The Requirement of Sox2 for the Spinal Cord Motor Neuron Development of Zebrafish

The Requirement of Sox2 for the Spinal Cord Motor Neuron Development of Zebrafish
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Sox2对斑马鱼脊髓运动神经元发育的要求

DOI:
10.3389/fnmol.2020.00034
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发表时间:
2020-03-27
影响因子:
4.8
通讯作者:
Liu, Dong
Liu, Dong
中科院分区:
医学2区
文献类型:
--
作者:
Gong, Jie;Hu, Songqun;Liu, Dong

文献摘要

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性别决定区Y盒2(Sox 2)作为一种转录因子在神经组织中表达,不仅在神经细胞的多能性和增殖中起重要作用,而且在细胞分化的相反功能中也起重要作用。然而,Sox 2如何与运动神经元发育联系仍然未知。在这里,我们发现,Sox 2定位在脊髓运动神经元的原位杂交和细胞分离,它作为一个积极的调节运动神经元的发育。斑马鱼幼虫Sox 2的缺乏导致中性粒细胞发育异常,包括CaP轴突截短但过度分支、MiP丢失和未分化神经元细胞增加。重要的是,转录组分析表明,Sox 2缺失的胚胎引起许多神经发生,轴突发生,轴突导向和分化相关的基因表达变化,这进一步支持了Sox 2在运动神经元发育中的重要功能。综上所述,这些数据表明Sox 2通过调节神经元分化和神经元轴突的形态在运动神经元发育中起着至关重要的作用。
Sex-determining region Y box 2 (Sox2), expressed in neural tissues, plays an important role as a transcription factor not only in the pluripotency and proliferation of neuronal cells but also in the opposite function of cell differentiation. Nevertheless, how Sox2 is linked to motor neuron development remains unknown. Here, we showed that Sox2 was localized in the motor neurons of spinal cord by in situ hybridization and cell separation, which acted as a positive regulator of motor neuron development. The deficiency of Sox2 in zebrafish larvae resulted in abnormal PMN development, including truncated but excessively branched CaP axons, loss of MiP, and increase of undifferentiated neuron cells. Importantly, transcriptome analysis showed that Sox2-depleted embryos caused many neurogenesis, axonogenesis, axon guidance, and differentiation-related gene expression changes, which further support the vital function of Sox2 in motor neuron development. Taken together, these data indicate that Sox2 plays a crucial role in the motor neuron development by regulating neuron differentiation and morphology of neuron axons.