Mechanisms Employed by Escherichia coli to Prevent Ribonucleotide Incorporation into Genomic DNA by Pol V 英文参考文献.docVIP

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Mechanisms Employed by Escherichia coli to Prevent Ribonucleotide Incorporation into Genomic DNA by Pol V 英文参考文献.doc

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Mechanisms Employed by Escherichia coli to Prevent Ribonucleotide Incorporation into Genomic DNA by Pol V 英文参考文献

MechanismsEmployedbyEscherichiacolitoPrevent RibonucleotideIncorporationintoGenomicDNAbyPolV JohnP.McDonald1,AlexandraVaisman1,WojciechKuban1,MyronF.Goodman2,RogerWoodgate1* 1Laboratory of Genomic Integrity, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America,2DepartmentsofBiologicalSciencesandChemistry,UniversityofSouthernCalifornia,LosAngeles,California,UnitedStatesofAmerica Abstract EscherichiacolipolV(UmuD92C),themaintranslesionDNApolymerase,ensurescontinuednascentstrandextensionwhen thecellular replicaseisblockedbyunrepairedDNAlesions.PolVischaracterized bylowsugarselectivity,whichcanbe furtherreducedbyaY11A‘‘steric-gate’’substitutioninUmuCthatenablespolVtopreferentiallyincorporaterNTPsover dNTPs in vitro. Despite efficient error-prone translesion synthesis catalyzed by UmuC_Y11A in vitro, strains expressing umuC_Y11AexhibitlowUVmutabilityandUVresistance.Here,weshowthatthesephenotypesresultfromtheconcomitant dual actions of Ribonuclease HII (RNase HII) initiating removal of rNMPs from the nascent DNA strand and nucleotide excisionrepair(NER)removingUVlesionsfromtheparentalstrand.Intheabsenceofeitherrepairpathway,UVresistance andmutagenesisconferredbyumuC_Y11Aissignificantlyenhanced,suggestingthatthecombinedactionsofRNaseHII andNERleadtodouble-strandbreaksthatresultinreducedcellviability.WepresentevidencethattheY11A-specificUV phenotype is tempered by pol IV in vivo. At physiological ratios of the two polymerases, pol IV inhibits pol V–catalyzed translesionsynthesis(TLS)pastUVlesionsandsignificantlyreducesthenumberofY11A-incorporatedrNTPsbylimitingthe length of the pol V–dependent TLS tract generated during lesion bypass in vitro. In a recA730 lexA(Def) DumuDC DdinB strain, plasmid-encoded wild-type pol V promotes high levels of spontaneous mutagenesis. However, umuC_Y11A- dependentspontaneousmutagenesisisonly,7%ofthatobservedwithwild-typepolV,butincreasesto,39%ofwild- type