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首页> 外文期刊>Genetics: A Periodical Record of Investigations Bearing on Heredity and Variation >Neural Maintenance Roles for the Matrix Receptor Dystroglycan and the Nuclear Anchorage Complex in Caenorhabditis elegans
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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) [DGN-1][1] functions to maintain the position of [lumbar neurons][2] during late embryonic and larval development. In the absence of [DGN-1][1] the cell bodies of multiple [lumbar neuron][3] classes are frequently displaced anterior of their normal positions. Early but not later embryonic panneural expression of [DGN-1][1] 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 [DGN-1][1] and may involve a novel extracellular partner for dystroglycan. A genetic screen for similar [lumbar][3] maintenance mutants revealed a role for the nesprin/SYNE family protein [ANC-1][4] as well as for the extracellular protein [DIG-1][5], previously implicated in [lumbar neuron][3] maintenance. The involvement of [ANC-1][4] reveals a previously unknown role for nucleus–cytoskeleton interactions in neural maintenance. Genetic analysis indicates that [lumbar neuron][3] position is maintained in late embryos by parallel [DGN-1][1]/[DIG-1][5] and [ANC-1][4]–dependent pathways, and in larvae by separate [DGN-1][1] and [ANC-1][4] pathways. The effect of muscle paralysis on late embryonic- or larval-stage maintenance defects in mutants indicates that [lumbar][3] 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. [1]: http://www.wormbase.org/db/get?name=DGN-1;class=Gene [2]: http://www.wormbase.org/db/ontology/anatomy?name=lumbar%20neuron;class=Anatomy_name [3]: http://www.wormbase.org/db/get?name=lumbar%20neuron;class=Anatomy_name [4]: http://www.wormbase.org/db/get?name=ANC-1;class=Gene [5]: http://www.wormbase.org/db/get?name=DIG-1;class=Gene
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）[DGN-1] [1]的功能是在后期胚胎和幼虫发育过程中维持[腰神经元] [2]的位置。在缺少[DGN-1] [1]的情况下，多个[腰腰神经元] [3]类的细胞体经常在其正常位置的前面移位。 [DGN-1] [1]的早期但并非后来的胚胎全神经表达可以挽救位置维持，这表明dystroglycan是建立贯穿整个后期发育阶段的关键维持途径所必需的。腰神经维持仅需要[DGN-1] [1]的膜拴N端结构域，并且可能涉及营养不良聚糖的新型胞外伴侣。相似的[lumbar] [3]维持突变体的遗传筛选揭示了nesprin / SYNE家族蛋白[ANC-1] [4]以及细胞外蛋白[DIG-1] [5]的作用，以前曾涉及[腰神经元] [3]维护。 [ANC-1] [4]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，[腰神经元] [3]的位置通过平行的[DGN-1] [1] / [DIG-1] [5]和[ANC-1] [4]依赖性途径得以维持，并且在幼虫中通过单独的[DGN-1] [1]和[ANC-1] [4]途径传播。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[腰] [3]神经元同时受到肌肉收缩依赖性和收缩非依赖性的置换压力的影响，并且不同的维持途径可能会预防特定的位移应力的类型。 [1]：http://www.wormbase.org/db/get?name=DGN-1;class=Gene [2]：http://www.wormbase.org/db/ontology/anatomy?name=lumbar ％20neuron; class =解剖名[3]：http://www.wormbase.org/db/get?name=lumbar%20neuron;class=解剖名[4]：http://www.wormbase.org/db/get名称= ANC-1;类别=基因[5]：http：//www.wormbase.org/db/get？名称= DIG-1;类别=基因

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