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首页> 外文期刊>Molecular and Cellular Biology >Role of Krüppel-Like Factor 4 in Neurogenesis and Radial Neuronal Migration in the Developing Cerebral Cortex
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Role of Krüppel-Like Factor 4 in Neurogenesis and Radial Neuronal Migration in the Developing Cerebral Cortex

机译：克虏伯样因子4在发展中的大脑皮层的神经发生和径向神经元迁移中的作用。

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Transcription factors play key roles in the formation of a multilayered cerebral cortex consisting of neurons and glial cells. Krüppel-like factor 4 (KLF4) is expressed in neural stem cells and controls axonal regeneration. Its dysregulation leads to hydrocephalus in postnatal mouse brains. Here, we further show that KLF4 regulates neurogenesis and radial migration of neurons in the developing cerebral cortex. Neural progenitors with constitutive expression of KLF4 fail to migrate and develop into mature neurons but, rather, form cells with a glial identity. Notably, the JAK-STAT pathway is altered by KLF4, with increased phosphorylation of STAT3 at tyrosine 705. Blocking STAT3 activation with a dominant negative form can rescue the migration defect induced by constitutive KLF4 expression. Furthermore, downregulation of endogenous KLF4 significantly promotes radial migration and the transition of newly born migrating neurons from multipolar to bipolar morphology. Together, these results suggest that precise regulation of KLF4 expression is critical to neuronal differentiation and migration during the formation of a cerebral cortex.
机译：转录因子在由神经元和神经胶质细胞组成的多层大脑皮层的形成中起关键作用。 Krüppel样因子4（KLF4）在神经干细胞中表达并控制轴突再生。它的失调导致出生后小鼠大脑中脑积水。在这里，我们进一步表明，KLF4调节发育中的大脑皮层中神经元的神经发生和径向迁移。具有KLF4组成型表达的神经祖细胞无法迁移并发育成成熟的神经元，而是形成具有神经胶质特性的细胞。值得注意的是，JAK-STAT途径被KLF4改变，酪氨酸705处的STAT3磷酸化增加。以显性负性形式阻断STAT3激活可以挽救由组成型KLF4表达诱导的迁移缺陷。此外，内源性KLF4的下调显着促进了径向迁移和新生迁移神经元从多极形态到双极形态的转变。总之，这些结果表明，KLF4表达的精确调节对于大脑皮层形成过程中的神经元分化和迁移至关重要。

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