生物
突触后电位
MEF2C公司
神经科学
突触后密度
兴奋性突触后电位
颅面
Mef2
神经发育障碍
抑制性突触后电位
原钙粘蛋白
转录组
突触发生
基因表达
增强子
神经传递
基因表达调控
核糖核酸
细胞生物学
神经鞘素
共域化
内含子
解剖
转录调控
表观遗传学
突触
神经嵴
作者
Liu‐Lin Xiong,Xinwei Huang,Qiu‐Xia Xiao,Yinggang Zheng,He Qin,Chang‐Le Fang,Li Chen,Ruo‐Lan Du,Qiulin Wang,Li‐Ren Huangfu,Yongshuai Fei,Yang‐Yang Zhao,Chen‐Yang Zhai,Zhen Chen,S. C. Yuan,Y Z Zhou,Xue He,Tingting Zhi,Xiaohe Tian,Ting‐Hua Wang
标识
DOI:10.1002/advs.202504191
摘要
Nonsyndromic cleft lip and palate (NSCLP) is a common craniofacial malformation increasingly recognized to involve neurodevelopmental abnormalities, though the molecular basis remains unclear. Here, single-nucleus RNA sequencing of the superior temporal plane from mid-gestation NSCLP fetuses is performed, and profound alterations in cell-type composition, intercellular communication, and transcriptional programs are uncovered. Integrative analyses with weighted gene co-expression network analysis and single-cell regulatory network interference and clustering based on single-nucleus transcriptomes identify myocyte enhancer factor 2C (MEF2C) as a shared transcriptional regulator consistently downregulated in excitatory and inhibitory neurons across mid-term gestation, which is validated in NSCLP fetal brain tissues. MEF2C expression is negatively correlated with synaptophysin immunofluorescence intensity. In MEF2C-deficient primary cortical neurons, impaired synaptic formation, reduced postsynaptic density protein-95 expression, and weakened excitatory postsynaptic transmission without altering intrinsic excitability are found. Upstream regulators of MEF2C are enriched for pathways controlling neuronal differentiation, synaptic plasticity, and epigenetic regulation, suggesting broad disruption of neurodevelopmental programs. Together, this study provides molecular evidence of disrupted brain development in NSCLP and implicates MEF2C as a potential mediator of neurodevelopmental impairments.
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