During embryonic development, radial glial cells give rise to neurons, then to astrocytes following the gliogenic switch. Timely regulation of the switch, operated by several transcription factors, is fundamental for allowing coordinated interactions between neurons and glia. We deleted the gene for one such factor, SOX9, early during mouse brain development and observed a significantly compromised dentate gyrus (DG). We dissected the origin of the defect, targeting embryonic Sox9 deletion to either the DG neuronal progenitor domain or the adjacent cortical hem (CH). We identified in the latter previously uncharacterized ALDH1L1+ astrocytic progenitors, which form a fimbrial-specific glial scaffold necessary for neuronal progenitor migration towards the developing DG. Our results highlight an early crucial role of SOX9 for DG development through regulation of astroglial potential acquisition in the CH. Moreover, we illustrate how formation of a local network, amidst astrocytic and neuronal progenitors originating from adjacent domains, underlays brain morphogenesis.

中文翻译：

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齿状回的发育需要皮质下摆衍生的星形细胞支架。

在胚胎发育期间，放射状神经胶质细胞产生神经元，然后在胶质发生转换后产生星形胶质细胞。由几个转录因子操纵的开关的及时调节，是允许神经元和神经胶质之间协调相互作用的基础。我们在小鼠大脑发育的早期就删除了一个这样的因子SOX9的基因，并观察到一个明显受损的齿状回（DG）。我们解剖了缺陷的起源，针对胚胎Sox9缺失到DG神经元祖域或相邻的皮质下摆（CH）。我们在后者先前未鉴定的ALDH1L1 +星形细胞祖细胞中鉴定出了神经元祖细胞向发育中的DG迁移所必需的纤维特异性神经胶质支架。我们的结果强调了SOX9在DG发育中的早期关键作用，即通过调节CH中星形胶质细胞的潜在捕获来发挥作用。此外，我们说明了本地网络的形成，其中来自相邻域的星形细胞和神经元祖细胞是脑形态发生的基础。