A Wnt-FoxQ2-nodal pathway links primary and secondary axis specification in sea urchin embryos.
A Wnt-FoxQ2-nodal pathway links primary and secondary axis specification in sea urchin embryos.
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Wnt-FoxQ2-nodal 通路连接海胆胚胎中主轴和次轴的规范。
DOI：
10.1016/j.devcel.2007.10.012
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发表时间：
2008
影响因子：
11.8
通讯作者：
Angerer,LynneM
中科院分区：
文献类型：
--
作者：
Yaguchi,Shunsuke;Yaguchi,Junko;Angerer,RobertC;Angerer,LynneM
海胆胚胎的初级（动物-植物）（AV）和次级（口-口）（OA）轴是通过不同的调节途径建立的。然而，由于AV模式的实验扰动也总是破坏OA模式和辐射胚胎，这两个轴必须机械地连接。在这里，我们表明，FoxQ 2，这是逐步限制在动物板在卵裂阶段，提供了这种联系。当通过阻断β-连环蛋白的核功能来阻止AV模式化时，表达FoxQ 2的动物板在整个未来的外胚层中扩展，并且启动OA极性的nodal的表达被阻断。令人惊讶的是，仅通过抑制FoxQ 2翻译就可以挽救转录和OA分化。因此，FoxQ 2限制于动物板是经典Wnt信号传导的关键要素，其协调沿着AV轴的模式化与OA特化的起始。
The primary (animal-vegetal) (AV) and secondary (oral-aboral) (OA) axes of sea urchin embryos are established by distinct regulatory pathways. However, because experimental perturbations of AV patterning also invariably disrupt OA patterning and radialize the embryo, these two axes must be mechanistically linked. Here we show that FoxQ2, which is progressively restricted to the animal plate during cleavage stages, provides this linkage. When AV patterning is prevented by blocking the nuclear function of β-catenin, the animal plate where FoxQ2 is expressed expands throughout the future ectoderm, and expression ofnodal, which initiates OA polarity, is blocked. Surprisingly,nodaltranscription and OA differentiation are rescued simply by inhibiting FoxQ2 translation. Therefore, restriction of FoxQ2 to the animal plate is a crucial element of canonical Wnt signaling that coordinates patterning along the AV axis with the initiation of OA specification.