Defects in pathfinding by cranial neural crest cells in mice lacking the neuregulin receptor ErbB4
Defects in pathfinding by cranial neural crest cells in mice lacking the neuregulin receptor ErbB4
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DOI：
10.1038/35000058
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发表时间：
2000-02-01
影响因子：
21.3
通讯作者：
Gassmann, M
中科院分区：
文献类型：
--
作者：
Golding, JP;Trainor, P;Gassmann, M
在编码受体酪氨酸激酶ErbB4的基因中具有功能缺失突变的小鼠胚胎表现出颅感觉神经节传入轴突的错误投射。在这里，我们分析ErbB4缺陷小鼠，发现野生型和突变颅神经节之间的形态差异与异常迁移的一个亚群的后脑源性颅神经嵴细胞内的近轴间充质环境。在移植实验中使用新的移植技术在培养的小鼠胚胎，我们确定，这种表型是非细胞自主的：野生型和突变的神经嵴细胞都迁移的模式与宿主环境一致，偏离正常的途径，只有当移植到突变的胚胎。因此，后脑内的ErbB4信号传导事件为颅旁轴间充质提供了模式化信息，这对于神经嵴细胞的适当迁移至关重要。
Mouse embryos with a loss-of-function mutation in the gene encoding the receptor tyrosine kinase ErbB4 exhibit misprojections of cranial sensory ganglion afferent axons. Here we analyse ErbB4-deficient mice, and find that morphological differences between wild-type and mutant cranial ganglia correlate with aberrant migration of a subpopulation of hindbrain-derived cranial neural crest cells within the paraxial mesenchyme environment. In transplantation experiments using new grafting techniques in cultured mouse embryos, we determine that this phenotype is non-cell-autonomous: wild-type and mutant neural crest cells both migrate in a pattern consistent with the host environment, deviating from their normal pathway only when transplanted into mutant embryos. ErbB4 signalling events within the hindbrain therefore provide patterning information to cranial paraxial mesenchyme that is essential for the proper migration of neural crest cells.