Genetic Variation for Cardiac Dysfunction in Drosophila 英文参考文献.docVIP

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Genetic Variation for Cardiac Dysfunction in Drosophila 英文参考文献.doc

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Genetic Variation for Cardiac Dysfunction in Drosophila 英文参考文献

GeneticVariationforCardiacDysfunctioninDrosophila KarenA.Ocorr1.,TimothyCrawley1.,GregGibson2*,RolfBodmer1* 1CenterforNeuroscienceand Aging,TheBurnhamInstitutefor MedicalResearch,LaJolla,California,UnitedStatesof America,2Departmentof Genetics,NorthCarolinaStateUniversity,Raleigh,NorthCarolina,UnitedStatesofAmerica Background.Commondiseasesmaybeattributedtocombinationsofvariantalleles,buttherearefewmodelsystemswhere theinteractionsamongsuchvariantscanbestudiedincontrolledgeneticcrosses.Whileassociationstudiesaredesignedto detect common polymorphisms of moderate effect, new approaches are required to characterize the impact on disease of interactions among rare alleles. Methodology/Principal Findings. We show that wild populations of Drosophila melanogaster harborrarepolymorphismsofmajoreffect(RAME)thatpredisposefliestoaspecificdiseasephenotype,age- dependent cardiac dysfunction. A screen of fifty inbred wild-type lines revealed a continuous spectrum of pacing-induced heartfailurethatgenerallyincreasesinfrequencywithage.High-speedvideoanalysisoftheinbredlineswithhighratesof inducible heart failure indicates specific defects in cardiac function, including arrhythmias and contractile disorders (‘cardiomyopathies’).Acombinationofbulkedsegregantanalysisandsinglefeaturepolymorphism(SFP)detectionlocalizes oneofthecardiacsusceptibilitylocitothe97Cintervalontheflygenome.Conclusions/Significance.Wild-typeDrosophila, likehumans,arepredisposedtocardiacdysfunction.Identificationoffactorsassociatedwiththesenaturallyoccurringcardiac traitspromisestoprovideimportantinsightsintotheepidemiologyofcardiacdisease. Citation: OcorrKA,CrawleyT,GibsonG,BodmerR(2007)GeneticVariationforCardiacDysfunctioninDrosophila.PLoSONE2(7):e601.doi:10.1371/ journal.pone.0000601 INTRODUCTION models also need to be considered. Rare alleles of major effect, includingcompletelossoffunctionmutations,individuallyarenot expected to contribute measurably to risk in a population, but hundredsofrecessi