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Neural Maintenance Roles for the Matrix Receptor Dystroglycan and the Nuclear Anchorage Complex in Caenorhabditis elegans

机译:秀丽隐杆线虫中基质受体dystroglycan和核锚固复合物的神经维持作用。

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Recent studies in Caenorhabditis elegans have revealed specific neural maintenance mechanisms that protect soma and neurites against mispositioning due to displacement stresses, such as muscle contraction. We report that C. elegans dystroglycan (DG) functions to maintain the position of during late embryonic and larval development. In the absence of the cell bodies of multiple classes are frequently displaced anterior of their normal positions. Early but not later embryonic panneural expression of rescues positional maintenance, suggesting that dystroglycan is required for establishment of a critical maintenance pathway that persists throughout later developmental stages. Lumbar neural maintenance requires only a membrane-tethered N-terminal domain of and may involve a novel extracellular partner for dystroglycan. A genetic screen for similar maintenance mutants revealed a role for the nesprin/SYNE family protein as well as for the extracellular protein , previously implicated in maintenance. The involvement of reveals a previously unknown role for nucleus–cytoskeleton interactions in neural maintenance. Genetic analysis indicates that position is maintained in late embryos by parallel / and –dependent pathways, and in larvae by separate and href="http://www.wormbase.org/db/get?name=ANC-1;class=Gene" data-ga-action="click_feat_suppl" ref="reftype=extlink&article-id=3316649&issue-id=208314&journal-id=301&FROM=Article%7CFront%20Matter&TO=External%7CLink%7CURI" target="_blank">ANC-1 pathways. The effect of muscle paralysis on late embryonic- or larval-stage maintenance defects in mutants indicates that href="http://www.wormbase.org/db/get?name=lumbar%20neuron;class=Anatomy_name" data-ga-action="click_feat_suppl" ref="reftype=extlink&article-id=3316649&issue-id=208314&journal-id=301&FROM=Article%7CFront%20Matter&TO=External%7CLink%7CURI" target="_blank">lumbar neurons are subject to both muscle contraction-dependent and contraction-independent displacement stresses, and that different maintenance pathways may protect against specific types of displacement stress.
机译:秀丽隐杆线虫的最新研究表明,特定的神经维持机制可保护躯体和神经突免于因位移应力(例如肌肉收缩)而发生错位。我们报告线虫dystroglycan(DG)的功能来维持后期胚胎和幼虫发育的位置。在不存在多个类别的细胞体的情况下,常常将它们的正常位置移位。早期但不是以后的胚胎胰腺表达可以挽救位置维持,这表明dystroglycan是建立在整个发育后期持续存在的关键维持途径所必需的。腰神经维持仅需要一个膜连接的N末端结构域,并且可能涉及营养不良聚糖的新型胞外伴侣。对相似的维持突变体进行的遗传筛选揭示了先前参与维持的nesprin / SYNE家族蛋白以及细胞外蛋白的作用。的参与揭示了神经维持过程中核-细胞骨架相互作用的先前未知的作用。遗传分析表明,通过平行/依赖途径可以在晚期胚胎中保持位置,而通过单独的href =“ http://www.wormbase.org/db/get?name=ANC-1;class = Gene“ data-ga-action =” click_feat_suppl“ ref =” reftype = extlink&article-id = 3316649&issue-id = 208314&journal-id = 301&FROM = Article%7CFront%20Matter&TO = External%7CLink%7CURI“ target =” _ blank“> ANC -1 途径。肌肉麻痹对突变体晚期胚胎或幼虫期维持缺陷的影响表明href =“ http://www.wormbase.org/db/get?name=lumbar%20neuron;class=Anatomy_name”数据- ga-action =“ click_feat_suppl” ref =“ reftype = extlink&article-id = 3316649&issue-id = 208314&journal-id = 301&FROM = Article%7CFront%20Matter&TO = External%7CLink%7CURI” target =“ _ blank”>腰部神经元既要承受肌肉收缩依赖性的压力,又要承受与收缩无关的位移的压力,并且不同的维持途径可以防止特定类型的位移压力。

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