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首页> 外文期刊>Neuron >An Isoform-Specific SnoN1-FOXO1 Repressor Complex Controls Neuronal Morphogenesis and Positioning in the Mammalian Brain.
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An Isoform-Specific SnoN1-FOXO1 Repressor Complex Controls Neuronal Morphogenesis and Positioning in the Mammalian Brain.

机译：一个特定的同工型SnoN1-FOXO1阻遏物复杂控制神经元形态发生和哺乳动物大脑中的位置。

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摘要

Control of neuronal positioning is fundamental to normal brain development. However, the cell-intrinsic mechanisms that govern neuronal positioning remain to be elucidated. Here, we report that the spliced protein products of the transcriptional regulator SnoN, SnoN1 and SnoN2, harbor opposing functions in the coordinate regulation of neuronal branching and positioning. Knockdown of SnoN2 stimulates axon branching in primary neurons and impairs migration of granule neurons in the rat cerebellar cortex in vivo. By contrast, SnoN1 knockdown suppresses SnoN2 knockdown-induced neuronal branching and strikingly triggers excessive migration of granule neurons in the cerebellar cortex. We also find that SnoN1 forms a complex with the transcription factor FOXO1 that represses the X-linked lissencephaly gene encoding doublecortin (DCX). Accordingly, repression of DCX mediates the ability of SnoN1 to regulate branching in primary neurons and granule neuron migration in vivo. These data define an isoform-specific SnoN1-FOXO1 transcriptional complex that orchestrates neuronal branching and positioning in the brain with important implications for the study of developmental disorders of cognition and epilepsy.
机译：控制神经元定位是正常大脑发育的基础。然而，控制神经元定位的细胞内在机制尚待阐明。在这里，我们报道转录调节器SnoN，SnoN1和SnoN2的剪接蛋白产物在神经元分支和定位的协调调控中具有相反的功能。击倒SnoN2会刺激大鼠小脑皮质中的神经元轴突分支，并削弱颗粒神经元在大鼠小脑皮质中的迁移。相比之下，SnoN1击倒抑制SnoN2击倒诱导的神经元分支，并惊人地触发小脑皮层中的颗粒神经元的过度迁移。我们还发现SnoN1与转录因子FOXO1形成复合物，该转录因子可抑制编码双皮质素（DCX）的X连锁的lissencephaly基因。因此，DCX的抑制介导SnoN1调节体内原代神经元和颗粒神经元迁移的能力。这些数据定义了一个异构体特异的SnoN1-FOXO1转录复合物，该复合物可协调大脑中神经元的分支和定位，对研究认知和癫痫的发展障碍具有重要意义。

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