Sex Reversal in C57BL6J XY Mice Caused by Increased Expression of Ovarian Genes and Insufficient Activation of the Testis Determining Pathway 英文参考文献.docVIP

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Sex Reversal in C57BL6J XY Mice Caused by Increased Expression of Ovarian Genes and Insufficient Activation of the Testis Determining Pathway 英文参考文献.doc

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Sex Reversal in C57BL6J XY Mice Caused by Increased Expression of Ovarian Genes and Insufficient Activation of the Testis Determining Pathway 英文参考文献

SexReversalinC57BL/6JXYMiceCausedbyIncreased ExpressionofOvarianGenesandInsufficientActivation oftheTestisDeterminingPathway StephanieM.Correa1,LindaL.Washburn2,RaviS.Kahlon1,MichelleC.Musson1,GerritJ.Bouma2,3, EvaM.Eicher2,KennethH.Albrecht1,2* 1DepartmentofMedicine,BiomedicalGenetics,BostonUniversitySchoolofMedicine,Boston,Massachusetts,UnitedStatesofAmerica,2TheJacksonLaboratory,Bar Harbor, Maine, United States of America, 3Animal Reproduction and Biotechnology Laboratory, Department of Biomedical Sciences, Colorado State University, Fort Collins,Colorado,UnitedStatesofAmerica Abstract SexreversalcanoccurinXYhumanswithonlyasinglefunctionalWT1orSF1alleleoraduplicationofthechromosome regioncontainingWNT4.Incontrast,XYmicewithonlyasinglefunctionalWt1,Sf1,orWnt4allele,ormicethatover-express Wnt4 from a transgene, reportedly are not sex-reversed. Because genetic background plays a critical role in testis differentiation,particularlyinC57BL/6J(B6)mice,wetestedthehypothesisthatWt1,Sf1,andWnt4aredosagesensitivein B6XYmice.WefoundthatreducedWt1orSf1dosageinB6XYB6miceimpairedtestisdifferentiation,butnoovariantissue AKR B6 developed.If,however,aY chromosomereplacedtheY chromosome,theseotherwisegeneticallyidenticalB6XYmice developedovariantissue.Incontrast,reducedWnt4dosageincreasedtheamountoftesticulartissuepresentinSf1+/2B6 ,Wt1 /2B6XY ,B6XY ,andB6XY AKR + AKR POS AKR B6 B6 fetuses.WeproposethatWt1 andSf1 arehypomorphicallelesoftestis- XY determiningpathwaygenesandthatWnt4B6 is ahypermorphic allele ofanovary-determiningpathwaygene.Thelatter hypothesisissupportedbythefindingthatexpressionofWnt4andfourothergenesintheovary-determiningpathwayare elevatedinnormalB6XXE12.5ovaries.WeproposethatB6micearesensitivetoXYsexreversal,atleastinpart,because they carry Wt1B6 and/or Sf1B6 alleles that compromise testis differentiation and a Wnt4B6 allele that promotes ovary differentiationandtherebyantagonizestestisdifferentiation.Additionofa