Methicillin-Resistance in Staphylococcus aureus Is Not Affected by the Overexpression in Trans of the mecA Gene Repressor A Surprising Observation 英文参考文献.docVIP

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Methicillin-Resistance in Staphylococcus aureus Is Not Affected by the Overexpression in Trans of the mecA Gene Repressor A Surprising Observation 英文参考文献.doc

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Methicillin-Resistance in Staphylococcus aureus Is Not Affected by the Overexpression in Trans of the mecA Gene Repressor A Surprising Observation 英文参考文献

Methicillin-ResistanceinStaphylococcusaureusIsNot AffectedbytheOverexpressioninTransofthemecA GeneRepressor:ASurprisingObservation DuarteC.Oliveira1,2*¤,Herm?′niadeLencastre1,2 1Laboratory of Molecular Genetics, Instituto de Tecnologia Qu?′mica e Biolo′gica, Universidade Nova de Lisboa, Oeiras, Portugal, 2Laboratory of Microbiology, The RockefellerUniversity,NewYork,NewYork,UnitedStatesofAmerica Abstract Methicillin-resistant Staphylococcus aureus (MRSA) is intrinsically cross-resistant to virtually all b-lactam antibiotics. The central determinant for the MRSA phenotype is the mecA gene, whose transcriptional control may be mediated by a repressor(mecI)andasensor/inducer(mecR1).ThemecI-mecR1-mediatedinductionofmecAtakesseveralhoursrendering thestrainsphenotypicallysusceptibleinspiteofthepresenceoftheresistancegene.Therefore,ithasbeenproposedthat thefullresistancetob-lactamsobservedinmanycontemporaryclinicalMRSAstrainsrequiresanon-functionalmecI-mecR1 regulatorysystem.ThemecAgeneisembeddedinalargechromosomalcassette(theSCCmecelement)forwhichseveral structural types have been described. Some epidemic MRSA clones, typically expressing full b-lactam resistance, carry SCCmecelementsthatcontainanintactmecI-mecR1locus(e.g.SCCmectypesIIandIII).Wehaveaddressedthisapparent contradictionbyfirstsequencingthemecIcodingregionandmecApromotersequencesinacollectionofprototypeMRSA strainscharacterizedbydifferentSCCmectypes.Aconservednon-sensemutationwithinmecIwasdetectedinallSCCmec typeIIIstrainstested,presumablyresponsibleforanon-functionaltruncatedMecIproteinand,therefore,explainingthefull resistancephenotype.InSCCmectypeIIstrainsnoconservedmutationswerefound.Wenexttransformedacollectionof prototypeMRSAepidemicstrainswitharecombinantplasmidoverexpressingawild-typecopyofmecI.Surprisingly,forthe greatmajorityofthestrainsnosignificantalterationsinthephenotypicexpressionofb-lactamresistancecouldbedetected. Thesefindingswereconfirmedandfurtherexplored,challengingthecurrentlyacceptedm