE-DSBrepairusingflanking repeatsappearstobecausedbytheaccumulationoflargequantitiesofssDNAthataccumulateatSpo11-DSBswhen Dmc1isabsent.WeproposethattheseresectedDSBssequesterbothresectionmachi