Department of Neuroscience, Washington University School of Medicine, St. Louis, MO 63110-1093, USA.
Department of Neuroscience, Washington University School of Medicine, St. Louis, MO 63110-1093, USA.
Mol Cell. 2020 Jan 16;77(2):279-293.e8. doi: 10.1016/j.molcel.2019.10.033. Epub 2019 Nov 26.
The genomes of mammalian neurons contain uniquely high levels of non-CG DNA methylation that can be bound by the Rett syndrome protein, MeCP2, to regulate gene expression. How patterns of non-CG methylation are established in neurons and the mechanism by which this methylation works with MeCP2 to control gene expression is unclear. Here, we find that genes repressed by MeCP2 are often located within megabase-scale regions of high non-CG methylation that correspond with topologically associating domains of chromatin folding. MeCP2 represses enhancers found in these domains that are enriched for non-CG and CG methylation, with the strongest repression occurring for enhancers located within MeCP2-repressed genes. These alterations in enhancer activity provide a mechanism for how MeCP2 disruption in disease can lead to widespread changes in gene expression. Hence, we find that DNA topology can shape non-CG DNA methylation across the genome to dictate MeCP2-mediated enhancer regulation in the brain.
哺乳动物神经元的基因组含有独特的高水平非 CG DNA 甲基化,这种甲基化可以被 Rett 综合征蛋白 MeCP2 结合,从而调节基因表达。然而,非 CG 甲基化的模式如何在神经元中建立,以及这种甲基化与 MeCP2 协同作用控制基因表达的机制尚不清楚。在这里,我们发现 MeCP2 抑制的基因通常位于具有高非 CG 甲基化的、与染色质折叠拓扑关联域对应的、兆碱基规模的区域内。MeCP2 抑制这些区域中的增强子,这些增强子富含非 CG 和 CG 甲基化,而位于 MeCP2 抑制基因内的增强子受到的抑制最强。这些增强子活性的改变为 MeCP2 功能障碍如何导致疾病中广泛的基因表达变化提供了一种机制。因此,我们发现 DNA 拓扑结构可以塑造基因组中的非 CG DNA 甲基化,从而在大脑中决定 MeCP2 介导的增强子调控。