Six3 inactivation causes progressive caudalization and aberrant patterning of the mammalian diencephalon
Six3 inactivation causes progressive caudalization and aberrant patterning of the mammalian diencephalon
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DOI：
10.1242/dev.010082
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发表时间：
2008-02-01
期刊：
影响因子：
4.6
通讯作者：
Oliver, Guillermo
中科院分区：
文献类型：
--
作者：
Lavado, Alfonso;Lagutin, Oleg V.;Oliver, Guillermo
同源盒基因Six3抑制Wnt1的转录。它也是哺乳动物喙侧前脑发育的前神经板所必需的。我们现在已经确定，在15- 17岁阶段，未来间脑是Six3-null大脑中最前部的结构，Wnt1的表达在前部扩展。因此，大脑呈尾状，在22到24岁的阶段，前瞻丘脑区域是最前面的结构。在E11.0左右，前盖取代了这个结构。Six3分析；Wnt1双缺失小鼠发现Six3介导的Wnt1抑制对于吻侧间脑的形成是必需的，而Six3活性对于端脑的形成是必需的。这些结果为在哺乳动物大脑发育中建立前后身份的机制提供了深入的见解。
The homeobox gene Six3 represses Wnt1 transcription. It is also required in the anterior neural plate for the development of the mammalian rostral forebrain. We have now determined that at the 15-to 17-somite stage, the prospective diencephalon is the most-anterior structure in the Six3-null brain, and Wnt1 expression is anteriorly expanded. Consequently, the brain caudalizes, and at the 22-to 24-somite stage, the prospective thalamic territory is the most-anterior structure. At around E11.0, the pretectum replaces this structure. Analysis of Six3; Wnt1 double-null mice revealed that Six3-mediated repression of Wnt1 is necessary for the formation of the rostral diencephalon and that Six3 activity is required for the formation of the telencephalon. These results provide insight into the mechanisms that establish anteroposterior identity in the developing mammalian brain.