An ALS-Linked Mutant SOD1 Produces a Locomotor Defect Associated with Aggregation and Synaptic Dysfunction When Expressed in Neurons of Caenorhabditis elegans 英文参考文献.docVIP
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An ALS-Linked Mutant SOD1 Produces a Locomotor Defect Associated with Aggregation and Synaptic Dysfunction When Expressed in Neurons of Caenorhabditis elegans 英文参考文献
AnALS-LinkedMutantSOD1ProducesaLocomotor
DefectAssociatedwithAggregationandSynaptic
DysfunctionWhenExpressedinNeuronsof
Caenorhabditiselegans
JiouWang1,2,GeorgeW.Farr1,2,DavidH.Hall3,FeiLi4,KrystynaFurtak1,2,LarsDreier5,ArthurL.
Horwich1,2
*
1HowardHughesMedicalInstitute,YaleSchoolofMedicine,NewHaven,Connecticut,UnitedStatesofAmerica,2DepartmentofGenetics,YaleSchoolofMedicine,New
Haven, Connecticut, United States of America, 3Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York, United States of America,
4DepartmentofMolecular,Cellular,andDevelopmentalBiology,UniversityofMichigan,AnnArbor,Michigan,UnitedStatesofAmerica,5DepartmentofNeurobiology,
DavidGeffenSchoolofMedicine,UniversityofCaliforniaLosAngeles,LosAngeles,California,UnitedStatesofAmerica
Abstract
Thenatureoftoxiceffectsexertedonneuronsbymisfoldedproteins,occurringinanumberofneurodegenerativediseases,
ispoorlyunderstood.Oneapproachtothisproblemistomeasureeffectswhensuchproteinsareexpressedinheterologous
neurons.WereportoneffectsofanALS-associated,misfolding-pronemutanthumanSOD1,G85R,whenexpressedinthe
neuronsofCaenorhabditiselegans.Stablemutanttransgenicanimals,butnotwild-typehumanSOD1transgenics,exhibited
a strong locomotor defect associated with the presence, specifically in mutant animals, of both soluble oligomers and
insolubleaggregatesofG85Rprotein.Awhole-genomeRNAiscreenidentifiedchaperonesandothercomponentswhose
deficiencyincreasedaggregationandfurtherdiminishedlocomotion.Thenatureofthelocomotordefectwasinvestigated.
Mutantanimalswereresistanttoparalysisbythecholinesteraseinhibitoraldicarb,whileexhibitingnormalsensitivitytothe
cholinergicagonistlevamisoleandnormalmusclemorphology.Whenfluorescentlylabeledpresynapticcomponentswere
examinedinthedorsalnervecord,decreasednumbersofpunctacorrespondingtoneuromuscularjunctionswereobserved
in mutant animals and brightnesswas also diminished. AttheEM level, mutant animals exhibited areduced number of
synapticvesicles.Neurotoxicit
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