Notch/Hes信号和miR-9参与复杂的反馈相互作用,控制神经祖细胞的增殖和分化。

Neurogenesis (Austin, Tex.) Pub Date : 2017-05-12 eCollection Date: 2017-01-01 DOI:10.1080/23262133.2017.1313647
Beate Roese-Koerner, Laura Stappert, Oliver Brüstle
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引用次数: 39

摘要

典型Notch信号在神经系统发育过程中具有多种功能,对神经祖细胞自我更新、分化时间和各种细胞命运的规范至关重要。Notch介导的自我更新的一个关键特征是其在神经祖细胞群中的波动活动以及Notch效应物Hes1及其靶基因的振荡表达模式。Hes1和神经源性microRNA miR-9之间的负反馈回路被发现是这个振荡时钟的一部分。在最近的一项研究中,我们发现Notch胞内结构域/RBPj转录复合物直接结合miR-9_2启动子可进一步调节miR-9的表达。反过来,miR-9不仅可以靶向Hes1,还可以靶向Notch2,从而减弱Notch信号,促进神经元分化。在这里,我们讨论了两个相互交织的反馈回路如何提供一个额外的失败保存机制来控制神经祖细胞群中的增殖和分化。此外,我们探讨了mir -9介导的Notch/Hes1信号调节在神经祖细胞稳态、模式、分化时间和肿瘤形成方面的潜在意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Notch/Hes signaling and miR-9 engage in complex feedback interactions controlling neural progenitor cell proliferation and differentiation.

Canonical Notch signaling has diverse functions during nervous system development and is critical for neural progenitor self-renewal, timing of differentiation and specification of various cell fates. A key feature of Notch-mediated self-renewal is its fluctuating activity within the neural progenitor cell population and the oscillatory expression pattern of the Notch effector Hes1 and its target genes. A negative feedback loop between Hes1 and neurogenic microRNA miR-9 was found to be part of this oscillatory clock. In a recent study we discovered that miR-9 expression is further modulated by direct binding of the Notch intracellular domain/RBPj transcriptional complex to the miR-9_2 promoter. In turn, miR-9 not only targets Hes1 but also Notch2 to attenuate Notch signaling and promote neuronal differentiation. Here, we discuss how the two interwoven feedback loops may provide an additional fail-save mechanism to control proliferation and differentiation within the neural progenitor cell population. Furthermore, we explore potential implications of miR-9-mediated regulation of Notch/Hes1 signaling with regard to neural progenitor homeostasis, patterning, timing of differentiation and tumor formation.

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