STING is known as a central adaptor for sensing cytosolic DNA sensing. Recent studies have provided evidence that STING response is divergent among different cell types. Here, this work demonstrates that STING controls neural progenitor cells (NPCs) by sensing DNA damage in NPCs. The deletion of STING reduces neuronal differentiation and increases proliferation of mouse and human NPCs. Furthermore, STING^cKO mice display autistic‐like behaviors. In NPCs, STING specifically recruits IKKβ and activates nuclear factor κB (NF‐κB) through phosphorylation. NF‐κB binds to ALX4 promoter and triggers ALX4 transcription. In addition, tumor necrosis factor α, an activator of NF‐κB, can rescue some phenotypes caused by STING deletion in mice. Together, the findings show that STING signaling is essential for neuronal gene expression program and has profound consequences on brain function.

中文翻译：

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胚胎性大脑皮层中STING信号的缺乏导致神经源性异常和自闭症行为

STING被称为用于感测胞质DNA感测的中央适配器。最近的研究提供了证据，表明STING反应在不同细胞类型之间存在差异。在这里，这项工作证明STING通过感知NPC中的DNA损伤来控制神经祖细胞（NPC）。STING的缺失减少神经元分化并增加小鼠和人NPC的增殖。此外，STING ^cKO小鼠表现出自闭症样行为。在的NPC，具体STING募集IKK β和激活核因子κ B（NF- κ通过磷酸B）。NF- κ乙结合于启动子ALX4和触发器ALX4转录。此外，肿瘤坏死因子α是NF‐ κ的激活因子B，可以挽救一些由STING缺失引起的小鼠表型。总之，这些发现表明STING信号对于神经元基因表达程序必不可少，并对脑功能产生深远影响。