The mouse Wnt/PCP protein Vangl2 is necessary for migration of facial branchiomotor neurons, and functions independently of Dishevelled.
The mouse Wnt/PCP protein Vangl2 is necessary for migration of facial branchiomotor neurons, and functions independently of Dishevelled.
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DOI：
10.1016/j.ydbio.2012.06.021
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发表时间：
2012-09-15
影响因子：
2.7
通讯作者：
Chandrasekhar, Anand
中科院分区：
文献类型：
--
作者：
Glasco, Derrick M.;Sittaramane, Vinoth;Bryant, Whitney;Fritzsch, Bernd;Sawant, Anagha;Paudyal, Anju;Stewart, Michelle;Andre, Philipp;Vilhais-Neto, Goncalo Cadete;Yang, Yingzi;Song, Mi-Ryoung;Murdoch, Jennifer N.;Chandrasekhar, Anand
关键词：
在发育过程中，支配脊椎动物头部肌肉的面鳃肌（FBM）神经元在脑干内向尾侧和径向迁移，在软膜表面形成运动核。Wnt/平面细胞极性（PCP）通路的几个组分，包括跨膜蛋白Vangl 2，调节斑马鱼FBM神经元的尾部迁移，但它们在小鼠神经元迁移中的作用尚未被详细研究。因此，我们分析了小鼠环尾（Lp）突变体中的FBM神经元迁移，其中Vangl 2失活。在Vangl 2 Lp/+和Vangl 2 Lp/Lp胚胎中，FBM神经元未能从菱形节（r）4向尾部迁移到r6。虽然尾部迁移在很大程度上被阻止，许多FBM神经元进行正常的径向迁移到软膜表面的神经管。此外，后脑图案和FBM祖规范是完整的，和FBM神经元没有transfate到其他非迁移神经元类型，表明尾部迁移的具体影响。由于一些斑马鱼Wnt/PCP基因的功能丧失并不影响FBM神经元的尾部迁移，我们测试了小鼠中是否也是这种情况。Ptk 7，PCP信号的调节器，胚胎无效，FBM神经元的尾部迁移有严重的缺陷。然而，FBM神经元迁移正常Dishevelled（Dvl）1/2双突变体，并在斑马鱼胚胎与破坏Dvl信号，这表明Dvl功能基本上是FBM神经元尾部迁移。与此一致，Vangl 2 Lp/+胚胎中Dvl 2功能的丧失不会加剧Vangl 2 Lp/+神经元迁移表型。这些数据表明FBM神经元的尾部迁移受Wnt/PCP通路的多个组分调节，但重要的是，可能不需要Dishevelled功能。有趣的是，遗传相互作用的实验表明，吻侧FBM神经元迁移，这通常是抑制，取决于Dvl功能。
During development, facial branchiomotor (FBM) neurons, which innervate muscles in the vertebrate head, migrate caudally and radially within the brainstem to form a motor nucleus at the pial surface. Several components of the Wnt/planar cell polarity (PCP) pathway, including the transmembrane protein Vangl2, regulate caudal migration of FBM neurons in zebrafish, but their roles in neuronal migration in mouse have not been investigated in detail. Therefore, we analyzed FBM neuron migration in mouse looptail (Lp) mutants, in which Vangl2 is inactivated. In Vangl2 Lp/+ and Vangl2 Lp/Lp embryos, FBM neurons failed to migrate caudally from rhombomere (r) 4 into r6. Although caudal migration was largely blocked, many FBM neurons underwent normal radial migration to the pial surface of the neural tube. In addition, hindbrain patterning and FBM progenitor specification were intact, and FBM neurons did not transfate into other non-migratory neuron types, indicating a specific effect on caudal migration. Since loss-of-function in some zebrafish Wnt/PCP genes does not affect caudal migration of FBM neurons, we tested whether this was also the case in mouse. Embryos null for Ptk7, a regulator of PCP signaling, had severe defects in caudal migration of FBM neurons. However, FBM neurons migrated normally in Dishevelled (Dvl) 1/2 double mutants, and in zebrafish embryos with disrupted Dvl signaling, suggesting that Dvl function is essentially dispensable for FBM neuron caudal migration. Consistent with this, loss of Dvl2 function in Vangl2 Lp/+ embryos did not exacerbate the Vangl2 Lp/+ neuronal migration phenotype. These data indicate that caudal migration of FBM neurons is regulated by multiple components of the Wnt/PCP pathway, but, importantly, may not require Dishevelled function. Interestingly, genetic-interaction experiments suggest that rostral FBM neuron migration, which is normally suppressed, depends upon Dvl function.
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