a Department of Medical Microbiology and Immunology, School of Medicine , Genome Center, MIND Institute, University of California , Davis , CA , USA.
Epigenetics. 2019 Jul;14(7):672-684. doi: 10.1080/15592294.2019.1609867. Epub 2019 May 6.
Down Syndrome (DS) is the most common genetic cause of intellectual disability, in which an extra copy of human chromosome 21 (HSA21) affects regional DNA methylation profiles across the genome. Although DNA methylation has been previously examined at select regulatory regions across the genome in a variety of DS tissues and cells, differentially methylated regions (DMRs) have yet to be examined in an unbiased sequencing-based approach. Here, we present the first analysis of DMRs from whole genome bisulfite sequencing (WGBS) data of human DS and matched control brain, specifically frontal cortex. While no global differences in DNA methylation were observed, we identified 3,152 DS-DMRs across the entire genome, the majority of which were hypermethylated in DS. DS-DMRs were significantly enriched at CpG islands and de-enriched at specific gene body and regulatory regions. Functionally, the hypermethylated DS-DMRs were enriched for one-carbon metabolism, membrane transport, and glutamatergic synaptic signalling, while the hypomethylated DMRs were enriched for proline isomerization, glial immune response, and apoptosis. Furthermore, in a cross-tissue comparison to previous studies of DNA methylation from diverse DS tissues and reference epigenomes, hypermethylated DS-DMRs showed a strong cross-tissue concordance, while a more tissue-specific pattern was observed for the hypomethylated DS-DMRs. Overall, this approach highlights that low-coverage WGBS of clinical samples can identify epigenetic alterations to known biological pathways, which are potentially relevant to therapeutic treatments and include metabolic pathways. These results also provide new insights into the genome-wide effects of genetic alterations on DNA methylation profiles indicative of altered neurodevelopment and brain function.
唐氏综合征(DS)是最常见的遗传性智力障碍,其病因是人类 21 号染色体(HSA21)多出一条,影响整个基因组的局部 DNA 甲基化谱。尽管之前已经在各种 DS 组织和细胞中对基因组中特定调控区域的 DNA 甲基化进行了研究,但尚未采用无偏测序方法研究差异甲基化区域(DMR)。在这里,我们首次分析了人类 DS 及配对对照大脑(特别是额叶皮质)全基因组亚硫酸氢盐测序(WGBS)数据中的 DMR。虽然没有观察到 DNA 甲基化的全局差异,但我们在整个基因组中鉴定出 3152 个 DS-DMR,其中大多数在 DS 中呈超甲基化。DS-DMR 在 CpG 岛显著富集,在特定基因体和调控区显著去富集。从功能上看,超甲基化的 DS-DMR 富含一碳代谢、膜转运和谷氨酸能突触信号传导,而低甲基化的 DMR 富含脯氨酸异构化、神经胶质免疫反应和细胞凋亡。此外,与来自不同 DS 组织和参考表观基因组的先前 DNA 甲基化研究进行跨组织比较时,超甲基化的 DS-DMR 表现出很强的跨组织一致性,而低甲基化的 DS-DMR 则表现出更具组织特异性的模式。总的来说,这种方法强调了对临床样本进行低覆盖率 WGBS 可以识别已知生物学途径的表观遗传改变,这些改变可能与治疗方法有关,包括代谢途径。这些结果还为遗传改变对指示神经发育和大脑功能改变的 DNA 甲基化谱的全基因组影响提供了新的见解。