Nodal activity in the node governs left-right asymmetry
Nodal activity in the node governs left-right asymmetry
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DOI：
10.1101/gad.1016202
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发表时间：
2002-09-15
影响因子：
10.5
通讯作者：
Robertson, EJ
中科院分区：
文献类型：
--
作者：
Brennan, J;Norris, DP;Robertson, EJ
Nodal 在小鼠节点的侧边缘表达，但由于 Nodal 突变胚胎的早期致死性，其在“组织者”组织中的功能仍然未知。在这里，我们使用遗传策略来选择性地从节点中删除节点活动。节点中缺乏节点的胚胎无法引发左侧板中胚层的分子不对称性，并表现出多个左右图案缺陷。交点也可以充当短程信号，以建立功能性中线屏障。我们的研究结果证实，小鼠节点有助于启动左右轴规范，并将 Nodal 确定为调节该过程的关键形态发生素。
Nodal is expressed at the lateral edges of the mouse node, but its function in this "organizer" tissue remains unknown due to the early lethality of Nodal mutant embryos. Here we used a genetic strategy to selectively remove Nodal activity from the node. Embryos lacking Nodal in the node fail to initiate molecular asymmetry in the left lateral plate mesoderm and exhibit multiple left-right patterning defects. Nodal may also act as a short-range signal to establish a functional midline barrier. Out findings confirm that the mouse node is instrumental in initiating left-right axis specification and identify Nodal as the key morphogen regulating this process.