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在ina-1整合素突变体中,神经元迁移和轴突成束受到破坏。

Neuronal migrations and axon fasciculation are disrupted in ina-1 integrin mutants.

作者信息

Baum P D, Garriga G

机构信息

Department of Molecular and Cell Biology, University of California, Berkeley 94720-3204, USA.

出版信息

Neuron. 1997 Jul;19(1):51-62. doi: 10.1016/s0896-6273(00)80347-5.

DOI:10.1016/s0896-6273(00)80347-5
PMID:9247263
Abstract

Integrins are heterodimeric cell surface receptors implicated in cell adhesion and signaling. Our analysis of C. elegans ina-1 alpha integrin mutants provides the first genetic evidence that migrating neurons require integrins. Mosaic analysis and expression studies show that ina-1 acts autonomously in cells to promote their migrations. Although axons generally extend to their normal targets in ina-1 mutants, bundling of axons into fascicles is defective, defining a previously unrecognized role for integrins. In addition to these neuronal phenotypes, ina-1 mutants also display many morphogenetic defects. Finally, we show that the C. elegans INA-1 alpha integrin subunit associates with the PAT-3beta subunit in vivo, suggesting that these proteins function together in cell migration, axon fasciculation, and morphogenesis.

摘要

整合素是参与细胞黏附和信号传导的异二聚体细胞表面受体。我们对线虫ina-1α整合素突变体的分析提供了首个遗传学证据,证明迁移神经元需要整合素。镶嵌分析和表达研究表明,ina-1在细胞中自主发挥作用以促进其迁移。虽然在ina-1突变体中轴突通常会延伸至其正常靶点,但轴突聚集成束存在缺陷,这确定了整合素一个以前未被认识到的作用。除了这些神经元表型外,ina-1突变体还表现出许多形态发生缺陷。最后,我们表明线虫INA-1α整合素亚基在体内与PAT-3β亚基相关联,这表明这些蛋白质在细胞迁移、轴突成束和形态发生中共同发挥作用。

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