A feedback regulatory loop involving microRNA-9 and nuclear receptor TLX in neural stem cell fate determination.
A feedback regulatory loop involving microRNA-9 and nuclear receptor TLX in neural stem cell fate determination.
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DOI：
10.1038/nsmb.1576
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发表时间：
2009-04
影响因子：
16.8
通讯作者：
中科院分区：
文献类型：
--
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microrna在干细胞生物学中扮演着重要的角色。其中，microRNA-9 （miR-9）在大脑的神经源性区域特异性表达。miR-9是否在神经干细胞自我更新和分化中发挥作用尚不清楚。我们之前已经证明核受体TLX是神经干细胞自我更新的重要调节因子。本研究表明，miR-9抑制TLX表达，负向调节神经干细胞增殖，加速神经分化。引入缺乏miR-9识别位点的TLX表达载体可挽救miR-9诱导的增殖缺陷并抑制早熟分化。胚胎脑内miR-9的子宫电穿孔导致转染的神经干细胞过早分化和向外迁移。此外，TLX抑制miR-9 pri-miRNA的表达。MiR-9通过与TLX形成负调控环，建立了控制神经干细胞增殖与分化平衡的模型。
MicroRNAs are important players in stem cell biology. Among them, microRNA-9 (miR-9) is expressed specifically in neurogenic areas of the brain. Whether miR-9 plays a role in neural stem cell self-renewal and differentiation is unknown. We showed previously that nuclear receptor TLX is an essential regulator of neural stem cell self-renewal. Here we show that miR-9 suppresses TLX expression to negatively regulate neural stem cell proliferation and accelerate neural differentiation. Introducing a TLX expression vector lacking the miR-9 recognition site rescued miR-9-induced proliferation deficiency and inhibited precocious differentiation. In utero electroporation of miR-9 in embryonic brains led to premature differentiation and outward migration of the transfected neural stem cells. Moreover, TLX represses miR-9 pri-miRNA expression. MiR-9, by forming a negative regulatory loop with TLX, establishes a model for controlling the balance between neural stem cell proliferation and differentiation.
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