Lack of the murine homeobox gene Hesx1 leads to a posterior transformation of the anterior forebrain
Lack of the murine homeobox gene Hesx1 leads to a posterior transformation of the anterior forebrain
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DOI：
10.1242/dev.02829
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发表时间：
2007-04-15
期刊：
影响因子：
4.6
通讯作者：
Martinez-Barbera, Juan Pedro
中科院分区：
文献类型：
--
作者：
Andoniadou, Cynthia L.;Signore, Massimo;Martinez-Barbera, Juan Pedro
同源框基因Hesx1是一种必不可少的抑制因子，在小鼠和人类的正常前脑发育中是前神经板所必需的。结合遗传细胞标记和标记分析，我们证明了Hesx1的缺失导致了小鼠发育过程中前脑(AFB)的后移。我们的数据表明，这种转化的机制是AFB中Hesx1表达区域内Wnt/β-catenin信号的异位激活。当Hesx1在发育中的小鼠胚胎中异位表达时，单独的Hesx1不能改变后脑神经组织的正常命运。然而，在AFB中条件性表达Hesx1可以挽救Hesx1突变体中观察到的前脑缺陷。这一结果为Hesx1在前脑形成中的作用提供了新的见解。
The homeobox gene Hesx1 is an essential repressor that is required within the anterior neural plate for normal forebrain development in mouse and humans. Combining genetic cell labelling and marker analyses, we demonstrate that the absence of Hesx1 leads to a posterior transformation of the anterior forebrain (AFB) during mouse development. Our data suggest that the mechanism underlying this transformation is the ectopic activation of Wnt/beta-catenin signalling within the Hesx1 expression domain in the AFB. When ectopically expressed in the developing mouse embryo, Hesx1 alone cannot alter the normal fate of posterior neural tissue. However, conditional expression of Hesx1 within the AFB can rescue the forebrain defects observed in the Hesx1 mutants. The results presented here provide new insights into the function of Hesx1 in forebrain formation.