Reevaluating the Role of Pou3f1 in Striatal Development: Evidence from Transgenic Mouse Models.

IF 3.5 3区医学 Q2 NEUROSCIENCES Brain Research Bulletin Pub Date : 2025-03-13 DOI:10.1016/j.brainresbull.2025.111302

Xiaolei Song, Fengzhu Zhang, Danyu Han, Jingzhe Yu, Qian Ren, Xiaoming Xin, Rongliang Guo, Weidong Le

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Abstract

The striatum, a critical component of the basal ganglia, is essential for motor control, cognitive processing, and emotional regulation. Medium spiny neurons (MSNs) are the primary neuronal population in the striatum, classified into D1 and D2 subtypes. The transcription factor Pou3f1 has been hypothesized to play a crucial role in the development of pyramidal neurons. Recently, a comprehensive analysis of the human embryonic scRNA-seq dataset predicted and emphasized the bridging function of POU3F1 between striatal progenitor cells and immature neurons, though this finding lacked genetic validation. In this study, we found that Pou3f1 expression was significantly reduced after Six3 deletion. However, Pou3f1 deletion does not significantly affect the number or subtype composition of MSNs, nor the proliferation and differentiation of progenitor cells, in our Pou3f1 conditional knockout (cko) mice, challenging the in silico predictions based on human data. These results suggest that Pou3f1 is not required for the specification, generation, or differentiation of MSNs, though its potential involvement in other aspects of striatal development cannot be entirely ruled out.

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纹状体是基底神经节的重要组成部分，对运动控制、认知处理和情绪调节至关重要。中刺神经元（MSN）是纹状体的主要神经元群，分为 D1 和 D2 亚型。转录因子 Pou3f1 被认为在锥体神经元的发育过程中起着至关重要的作用。最近，一项对人类胚胎scRNA-seq数据集的综合分析预测并强调了POU3F1在纹状体祖细胞和未成熟神经元之间的桥接功能，但这一发现缺乏基因验证。在本研究中，我们发现在缺失 Six3 后，Pou3f1 的表达显著减少。然而，在我们的 Pou3f1 条件性基因敲除（ckout，cko）小鼠中，Pou3f1 基因缺失并不明显影响 MSN 的数量或亚型组成，也不影响祖细胞的增殖和分化，这对基于人类数据的硅学预测提出了挑战。这些结果表明，Pou3f1不是MSN的规范、生成或分化所必需的，尽管不能完全排除它可能参与纹状体发育的其他方面。

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来源期刊

Brain Research Bulletin 医学-神经科学

CiteScore

6.90

自引率

2.60%

发文量

253

审稿时长

67 days

期刊介绍： The Brain Research Bulletin (BRB) aims to publish novel work that advances our knowledge of molecular and cellular mechanisms that underlie neural network properties associated with behavior, cognition and other brain functions during neurodevelopment and in the adult. Although clinical research is out of the Journal''s scope, the BRB also aims to publish translation research that provides insight into biological mechanisms and processes associated with neurodegeneration mechanisms, neurological diseases and neuropsychiatric disorders. The Journal is especially interested in research using novel methodologies, such as optogenetics, multielectrode array recordings and life imaging in wild-type and genetically-modified animal models, with the goal to advance our understanding of how neurons, glia and networks function in vivo.