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A cross-study analysis of prenatal exposures to environmental contaminants and the epigenome: support for stress-responsive transcription factor occupancy as a mediator of gene-specific CpG methylation patterning

机译：产前暴露于环境污染物和表观基因组的交叉研究分析：支持应激反应转录因子的占用作为基因特异性CpG甲基化模式的中介

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摘要

A biological mechanism by which exposure to environmental contaminants results in gene-specific CpG methylation patterning is currently unknown. We hypothesize that gene-specific CpG methylation is related to environmentally perturbed transcription factor occupancy. To test this hypothesis, a database of 396 genes with altered CpG methylation either in cord blood leukocytes or placental tissue was compiled from 14 studies representing assessments of six environmental contaminants. Subsequently, an in silico approach was used to identify transcription factor binding sites enriched among the genes with altered CpG methylation in relationship to the suite of environmental contaminants. For each study, the sequences of the promoter regions (representing ?1000 to +500?bp from the transcription start site) of all genes with altered CpG methylation were analyzed for enrichment of transcription factor binding sites. Binding sites for a total of 56 unique transcription factors were identified to be enriched within the promoter regions of the genes. Binding sites for the Kidney-Enriched Krupple-like Factor 15, a known responder to endogenous stress, were enriched ( P
机译：目前尚不清楚通过生物污染物暴露于环境污染物导致基因特异性CpG甲基化模式的生物学机制。我们假设基因特异性CpG甲基化与环境扰动的转录因子占用有关。为了检验这一假设，从14个代表6种环境污染物评估的研究中，收集了396个脐带血白细胞或胎盘组织中CpG甲基化改变的基因的数据库。随后，采用计算机模拟方法来鉴定转录因子结合位点，该位点在与环境污染物相关的CpG甲基化改变的基因中富集。对于每项研究，分析了所有具有改变的CpG甲基化基因的启动子区域的序列（代表从转录起始位点开始的1000到+500 bp），以丰富转录因子结合位点。鉴定出总共56个独特转录因子的结合位点在基因的启动子区域内富集。在与六种环境污染物中的五种相关的CpG甲基化改变的基因中，富含肾脏的Krupple样因子15（已知的内源性应激反应物）的结合位点被富集（P <？0.001-0.041）。这些数据支持转录因子占用理论作为环境诱导的基因特异性CpG甲基化基础的潜在机制。

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