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首页> 外文期刊>Neuron >Neural RNA-binding protein Musashi1 controls midline crossing of precerebellar neurons through posttranscriptional regulation of Robo3/Rig-1 expression.
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Neural RNA-binding protein Musashi1 controls midline crossing of precerebellar neurons through posttranscriptional regulation of Robo3/Rig-1 expression.

机译：神经RNA结合蛋白Musashi1通过Robo3 / Rig-1表达的转录后调控来控制小脑前神经元的中线交叉。

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摘要

Precisely regulated spatiotemporal gene expression is essential for the establishment of neural circuits. In contrast to the increasing evidence for transcriptional regulation of axon guidance cues and receptors, the role of posttranscriptional regulation in axon guidance, especially in vivo, remains poorly characterized. Here, we demonstrate that the expression of Slit receptor Robo3/Rig-1, which plays crucial roles in axonal midline crossing, is regulated by a neural RNA-binding protein Musashi1 (Msi1). Msi1 binds to Robo3 mRNA through RNA recognition motifs and increases the protein level of Robo3 without affecting its mRNA level. In Msi1-deficient precerebellar neurons, Robo3 protein, but not its mRNA, is dramatically reduced. Moreover, similar to defects in Robo3-deficient mice, axonal midline crossing and neuronal migration of precerebellar neurons are severely impaired in Msi1-deficient mice. Together, these findings indicate that Msi1-mediated posttranscriptional regulation of Robo3 controls midline crossing of precerebellar neurons.
机译：精确调控的时空基因表达对于神经回路的建立至关重要。与轴突引导提示和受体的转录调控的越来越多的证据相反，转录后调控在轴突引导中的作用，尤其是在体内，仍缺乏很好的表征。在这里，我们证明了Slit受体Robo3 / Rig-1的表达在轴突中线交叉中起关键作用，它是由神经RNA结合蛋白Musashi1（Msi1）调节的。 Msi1通过RNA识别基序与Robo3 mRNA结合，并在不影响其mRNA水平的情况下增加Robo3的蛋白水平。在Msi1缺陷的小脑前神经元中，Robo3蛋白（而不是其mRNA）显着降低。此外，类似于Robo3缺陷小鼠的缺陷，Msi1缺陷小鼠的轴突中线交叉和小脑前神经元的神经元迁移受到严重损害。在一起，这些发现表明Robo3的Msi1介导的转录后调控控制小脑前神经元的中线交叉。

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