The bHLH transcription factor Olig2 promotes oligodendrocyte differentiation in collaboration with Nkx2.2
The bHLH transcription factor Olig2 promotes oligodendrocyte differentiation in collaboration with Nkx2.2
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DOI：
10.1016/s0896-6273(01)00414-7
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发表时间：
2001-09-13
期刊：
影响因子：
16.2
通讯作者：
Anderson, DJ
中科院分区：
文献类型：
--
作者：
Zhou, Q;Choi, G;Anderson, DJ
Olig2是一种碱性螺旋-环-螺旋（bHLH）转录因子，在脊髓心室区的限制性结构域中表达，该区域依次产生运动神经元和少突胶质细胞。就在少突胶质细胞前体形成之前，Olig2和Nkx2.2表达的结构域从相互排斥切换到重叠，并且Neurogenins 1和2在该区域内消失。Olig2与Nkx2.2在脊髓中的共表达促进异位和早熟少突胶质细胞分化这两种蛋白质在本试验中均作为转录抑制因子发挥作用。这种作用被神经生成素1的强制表达阻断。相比之下，Olig2单独的错误表达解除神经生成素的抑制并促进运动神经元分化。因此，Olig2在运动神经元和少突胶质细胞中依次起作用，命运特化。这种双重作用是通过Olig2功能性相互作用的其他转录因子的表达结构域的时空变化来实现的。
Olig2, a basic helix-loop-helix (bHLH) transcription factor, is expressed in a restricted domain of the spinal cord ventricular zone that sequentially generates motoneurons and oligodendrocytes. Just prior to oligodendrocyte precursor formation, the domains of Olig2 and Nkx2.2 expression switch from being mutually exclusive to overlapping, and Neurogenins1 and 2 are extinguished within this region. Coexpression of Olig2 with Nkx2.2 in the spinal cord promotes ectopic and precocious oligodendrocyte differentiation. Both proteins function as transcriptional repressors in this assay. This effect is blocked by forced expression of Neurogenin1. By contrast, misexpression of Olig2 alone derepresses Neurogenins and promotes motoneuron differentiation. Olig2 therefore functions sequentially in motoneuron and oligodendrocyte, fate specification. This dual action is enabled by spatio-temporal changes in the expression domains of other transcription factors with which Olig2 functionally interacts.