奥利格2
重编程
体内
化学
下调和上调
细胞生物学
转录因子
索克斯10
异位表达
基因表达
星形胶质细胞
基因表达调控
抄写(语言学)
祖细胞
转录组
电穿孔
癌症研究
分子生物学
转染
转化(遗传学)
水通道蛋白
神经干细胞
细胞分化
微量注射
体外
生物
祖细胞
转基因
基因
HEK 293细胞
细胞培养
作者
Chuying Lai,Kaiyu Hou,Wenyu Li,Jiahui Wang,Xiaoman Cai,Ya Shi,Miao Yang,Danting Yu,Kang Lu,Wen Li,Gong Chen,Zheng Wu
标识
DOI:10.1038/s41467-026-68869-4
摘要
In vivo astrocyte-to-neuron (AtN) conversion suffers low efficiency due to pre-existing intrinsic barriers. However, it is unclear whether astrocytes have inducible barriers to reprogramming. Here, we identify Olig2, a basic helix-loop-helix (bHLH) transcription factor, as an inducible barrier to Ngn2-mediated AtN conversion. Olig2 is strongly upregulated in cortical astrocytes following the ectopic expression of bHLH neuronal reprogramming factors such as Ngn2, NeuroD1, and Ascl1, but is barely expressed in normal astrocytes. Knocking down Olig2 in Ngn2-transduced astrocytes reduces astrocyte-specific gene expression, enhances neurogenesis-related gene expression, and increases AtN conversion efficiency by approximately threefold. Further multi-omics analysis shows that astrocytic Olig2 directly binds to regulatory regions of pro-neurogenic genes, including Ngn2, inhibiting their expression and impeding the expression of neural progenitor genes. Collectively, our findings reveal Olig2 as an inducible barrier to AtN conversion, providing insights into the regulation of neuronal reprogramming. Astrocyte-to-neuron (AtN) conversion is limited by intrinsic barriers, hindering its efficiency. Here, the authors show that Olig2 acts as an inducible barrier to in vivo Ngn2-mediated AtN conversion, reducing reprogramming efficiency.
科研通智能强力驱动
Strongly Powered by AbleSci AI