Neurophysiological Defects and Neuronal Gene Deregulation in Drosophila mir-124 Mutants 英文参考文献.docVIP

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Neurophysiological Defects and Neuronal Gene Deregulation in Drosophila mir-124 Mutants 英文参考文献.doc

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Neurophysiological Defects and Neuronal Gene Deregulation in Drosophila mir-124 Mutants 英文参考文献

NeurophysiologicalDefectsandNeuronalGene DeregulationinDrosophilamir-124Mutants KailiangSun1,2,JakubOrzechowskiWestholm1,KazuyaTsurudome3,JoshuaW.Hagen1,YubingLu4, MinoreeKohwi5,DoronBetel6,7,Fen-BiaoGao4,A.PejmunHaghighi3,ChrisQ.Doe5,EricC.Lai1* 1Department ofDevelopmental Biology, Sloan-Kettering Institute, NewYork,New York, United States ofAmerica, 2NeuroscienceProgram,WeillGraduate School of MedicalSciences,CornellUniversity,NewYork,NewYork,UnitedStatesofAmerica,3DepartmentofPhysiology,McGillUniversity,Montreal,Canada,4Departmentof Neurology, University of Massachusetts Medical School, Worcester, Massachusetts, United States of America, 5Institute of Molecular Biology, University of Oregon, Eugene, Oregon, United States of America, 6Department of Medicine, Weill Cornell Medical School, New York, New York, United States of America, 7Institute of ComputationalBiomedicine,WeillCornellMedicalSchool,NewYork,NewYork,UnitedStatesofAmerica Abstract miR-124isconservedinsequenceandneuronalexpressionacrosstheanimalkingdomandispredictedtohavehundredsof mRNA targets. Diverse defects in neural development and function were reported from miR-124 antisense studies in vertebrates, but a nematode knockout of mir-124 surprisingly lacked detectable phenotypes. To provide genetic insight fromDrosophila,wedeleteditssinglemir-124locusandfoundthatitisdispensableforgrossaspectsofneuralspecification and differentiation. On the other hand, we detected a variety of mutant phenotypes that were rescuable by a mir-124 genomictransgene,includingshortlifespan,increaseddendritevariation,impairedlarvallocomotion,andaberrantsynaptic release at the NMJ.These phenotypes reflect extensiverequirements of miR-124 even under optimal culture conditions. Comparison of the transcriptomes of cells from wild-type and mir-124 mutant animals, purified on the basis of mir-124 promoter activity, revealed broad upregulation of direct miR-124 targets. However, in contrast to the proposed mutual exclusionmodelf