Olig2 transcription factor is essential for the maintenance of neural progenitor cells (NPCs) in the pMN domain and their sequential specification into motor neurons (MNs) and oligodendrocyte precursor cells (OPCs). The expression of Olig2 rapidly declines in newly generated MNs. However, Olig2 expression persists in later-born OPCs and antagonizes the expression of MN-related genes. The mechanism underlying the differential expression of Olig2 in MNs and oligodendrocytes remains unknown. Here, we report that activation of WNT/β-catenin signaling in pMN lineage cells abolished Olig2 expression coupled with a dramatic increase of Ngn2 expression. Luciferase reporter assay showed that Ngn2 inhibited Olig2 promoter activity. Overexpression of Ngn2-EnR transcription repressor blocked the expression of Olig2 in ovo. Our results suggest that down-regulation of WNT-Ngn2 signaling contributes to oligodendrogenesis from the pMN domain and the persistent Olig2 expression in OPCs.

中文翻译：

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WNT 信号通过 Ngn2 依赖性直接抑制 Olig2 表达抑制少突胶质细胞生成

Olig2 转录因子对于维持 pMN 域中的神经祖细胞 (NPC) 及其序列规范为运动神经元 (MN) 和少突胶质细胞前体细胞 (OPC) 至关重要。Olig2 的表达在新生成的 MN 中迅速下降。然而，Olig2 表达在后来出生的 OPCs 中持续存在并拮抗 MN 相关基因的表达。Olig2 在 MN 和少突胶质细胞中差异表达的机制尚不清楚。在这里，我们报告了 pMN 谱系细胞中 WNT/β-连环蛋白信号传导的激活消除了 Olig2 表达，同时 Ngn2 表达显着增加。荧光素酶报告基因检测表明 Ngn2 抑制 Olig2 启动子活性。Ngn2-EnR 转录阻遏物的过度表达阻止 Olig2 在卵内的表达。