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首页> 外文期刊>Molecular and Cellular Biology >Disruption of CK2β in Embryonic Neural Stem Cells Compromises Proliferation and Oligodendrogenesis in the Mouse Telencephalon
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Disruption of CK2β in Embryonic Neural Stem Cells Compromises Proliferation and Oligodendrogenesis in the Mouse Telencephalon

机译：胚胎神经干细胞中CK2β的破坏损害小鼠端脑的增殖和少突胶质生成。

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Genetic programs that govern neural stem/progenitor cell (NSC) proliferation and differentiation are dependent on extracellular cues and a network of transcription factors, which can be regulated posttranslationally by phosphorylation. However, little is known about the kinase-dependent pathways regulating NSC maintenance and oligodendrocyte development. We used a conditional knockout approach to target the murine regulatory subunit (beta) of protein kinase casein kinase 2 (CK2β) in embryonic neural progenitors. Loss of CK2β leads to defects in proliferation and differentiation of embryonic NSCs. We establish CK2β as a key positive regulator for the development of oligodendrocyte precursor cells (OPCs), both in vivo and in vitro. We show that CK2β directly interacts with the basic helix-loop-helix (bHLH) transcription factor Olig2, a critical modulator of OPC development, and activates the CK2-dependent phosphorylation of its serine-threonine-rich (STR) domain. Finally, we reveal that the CK2-targeted STR domain is required for the oligodendroglial function of Olig2. These findings suggest that CK2 may control oligodendrogenesis, in part, by regulating the activity of the lineage-specific transcription factor Olig2. Thus, CK2β appears to play an essential and uncompensated role in central nervous system development.
机译：控制神经干/祖细胞（NSC）增殖和分化的遗传程序取决于细胞外信号和转录因子网络，转录因子网络可以通过磷酸化进行翻译后调控。但是，关于调节NSC维持和少突胶质细胞发育的激酶依赖性途径知之甚少。我们使用了条件敲除方法来靶向胚胎神经祖细胞中蛋白激酶酪蛋白激酶2（CK2β）的小鼠调节亚基（beta）。 CK2 β的缺失导致胚胎NSC增殖和分化的缺陷。我们将 CK2 β建立为体内 和 的少突胶质细胞前体细胞（OPC）发育的关键正调节剂。我们显示CK2β直接与基本螺旋-环-螺旋（bHLH）转录因子Olig2相互作用，这是OPC发展的关键调节剂，并激活其富含丝氨酸-苏氨酸（STR）域的CK2依赖性磷酸化。最后，我们揭示了Olig2的少突神经胶质功能需要CK2靶向的STR域。这些发现表明CK2可能部分地通过调节谱系特异性转录因子Olig2的活性来控制少突胶质生成。因此，CK2β在中枢神经系统发育中似乎起着必不可少的作用。

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