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Maintenance of neuronal positions in organized ganglia by SAX-7, a Caenorhabditis elegans homologue of L1

机译:SAX-7(一种秀丽隐杆线虫的同源物)维持组织神经节的神经元位置

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摘要

The L1 family of cell adhesion molecules is predominantly expressed in the nervous system. Mutations in human L1 cause neuronal diseases such as HSAS, MASA, and SPG1. Here we show that sax-7 gene encodes an L1 homologue in Caenorhabditis elegans. In sax-7 mutants, the organization of ganglia and positioning of neurons are abnormal in the adult stage, but these abnormalities are not observed in early larval stage. Misplacement of neurons in sax-7 mutants is triggered by mechanical force linked to body movement. Short and long forms of SAX-7 exhibited strong and weak homophilic adhesion activities in in vitro aggregation assay, respectively, which correlated with their different activities in vivo. SAX-7 was localized on plasma membranes of neurons in vivo. Expression of SAX-7 only in a single neuron in sax-7 mutants cell-autonomously restored its normal neuronal position. Expression of SAX-7 in two different head neurons in sax-7 mutants led to the forced attachment of these neurons. We propose that both homophilic and heterophilic interactions of SAX-7 are essential for maintenance of neuronal positions in organized ganglia.
机译:L1家族的细胞粘附分子主要在神经系统中表达。人L1中的突变会引起神经元疾病,例如HSAS,MASA和SPG1。在这里,我们显示sax-7基因编码秀丽隐杆线虫的L1同源物。在sax-7突变体中,成年期神经节的组织和神经元的位置异常,但在幼虫早期未观察到这些异常。 sax-7突变体中神经元的错位是由与身体运动有关的机械力触发的。短和长形式的SAX-7分别在体外聚集试验中表现出强和弱的同源性粘附活性,这与其体内不同的活性有关。 SAX-7体内定位在神经元的质膜上。 SAX-7仅在sax-7突变体的单个神经元中表达,可自动恢复其正常的神经元位置。 SAX-7在sax-7突变体的两个不同的头部神经元中的表达导致这些神经元的强迫附着。我们建议SAX-7的同型和异型相互作用对于维持有组织的神经节中的神经元位置至关重要。

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