Mice Lacking Alkbh1 Display Sex-Ratio Distortion and Unilateral Eye Defects 英文参考文献.docVIP

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Mice Lacking Alkbh1 Display Sex-Ratio Distortion and Unilateral Eye Defects 英文参考文献.doc

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Mice Lacking Alkbh1 Display Sex-Ratio Distortion and Unilateral Eye Defects 英文参考文献

MiceLackingAlkbh1DisplaySex-RatioDistortionand UnilateralEyeDefects LineM.Nordstrand1,JessicaSva¨rd1.,ElisabethLarsen1,2.,AnjaNilsen1.,RuneOugland1,2.,KariFuru1. , GuroF.Lien1,Torbj?rnRognes1,3,SatoshiH.Namekawa2,JeannieT.Lee2,5,ArneKlungland1,4 * 1Centre for Molecular Biology and Neuroscience, Institute of Medical Microbiology, Oslo University Hospital and University of Oslo, Oslo, Norway, 2Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts, United States of America, 3Department of Informatics, University of Oslo, Oslo, Norway, 4InstituteofBasicMedicalSciences,UniversityofOslo,Oslo,Norway,5HowardHughesMedicalInstitute,MassachusettsGeneralHospital,Boston,Massachusetts,United StatesofAmerica Abstract Background:EschericiacoliAlkBisa2-oxoglutarate-andiron-dependentdioxygenasethatreversesalkylatedDNAdamage byoxidativedemethylation.MouseAlkBhomolog1(Alkbh1)isoneofeightmembersofthenewlydiscoveredfamilyof mammaliandioxygenases. MethodsandFindings:Inthepresentstudyweshownon-MendelianinheritanceoftheAlkbh1targetedalleleinmice.Both Alkbh12/2 and heterozygous Alkbh1+/2 offspring are born at a greatly reduced frequency. Additionally, the sex-ratio is considerablyskewedagainstfemaleoffspring,withonefemalebornforeverythreetofourmales.Mostmechanismsthat causesegregationdistortion,actinthemalegametesandaffectmalefertility.Theskewingofthesexesappearstobeof paternal origin, and might be set in the pachythene stage of meiosis during spermatogenesis, in which Alkbh1 is upregulatedmorethan10-fold.Intestes,apoptoticspermatidswererevealedin5–10%ofthetubulesinAlkbh12/2 adults. The deficiency of Alkbh1 also causes misexpression of Bmp2, 4 and 7 at E11.5 during embryonic development. This is consistent with the incompletely penetrant phenotypes observed, particularly recurrent unilateral eye defects and craniofacialmalformations. Conclusions:GeneticandphenotypicassessmentsuggeststhatAlkbh1mediatesgeneregulationinspermatogenesis,and thatAlkbh1isessentia