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首页> 外文期刊>Developmental biology >The characterization of zebrafish antimorphic mib alleles reveals that Mib and Mind bomb-2 (Mib2) function redundantly
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The characterization of zebrafish antimorphic mib alleles reveals that Mib and Mind bomb-2 (Mib2) function redundantly

机译:斑马鱼变形mib等位基因的特征表明Mib和心灵炸弹2(Mib2)多余地发挥作用。

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Bothemmindbomb/em(emmib/em)andemmindbomb-2/em(emmib2/em)encodeRINGE3ubiquitinligasesthatpromoteDeltaubiquitylationandendocytosisinNotchactivation.Detailedmorphologicalandmolecularexaminationsrevealedthatzebrafishemmib/emsupemta52b/em/sup(missensemutationintheC-terminalRINGFinger(RF),M1013R)andemmib/emsupemm132/em/sup(nonsensemutationresultinginatruncatedproteinthatlosesallthreeRFs,C785stop)arestrongandweakantimorphicalleles,respectively,comparedtothenullallele,emmib/emsupemtfi91/em/sup(nonsensemutationresultinginatruncatedproteinofonly60aminoacids,Y60stop).Zebrafishemmib2/emorthologwasidentifiedinthisstudy.ZebrafishMibandMib2arecolocalizedintransfectedcellsandfunctionredundantlyinregulatingNotchsignalinginembryos.Mibsupta52b/supandMibsupm132/suphaveadosage-dependentdominant-negativeeffect,atleast,onMib2,whichisamolecularbasisfortheantimorphicphenotypes.ItwasalsoshownthatNotchsignalingnegativelyregulatesemmib/emexpressioninaSu(H)-dependentmanner,forminganegativefeedbackloopinmodulatingNotchactivation./p/div
机译: mindbomb mib )和 mindbomb-2 mib2 )都编码能促进Notchactivation的DeltaE泛素化和内吞作用的RINGE3泛素连接酶。详细的形态学和分子检验> ta52b (C端RINGFinger(RF),M1013R中的缺失突变)和 mib m132 (无义突变导致缺失所有三个RFs的截短的蛋白)的强度和弱反形态细胞分别与nullallele, mib tfi91 (nonsensemutyresemememisemisemisememem60)斑马鱼Miband Mib2共同定位在转染细胞中,并冗余地调节Notchsignalinginembryos.MIB ta52b 和MIB m132 具有依赖于年龄的显性负效应,至少,在MIB2上有肠溶oninaSu(H)依赖性,形成负反馈回路,调节Notch激活。

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