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Sox9 overexpression exerts multiple stage-dependent effects on mouse spinal cord development.
Glia ( IF 5.4 ) Pub Date : 2019-11-14 , DOI: 10.1002/glia.23752
Julia K Vogel 1 , Matthias Weider 1 , Lisa A Engler 1 , Simone Hillgärtner 1 , Christian Schmitt 1 , Irm Hermans-Borgmeyer 2 , Michael Wegner 1
Affiliation  

The high-mobility-group (HMG)-domain protein Sox9 is one of few transcription factors implicated in gliogenesis in the vertebrate central nervous system. To further study the role of Sox9 in early spinal cord development, we generated a mouse that allows expression of Sox9 in a temporally and spatially controlled manner. Using this mouse, we show that premature Sox9 expression in neural precursor cells disrupted the neuroepithelium of the ventricular zone. Sox9 also compromised development and survival of neuronal precursors and neurons. Additionally, we observed in these mice substantial increases in oligodendroglial and astroglial cells. Reversing the normal order of appearance of essential transcriptional regulators during oligodendrogenesis, Sox10 preceded Olig2. Our study reinforces the notion that Sox9 has a strong gliogenic activity. It also argues that Sox9 expression has to be tightly controlled to prevent negative effects on early spinal cord structure and neuronal development.

中文翻译:

Sox9过表达对小鼠脊髓发育产生多个阶段依赖性的影响。

高迁移率族(HMG)域蛋白Sox9是与脊椎动物中枢神经系统的胶质发生有关的少数转录因子之一。为了进一步研究Sox9在早期脊髓发育中的作用,我们产生了一种小鼠,该小鼠允许以时间和空间控制的方式表达Sox9。使用此小鼠,我们显示神经前体细胞中过早的Sox9表达破坏了心室区的神经上皮细胞。Sox9还损害了神经元前体和神经元的发育和存活。此外,我们在这些小鼠中观察到了少突胶质细胞和星形胶质细胞的大量增加。在少突胶质形成过程中,逆转了必需转录调节因子的正常出现顺序,Sox10先于Olig2。我们的研究强化了Sox9具有很强的胶质生成活性的观念。
更新日期:2019-11-14
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