Regulation of Zebrafish Skeletogenesis by ext2dackel and papst1pinscher 英文参考文献.docVIP

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Regulation of Zebrafish Skeletogenesis by ext2dackel and papst1pinscher 英文参考文献.doc

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Regulation of Zebrafish Skeletogenesis by ext2dackel and papst1pinscher 英文参考文献

RegulationofZebrafishSkeletogenesisbyext2/dackel andpapst1/pinscher Aure′lieCle′ment1,2,MalgorzataWiweger1,2,SophiavonderHardt3,MelissaA.Rusch4,5,ScottB. Selleck4,5,Chi-BinChien6,7,HenryH.Roehl1,2 * 1MRCCentreforDevelopmentalandBiomedicalGenetics,UniversityofSheffield,Sheffield,UnitedKingdom,2DepartmentofBiomedicalScience,UniversityofSheffield, Sheffield,UnitedKingdom,3AbteilungGenetik,MPIfu¨rEntwicklungsbiologie,Tuebingen,Germany,4DepartmentofPediatrics,UniversityofMinnesota,Minneapolis, Minnesota, United States of America, 5Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, Minnesota, United States of America,6DepartmentofNeurobiologyandAnatomy,UniversityofUtah,SaltLakeCity,Utah,UnitedStatesofAmerica,7BrainInstitute,UniversityofUtah,SaltLakeCity, Utah,UnitedStatesofAmerica Abstract Mutations in human Exostosin genes (EXTs) confer a disease called Hereditary Multiple Exostoses (HME) that affects 1 in 50,000 among the general population. Patients with HME have a short stature and develop osteochondromas during childhood.Hereweshowthattwozebrafishmutants,dackel(dak)andpinscher(pic),havecartilagedefectsthatstrongly resemblethoseseeninHMEpatients.WehavepreviouslydeterminedthatdakencodeszebrafishExt2.Positionalcloningof picrevealsthatitencodesasulphatetransporterrequiredforsulphationofglycans(Papst1).Weshowthatalthoughboth dak and pic are required during cartilage morphogenesis, they are dispensable for chondrocyte and perichondral cell differentiation. They are also required for hypertrophic chondrocyte differentiation and osteoblast differentiation. Transplantationanalysisindicatesthatdak2/2cellsareusuallyrescuedbyneighbouringwild-typechondrocytes.Incontrast, pic2/2 chondrocytes always act autonomously and can disrupt the morphology of neighbouring wild-type cells. These findingsleadtothedevelopmentofanewmodeltoexplaintheaetiologyofHME. Citation: Cle′ment A, Wiweger M, von der Hardt S, Rusch MA, Selleck SB, et al. (2008) Regu