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首页> 外文期刊>Developmental biology >The C. elegans M3 neuron guides the growth cone of its sister cell M2 via the Krüppel-like zinc finger protein MNM-2
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The C. elegans M3 neuron guides the growth cone of its sister cell M2 via the Krüppel-like zinc finger protein MNM-2

机译:秀丽隐杆线虫M3神经元通过类似Krppel锌指蛋白MNM-2引导其姊妹细胞M2的生长锥

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摘要

Theinvariantcellndash;cellinteractionsoccurringduringemC.elegans/emdevelopmentofferuniqueopportunitiestodiscoverhowgrowingaxonsmayreceiveguidancecuesfromneighboringcells.Theemmnm-2/emmutantwasisolatedbecauseofitsdefectsintheaxontrajectoryofthebilateralM2pharyngealneuronsinemC.elegans/em.Wefoundthatemmnm-2/emenhancestheeffectsofmanygrowthconeguidancemutationsontheseaxons,suggestingthatitperformsanovelfunctionduringaxonguidance.Weclonedemmnm-2/emandfoundthatitencodesaproteinwiththreeC2H2zincfingerdomainsrelatedtotheKruuml;ppel-likeFactorproteinfamily.emmnm-2/emisexpressedonlytransientlyintheM2neuron,butexhibitsasustainedexpressioninitssistercell,theM3neuron.Strikingly,theexpressionofemmnm-2/emisnotsustainedintheM3celloftheemmnm-2/emmutant,indicatingthatthisgenepositivelyregulatesitselfinthatcell.ElectropharyngeogramsalsoindicatethattheM3cellisfunctionallyimpairedintheemmnm-2/emmutant.WeusedanM3-specificpromotertoshowthattheM2axondefectcanberescuedbyexpressionofemmnm-2/eminitssistercellM3.Thesamepromoterwasusedtoexpressthepro-apoptoticgeneemegl-1/emtokilltheM3cell,whichresultedinanM2axonguidancedefectsimilartothatfoundintheemmnm-2/emmutant.OurresultssuggestanM2axonguidancemodelinwhichtheM3cellprovidesanimportantsignaltothegrowthconeofitssisterM2andthatthissignalandtheproperdifferentiationofM3bothdependonemmnm-2/emexpression.Thismechanismofaxonguidanceregulationallowsfine-tuningoftrajectoriesbetweensistercells./p/div
机译:Theinvariantcellndash; cellinteractionsoccurringduring <位置>线虫的developmentofferuniqueopportunitiestodiscoverhowgrowingaxonsmayreceiveguidancecuesfromneighboringcells.The <位置> MNM-2 的mutantwasisolatedbecauseofitsdefectsintheaxontrajectoryofthebilateralM2pharyngealneuronsin <位置>线虫的.Wefoundthat <位置> MNM-2 的enhancestheeffectsofmanygrowthconeguidancemutationsontheseaxons ,suggestingthatitperformsanovelfunctionduringaxonguidance.Wecloned <位置> MNM-2 的andfoundthatitencodesaproteinwiththreeC2H2zincfingerdomainsrelatedtotheKruuml ;. ppel-likeFactorproteinfamily <位置> MNM-2 的isexpressedonlytransientlyintheM2neuron,butexhibitsasustainedexpressioninitssistercell,theM3neuron.Strikingly,theexpressionof <位置> MNM-2 的isnotsustainedintheM3cellofthe mnm-2 突变体,表明该基因正向调节该细胞本身。人体电生理曲线图还表明M3细胞在 mnm-2 突变体中具有功能性。我们使用M3特异性启动子来表明该M2轴缺陷得以消除。 ressionof <位置> MNM-2 的initssistercellM3.Thesamepromoterwasusedtoexpressthepro-apoptoticgene <位置> EGL-1 的tokilltheM3cell,whichresultedinanM2axonguidancedefectsimilartothatfoundinthe <位置> MNM-2 的mutant.OurresultssuggestanM2axonguidancemodelinwhichtheM3cellprovidesanimportantsignaltothegrowthconeofitssisterM2andthatthissignalandtheproperdifferentiationofM3bothdependon <位置> MNM-2

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