Evolution of a New Function by Degenerative Mutation in Cephalochordate Steroid Receptors 英文参考文献.docVIP

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Evolution of a New Function by Degenerative Mutation in Cephalochordate Steroid Receptors 英文参考文献.doc

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Evolution of a New Function by Degenerative Mutation in Cephalochordate Steroid Receptors 英文参考文献

EvolutionofaNewFunctionbyDegenerativeMutation inCephalochordateSteroidReceptors JamieT.Bridgham1,JustineE.Brown1,AdrianaRodr?′guez-Mar?′2,JulianM.Catchen2,3,JosephW. Thornton1* 1CenterforEcologyandEvolutionaryBiology,UniversityofOregon,Eugene,Oregon,UnitedStatesofAmerica,2InstituteofNeuroscience,UniversityofOregon,Eugene, Oregon,UnitedStatesofAmerica,3DepartmentofComputerandInformationScience,UniversityofOregon,Eugene,Oregon,UnitedStatesofAmerica Abstract Gene duplication is the predominant mechanism for the evolution of new genes. Major existing models of this process assume that duplicate genes are redundant; degenerative mutations in one copy can therefore accumulate close to neutrally,usuallyleadingtolossfromthegenome.Whengeneproductsdimerizeorinteractwithothermoleculesfortheir functions,however,degenerativemutationsinonecopymayproducerepressorallelesthatinhibitthefunctionoftheother andarethereforeexposedtoselection.Here,wedescribetheevolutionofaduplicaterepressorbysimpledegenerative mutations in the steroid hormone receptors (SRs), a biologically crucial vertebrate gene family. We isolated and characterized the SRs of the cephalochordate Branchiostoma floridae, which diverged from other chordates just after duplication of the ancestral SR. The B. floridae genome contains two SRs: BfER, an ortholog of the vertebrate estrogen receptors, and BfSR, an ortholog of the vertebrate receptors for androgens, progestins, and corticosteroids. BfSR is specifically activated by estrogens and recognizes estrogen response elements (EREs) in DNA; BfER does not activate transcription in responsetosteroid hormones but binds EREs, where itcompetitively repressesBfSR. The twogenesare partiallycoexpressed,particularlyinovaryandtestis,suggestinganancientroleingermcelldevelopment.Theseresults corroboratepreviousfindingsthattheancestralsteroidreceptorwasestrogen-sensitiveandindicatethat,afterduplication, BfSRretainedtheancestralfunction,whileBfERevolvedthecapacitytonegativelyregulate