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转录因子促进直接通路中型多棘神经元(D1 MSN)的特性,并抑制间接通路中型多棘神经元(D2 MSN)的特性。

The transcription factor promotes the D1 MSN identity and represses the D2 MSN identity.

作者信息

Shang Zicong, Yang Lin, Wang Ziwu, Tian Yu, Gao Yanjing, Su Zihao, Guo Rongliang, Li Weiwei, Liu Guoping, Li Xiaosu, Yang Zhengang, Li Zhenmeiyu, Zhang Zhuangzhi

机构信息

Key Laboratory of Birth Defects, Children's Hospital of Fudan University, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, China.

出版信息

Front Cell Dev Biol. 2022 Aug 23;10:948331. doi: 10.3389/fcell.2022.948331. eCollection 2022.

DOI:10.3389/fcell.2022.948331
PMID:36081908
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9445169/
Abstract

The striatum is primarily composed of two types of medium spiny neurons (MSNs) expressing either D1- or D2-type dopamine receptors. However, the fate determination of these two types of neurons is not fully understood. Here, we found that D1 MSNs undergo fate switching to D2 MSNs in the absence of . Furthermore, scRNA-seq revealed that the transcription factor affects the differentiation of these progenitor cells in the lateral ganglionic eminence (LGE). More importantly, we found that the transcription factors , which are required for the differentiation of D2 MSNs, are repressed by . Finally, sustained expression in LGE progenitor cells promoted the D1 MSN identity and repressed the D2 MSN identity. Overall, our findings indicated that promotes the D1 MSN identity and represses the D2 MSN identity by regulating expression during striatal MSN development.

摘要

纹状体主要由表达D1型或D2型多巴胺受体的两种中型多棘神经元(MSN)组成。然而,这两种类型神经元的命运决定尚未完全明确。在此,我们发现D1 MSN在缺乏……的情况下会发生命运转换成为D2 MSN。此外,单细胞RNA测序显示转录因子影响外侧神经节隆起(LGE)中这些祖细胞的分化。更重要的是,我们发现D2 MSN分化所需的转录因子被……抑制。最后,LGE祖细胞中持续的……表达促进了D1 MSN特性并抑制了D2 MSN特性。总体而言,我们的研究结果表明……在纹状体MSN发育过程中通过调节……表达来促进D1 MSN特性并抑制D2 MSN特性。

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Cell Death Discov. 2022 Jun 30;8(1):301. doi: 10.1038/s41420-022-01088-0.
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Development. 2022 Feb 15;149(4). doi: 10.1242/dev.200035. Epub 2022 Feb 23.
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