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去极化释放的印记miR-184受MeCP2依赖性抑制。

MeCP2-dependent repression of an imprinted miR-184 released by depolarization.

作者信息

Nomura Tasuku, Kimura Mika, Horii Takuro, Morita Sumiyo, Soejima Hidenobu, Kudo Shinichi, Hatada Izuho

机构信息

Laboratory of Genome Science, Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University, 3-39-15 Showa-machi, Maebashi 371-8512, Japan

出版信息

Hum Mol Genet. 2008 Apr 15;17(8):1192-9. doi: 10.1093/hmg/ddn011. Epub 2008 Jan 18.

Abstract

Both fragile X syndrome and Rett syndrome are commonly associated with autism spectrum disorders and involve defects in synaptic plasticity. MicroRNA is implicated in synaptic plasticity because fragile X mental retardation protein was recently linked to the microRNA pathway. DNA methylation is also involved in synaptic plasticity since methyl CpG-binding protein 2 (MeCP2) is mutated in patients with Rett syndrome. Here we report that expression of miR-184, a brain-specific microRNA repressed by the binding of MeCP2 to its promoter, is upregulated by the release of MeCP2 after depolarization. The restricted release of MeCP2 from the paternal allele results in paternal allele-specific expression of miR-184. Our finding provides a clue to the link between the microRNA and DNA methylation pathways.

摘要

脆性X综合征和雷特综合征都通常与自闭症谱系障碍相关,且涉及突触可塑性缺陷。微小RNA与突触可塑性有关,因为脆性X智力低下蛋白最近与微小RNA途径相关联。DNA甲基化也参与突触可塑性,因为甲基CpG结合蛋白2(MeCP2)在雷特综合征患者中发生突变。在此我们报告,miR-184(一种被MeCP2与其启动子结合所抑制的脑特异性微小RNA)的表达在去极化后因MeCP2的释放而上调。MeCP2从父本等位基因的受限释放导致miR-184的父本等位基因特异性表达。我们的发现为微小RNA和DNA甲基化途径之间的联系提供了线索。

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