Functional Conservation of Asxl2, a Murine Homolog for the Drosophila Enhancer of Trithorax and Polycomb Group Gene Asx 英文参考文献.docVIP

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Functional Conservation of Asxl2, a Murine Homolog for the Drosophila Enhancer of Trithorax and Polycomb Group Gene Asx 英文参考文献.doc

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Functional Conservation of Asxl2, a Murine Homolog for the Drosophila Enhancer of Trithorax and Polycomb Group Gene Asx 英文参考文献

FunctionalConservationofAsxl2,aMurineHomologfor theDrosophilaEnhancerofTrithoraxandPolycomb GroupGeneAsx HeatherA.Baskind1,LucyNa1,QuanhongMa1,MayurP.Patel1,DavidL.Geenen2,Q.TianWang1* 1DepartmentofBiologicalSciences,UniversityofIllinoisatChicago,Chicago,Illinois,UnitedStatesofAmerica,2DepartmentofMedicine,SectionofCardiologyandthe CenterforCardiovascularResearch,UniversityofIllinoisatChicago,Chicago,Illinois,UnitedStatesofAmerica Abstract Background:Polycomb-group(PcG)andtrithorax-group(trxG)proteinsregulatehistonemethylationtoestablishrepressive andactivechromatinconfigurationsattargetloci,respectively.Thesechromatinconfigurationsarepassedonfrommother to daughter cells, thereby causing heritable changes in gene expression. The activities of PcG and trxG proteins are regulatedbyaspecialclassofproteinsknownasEnhancersoftrithoraxandPolycomb(ETP).TheDrosophilageneAdditional sexcombs(Asx)encodesanETPproteinandmutationsinAsxenhancebothPcGandtrxGmutantphenotypes.Themouse and human genomes each contain three Asx homologues, Asx-like 1, 2, and 3. In order to understand the functions of mammalianAsx-like(Asxl)proteins,wegeneratedanAsxl2mutantmousefromagene-trapEScellline. Methodology/PrincipalFindings:WeshowthattheAsxl2genetrapisexpressedathighlevelsinspecifictissuesincluding theheart,theaxialskeleton,theneocortex,theretina,spermatogoniaanddevelopingoocytes.Thegenetrapmutationis partially embryonic lethal and approximately half of homozygous animals die before birth. Homozygotes that survive embryogenesisaresignificantlysmallerthancontrolsandhaveashortenedlifespan.Asxl22/2micedisplaybothposterior transformationsandanteriortransformationintheaxialskeleton,suggestingthatthelossofAsxl2disruptstheactivitiesof bothPcGandtrxGproteins.ThePcG-associatedhistonemodification,trimethylationofhistoneH3lysine27,isreducedin Asxl22/2 heart. Necropsy and histological analysis show that mutant mice haveenlarged hearts and may have impaired heartfunction. Conclusions/Significance: Our resul