Grech Godwin M, Fawcett Katherine A, Hall Robert J, Grech Godfrey, Ellul-Micallef Roger, Hall Ian P, Fenech Anthony G
Department of Clinical Pharmacology and Therapeutics, Faculty of Medicine & Surgery, University of Malta, Msida, Malta.
Department of Population Health Sciences, University of Leicester, Leicester, UK.
FASEB J. 2025 Jun 30;39(12):e70689. doi: 10.1096/fj.202403208R.
SNV rs12477314 (C>T; 1000G MAF = 0.14), which maps to an intergenic region on 2q37.3, is a genome-wide significant association signal for pulmonary function in genome-wide association study meta-analyses. Bioinformatic analysis revealed that the intergenic region in proximity to the sentinel SNV is enriched for histone methylation markers suggestive of active enhancer regions modifiable by DNA methylation. The aim of this study was to investigate the functionality of putative enhancer/s and their potential interaction with CpG islands in the genomic region tagged by rs12477314 and their relevance to lung disease, in particular COPD. Two independent CRISPR/Cas9n-targeted deletions of the putative enhancer/s were performed in an airway epithelial cell line (NCI-H460). Deletion clones were subjected to RNA-Seq, and differential expression gene (DEG) datasets were generated using the Cufflinks version 2.2.1 pipeline (p-FDR < 0.05). Biological pathway analysis was performed using Qiagen's Ingenuity Pathway Analysis. Associations with the blood proteome were explored in UK Biobank. Our results suggest that the deleted regions are co-acting enhancers regulating overlapping gene expression patterns. The DEG datasets from the two genomic deletions are enriched for similar canonical pathways, which may contribute to a pro-inflammatory phenotype. Pathway-based regulatory effects analysis of the two DEG datasets resulted in identifying potential downstream biological processes. There was overlap between the pathways identified in protein association datasets and the DEG datasets. Our results suggest that the genomic region tagged by SNV rs12477314 constitutes a regulatory region responsible for regulating biological pathways conducive to a systemic inflammatory phenotype.
单核苷酸变异体rs12477314(C>T;1000基因组MAF = 0.14)定位于2q37.3的基因间区域,是全基因组关联研究荟萃分析中肺功能的全基因组显著关联信号。生物信息学分析表明,前哨单核苷酸变异体附近的基因间区域富含组蛋白甲基化标记,提示存在可被DNA甲基化修饰的活性增强子区域。本研究的目的是调查rs12477314标记的基因组区域中假定增强子的功能及其与CpG岛的潜在相互作用,以及它们与肺部疾病尤其是慢性阻塞性肺疾病(COPD)的相关性。在气道上皮细胞系(NCI-H460)中对假定增强子进行了两次独立的CRISPR/Cas9n靶向缺失。对缺失克隆进行RNA测序,并使用Cufflinks 2.2.1版本流程生成差异表达基因(DEG)数据集(p-FDR < 0.05)。使用Qiagen的Ingenuity Pathway Analysis进行生物通路分析。在英国生物银行中探索了与血液蛋白质组的关联。我们的结果表明,缺失区域是共同作用的增强子,调节重叠的基因表达模式。来自两次基因组缺失的DEG数据集富含相似的经典通路,这可能导致促炎表型。对两个DEG数据集进行基于通路的调控效应分析,从而确定潜在的下游生物学过程。蛋白质关联数据集和DEG数据集中鉴定出的通路存在重叠。我们的结果表明,单核苷酸变异体rs12477314标记的基因组区域构成了一个调控区域,负责调节有助于全身性炎症表型的生物学通路。