Embryonic mesodermal defects in alpha 5 integrin-deficient mice.
Embryonic mesodermal defects in alpha 5 integrin-deficient mice.
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发表时间：
1993-12
期刊：
影响因子：
4.6
通讯作者：
Joy T. Yang;H. Rayburn;R. Hynes
中科院分区：
文献类型：
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作者：
Joy T. Yang;H. Rayburn;R. Hynes
在胚胎干细胞中通过基因靶向产生的鼠α 5整联蛋白基因的功能缺失突变是隐性胚胎致死性的。突变胚胎在妊娠第9天开始显示出可观察到的缺陷，并在第10-11天左右死亡。α 5-null胚胎在后干和卵黄囊中胚层结构中具有明显的缺陷，表明α 5 β 1整合素在中胚层形成、运动或功能中的作用。然而，胚胎比纤连蛋白缺失的胚胎进展显著更远，α 5 β 1整联蛋白是纤连蛋白的受体，这表明其他纤连蛋白受体的参与。对源自α 5缺失胚胎的细胞的体外研究证实α 5 β 1整联蛋白在突变细胞上不表达，并显示突变细胞能够组装纤连蛋白基质，形成焦点接触，并在纤连蛋白上迁移，尽管完全不存在α 5 β 1纤连蛋白受体整联蛋白。所有这些功能以前都被认为涉及或需要α 5 β 1。结果表明，这些涉及纤连蛋白的细胞功能可以使用其他受体进行。
A loss of function mutation of the murine alpha 5 integrin gene generated by gene targeting in embryonic stem cells is a recessive embryonic lethal. The mutant embryos start to show observable defects by day 9 of gestation and die around day 10-11. The alpha 5-null embryos have pronounced defects in posterior trunk and yolk sac mesodermal structures, suggesting a role for alpha 5 beta 1 integrin in mesoderm formation, movement or function. However, the embryos progress significantly further than embryos null for fibronectin, for which alpha 5 beta 1 integrin is a receptor, suggesting the involvement of other fibronectin receptors. In vitro studies on cells derived from the alpha 5-null embryos confirm that the alpha 5 beta 1 integrin is not expressed on mutant cells and show that the mutant cells are able to assemble fibronectin matrix, form focal contacts, and migrate on fibronectin despite the complete absence of the alpha 5 beta 1 fibronectin receptor integrin. All these functions have previously been thought to involve or require alpha 5 beta 1. The results presented show that these cellular functions involving fibronectin can proceed using other receptors.