Mutation in utp15 Disrupts Vascular Patterning in a p53-Dependent Manner in Zebrafish Embryos 英文参考文献.docVIP

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Mutation in utp15 Disrupts Vascular Patterning in a p53-Dependent Manner in Zebrafish Embryos 英文参考文献.doc

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Mutation in utp15 Disrupts Vascular Patterning in a p53-Dependent Manner in Zebrafish Embryos 英文参考文献

Mutationinutp15DisruptsVascularPatterninginap53- DependentMannerinZebrafishEmbryos KevinMouillesseaux1,Jau-NianChen1,2,3,4* 1DepartmentofMolecular,Cell,andDevelopmentalBiology,UniversityofCaliforniaLosAngeles,LosAngeles,California,UnitedStatesofAmerica,2MolecularBiology Institute, University of California Los Angeles, Los Angeles, California, United States of America, 3Jonsson Comprehensive Cancer Center, University of California Los Angeles,LosAngeles,California,UnitedStatesofAmerica,4CardiovascularResearchLaboratory,UniversityofCaliforniaLosAngeles,LosAngeles,California,UnitedStates ofAmerica Abstract Background:Angiogenesisistheprocessbywhichthehighlybranchedandfunctionalvasculaturearisesfromthemajor vessels, providing developing tissues with nutrients, oxygen, and removing metabolic waste. During embryogenesis, vascularpatterningisdependentonatightlyregulatedbalancebetweenpro-andanti-angiogenicsignals,andfailureof angiogenesis leads to embryonic lethality. Using the zebrafish as a model organism, we sought to identify genes that influencenormalvascularpatterning. MethodologyandPrincipalFindings:Inaforwardgeneticscreen,weidentifiedmutantLA1908,whichmanifestsmassive apoptosis during early embryogenesis, abnormal expression of several markers of arterial-venous specification, delayed angiogenic sprouting oftheintersegmentalvessels (ISV),andmalformationofthecaudal veinplexus(CVP),indicatinga criticalroleforLA1908incellsurvivalandangiogenesis.GeneticmappingandsequencingidentifiedaGtoAtransitionin thesplicesiteprecedingexon11ofutp15inLA1908mutantembryos.Overexpressionofwildtypeutp15mRNAsuppresses all observed mutant phenotypes, demonstrating a causative relationship between utp15 and LA1908. Furthermore, we foundthat injecting morpholinooligonucleotides inhibiting p53 translation prevents celldeath and rescuesthe vascular abnormalities,indicatingthatp53isdownstreamofUtp15deficiencyinmediatingtheLA1908phenotypes. ConclusionsandSignificance:Takentogether,ourdatadem