During early development, signaling centers, such as the cortical hem and the preoptic area (POA), are critical for telencephalic patterning. However, the mechanisms underlying the maintenance of signal centers are poorly understood. Here, we report that the transcription factor Foxg1 is required to confine the POA, a resource of Sonic Hedgehog (Shh) that is pivotal for ventral telencephalic development. Cell-specific deletion of Foxg1 achieved by crossing Foxg1fl/fl with Dbx1-cre or Nestin-CreER combined with tamoxifen induction results in a dramatic expansion of the POA accompanied by the significantly increased activity of the Shh signaling pathway. Ventral pattern formation was severely impaired. Moreover, we demonstrated that Foxg1 directly represses Dbx1 to restrict the POA. Furthermore, we found that the ventral pallium was expanded, which might also contribute to the observed patterning defects. These findings will improve our understanding of the maintenance of signal centers and help to elucidate the mechanisms underlying ventral telencephalic patterning.

中文翻译：

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Foxg1直接抑制Dbx1以限制POA，并随后调节腹侧脑脊髓形态。

在早期开发期间，信号传输中心（例如皮质下摆和视前区（POA））对于端脑模式至关重要。但是，对信号中心维护的基本机制了解甚少。在这里，我们报告需要转录因子Foxg1来限制POA，而POA是Sonic Hedgehog（Shh）的资源，对于腹侧脑神经发育至关重要。通过将Foxg1fl / fl与Dbx1-cre或Nestin-CreER与他莫昔芬诱导相结合而实现的Foxg1的细胞特异性缺失导致POA的急剧扩增，同时伴随着Shh信号通路活性的显着增加。腹型形成严重受损。此外，我们证明了Foxg1直接抑制Dbx1来限制POA。此外，我们发现腹侧掌骨扩张，这也可能有助于观察到的图案缺陷。这些发现将增进我们对维持信号中心的理解，并有助于阐明腹侧脑脑模式的机制。