Cdx2 is essential for axial elongation in mouse development
Cdx2 is essential for axial elongation in mouse development
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DOI：
10.1073/pnas.0401654101
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发表时间：
2004-05-18
影响因子：
11.1
通讯作者：
Beck, F
中科院分区：
文献类型：
--
作者：
Chawengsaksophak, K;de Graaff, W;Beck, F
CDX2的失活导致植入前胚胎致死性。四倍体融合的植入缺陷的营救确定，CDX2对于滋养细胞发育，蛋黄囊中胚层中的血管生成，藻类生长，藻类生长和绒毛膜甲抗体融合是必不可少的。由于胎盘发育的失败，“救出” CDX2突变体在晚期胃阶段死亡。还需要CDX2才能完成正常的胃结构和尾芽伸长过程。预段性中胚层受到严格限制的数量，在节后5的节点异常。 CDX2突变（例如突变损害了作用和FGF信号传导）会导致胚胎结构的后部截断并打扰轴向图案，这是由HOX表达域的变化所表明的。该基因似乎在控制胚胎轴向伸长和前后图案的途径的整合中很重要。
Inactivation of Cdx2 leads to preimplantation embryonic lethality. Rescue of the implantation defect by tetraploid fusion established that Cdx2 is necessary for trophoblastic development, vasculogenesis in the yolk sac mesoderm, allantoic growth, and chorioallantoic fusion. "Rescued" Cdx2 mutants die at late gastrulation stages because of failure of placental development. Cdx2 is also needed for the completion of the normal process of gastrulation and tail bud elongation. Presegmental paraxial mesoderm is severely restricted in amount and somites posterior to somite 5 are abnormal. The Cdx2 mutation, like mutations impairing Writ and Fgf signaling, causes posterior truncations and disturbs axial patterning of the embryonic structures, indicated by changes in the Hox expression domains. The gene appears to be important in the integration of the pathways controlling embryonic axial elongation, and anterior-posterior patterning.