Maggio Angela G, Shu Henry T, Laufer Benjamin I, Bi Chongfeng, Lai Yinglei, LaSalle Janine M, Hu Valerie W
Department of Biochemistry and Molecular Medicine, The George Washington University School of Medicine and Health Sciences, Washington, DC, United States.
The Johns Hopkins University, School of Medicine, Baltimore, MD, United States.
Front Genet. 2022 Aug 11;13:929471. doi: 10.3389/fgene.2022.929471. eCollection 2022.
Environmental exposures to endocrine disrupting compounds (EDCs) such as the organochlorines have been linked with various diseases including neurodevelopmental disorders. Autism spectrum disorder (ASD) is a highly complex neurodevelopmental disorder that is considered strongly genetic in origin due to its high heritability. However, the rapidly rising prevalence of ASD suggests that environmental factors may also influence risk for ASD. In the present study, whole genome bisulfite sequencing was used to identify genome-wide differentially methylated regions (DMRs) in a total of 52 sperm samples from a cohort of men from the Faroe Islands (Denmark) who were equally divided into high and low exposure groups based on their serum levels of the long-lived organochlorine 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE), a primary breakdown product of the now banned insecticide dichlorodiphenyltrichloroethane (DDT). Aside from being considered a genetic isolate, inhabitants of the Faroe Islands have a native diet that potentially exposes them to a wide range of seafood neurotoxicants in the form of persistent organic pollutants (POPs). The DMRs were mapped to the human genome using Bismark, a 3-letter aligner used for methyl-seq analyses. Gene ontology, functional, and pathway analyses of the DMR-associated genes showed significant enrichment for genes involved in neurological functions and neurodevelopmental processes frequently impacted by ASD. Notably, these genes also significantly overlap with autism risk genes as well as those previously identified in sperm from fathers of children with ASD in comparison to that of fathers of neurotypical children. These results collectively suggest a possible mechanism involving altered methylation of a significant number of neurologically relevant ASD risk genes for introducing epigenetic changes associated with environmental exposures into the sperm methylome. Such changes may provide the potential for transgenerational inheritance of ASD as well as other disorders.
接触环境中的内分泌干扰化合物(EDC),如有机氯,与包括神经发育障碍在内的各种疾病有关。自闭症谱系障碍(ASD)是一种高度复杂的神经发育障碍,由于其高遗传性,被认为主要源于遗传。然而,ASD患病率的迅速上升表明环境因素也可能影响ASD的风险。在本研究中,全基因组亚硫酸氢盐测序用于识别来自法罗群岛(丹麦)一组男性的总共52个精子样本中的全基因组差异甲基化区域(DMR)。这些男性根据其血清中长寿命有机氯1,1-二氯-2,2-双(对氯苯基)乙烯(DDE)的水平分为高暴露组和低暴露组,DDE是现已禁用的杀虫剂二氯二苯三氯乙烷(DDT)的主要分解产物。除了被认为是一个遗传隔离群体外,法罗群岛居民的本地饮食可能使他们以持久性有机污染物(POPs)的形式接触到多种海鲜神经毒素。使用Bismark(一种用于甲基测序分析的三字母比对工具)将DMR定位到人类基因组。对与DMR相关基因的基因本体论、功能和通路分析显示,参与神经功能和经常受ASD影响的神经发育过程的基因有显著富集。值得注意的是,与神经正常儿童的父亲相比,这些基因也与自闭症风险基因以及先前在ASD儿童父亲的精子中鉴定出的基因有显著重叠。这些结果共同表明了一种可能的机制,即大量与神经相关的ASD风险基因的甲基化改变,将与环境暴露相关的表观遗传变化引入精子甲基化组。这种变化可能为ASD以及其他疾病的跨代遗传提供可能性。