microRNA对神经前体自我更新和分化的调控。

Neurogenesis (Austin, Tex.) Pub Date : 2014-11-17 eCollection Date: 2014-01-01 DOI:10.4161/23262133.2014.976018
Laura I Hudish, Bruce Appel
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引用次数: 2

摘要

在脊椎动物中枢神经系统发育的早期阶段,神经前体对称分裂产生新的前体,从而扩大了前体种群。在神经发育的中期,前体转变为不对称分裂模式,即每次有丝分裂产生一个新的前体和一个分化为神经元或胶质细胞的细胞。在发育的后期,大多数前体停止分裂并最终分化。Par复合物蛋白与神经前体的顶膜有关,促进前体的自我更新。Par蛋白如何下调以结束前体自我更新尚不清楚。我们对斑马鱼神经发育的研究发现,microRNA miR-219负调控顶端Par蛋白,从而促进神经前体分裂的停止和末梢分化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
microRNA regulation of neural precursor self-renewal and differentiation.

During early stages of development of the vertebrate central nervous system, neural precursors divide symmetrically to produce new precursors, thereby expanding the precursor population. During middle stages of neural development, precursors switch to an asymmetric division pattern whereby each mitosis produces one new precursor and one cell that differentiates as a neuron or glial cell. At late stages of development, most precursors stop dividing and terminally differentiate. Par complex proteins are associated with the apical membrane of neural precursors and promote precursor self-renewal. How Par proteins are down regulated to bring precursor self-renewal to an end has not been known. Our investigations of zebrafish neural development revealed that the microRNA miR-219 negatively regulates apical Par proteins, thereby promoting cessation of neural precursor division and driving terminal differentiation.

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