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首页> 外文期刊>Neuron >Spatiotemporal 16p11.2 Protein Network Implicates Cortical Late Mid-Fetal Brain Development and KCTD13-Cul3-RhoA Pathway in Psychiatric Diseases
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Spatiotemporal 16p11.2 Protein Network Implicates Cortical Late Mid-Fetal Brain Development and KCTD13-Cul3-RhoA Pathway in Psychiatric Diseases

机译：时空16p11.2蛋白质网络牵涉到精神疾病中的皮质中晚期胎儿大脑发育和KCTD13-Cul3-RhoA途径。

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The psychiatric disorders autism and schizophrenia have a strong genetic component, and copy number variants (CNVs) are firmly implicated. Recurrent deletions and duplications of chromosome 16p11.2 confer a high risk for both diseases, but the pathways disrupted by this CNV are poorly defined. Here we investigate the dynamics of the 16p11.2 network by integrating physical interactions of 16p11.2 proteins with spatiotemporal gene expression from the developing human brain. We observe profound changes in protein interaction networks throughout different stages of brain development and/or in different brain regions. We identify the late mid-fetal period of cortical development as most critical for establishing the connectivity of 16p11.2 proteins with their co-expressed partners. Furthermore, our results suggest that the regulation of the KCTD13-Cul3-RhoA pathway in layer 4 of the inner cortical plate is crucial for controlling brain size and connectivity and that its dysregulation by de novo mutations may be a potential determinant of 16p11.2 CNV deletion and duplication phenotypes.
机译：精神病性自闭症和精神分裂症具有很强的遗传成分，与拷贝数变异（CNV）密切相关。染色体16p11.2的反复缺失和重复会给这两种疾病带来很高的风险，但是被这种CNV破坏的途径定义不清。在这里，我们通过将16p11.2蛋白与时空基因表达的物理相互作用整合在一起来研究16p11.2网络的动力学，该时空基因表达来自人类大脑。我们观察到大脑发育不同阶段和/或不同大脑区域中蛋白质相互作用网络的深刻变化。我们确定胎儿发育后期的中期皮质对于建立16p11.2蛋白与其共表达伴侣的连接性至关重要。此外，我们的结果表明，内皮质板第4层中KCTD13-Cul3-RhoA途径的调控对于控制大脑的大小和连通性至关重要，并且其从头突变引起的失调可能是16p11.2 CNV的潜在决定因素。删除和重复表型。

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