Dong Shan-Shan, Duan Yuan-Yuan, Zhu Ren-Jie, Jia Ying-Ying, Chen Jia-Xin, Huang Xiao-Ting, Tang Shi-Hao, Yu Ke, Shi Wei, Chen Xiao-Feng, Jiang Feng, Hao Ruo-Han, Liu Yunlong, Liu Zhongbo, Guo Yan, Yang Tie-Lin
Key Laboratory of Biomedical Information Engineering of Ministry of Education, Key Laboratory of Biology Multiomics and Diseases in Shaanxi Province Higher Education Institutions, Biomedical Informatics & Genomics Center, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, Shaanxi, China.
Key Laboratory of Biomedical Information Engineering of Ministry of Education, Key Laboratory of Biology Multiomics and Diseases in Shaanxi Province Higher Education Institutions, Biomedical Informatics & Genomics Center, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, Shaanxi, China; Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an 710004, Shaanxi, China.
Am J Hum Genet. 2025 Jan 2;112(1):116-134. doi: 10.1016/j.ajhg.2024.11.005.
Central obesity is associated with higher risk of developing a wide range of diseases independent of overall obesity. Genome-wide association studies (GWASs) have identified more than 300 susceptibility loci associated with central obesity. However, the functional understanding of these loci is limited by the fact that most loci are in non-coding regions. To address this issue, our study first prioritized 2,034 single-nucleotide polymorphisms (SNPs) based on fine-mapping and epigenomic annotation analysis. Subsequently, we employed self-transcribing active regulatory region sequencing (STARR-seq) to systematically evaluate the enhancer activity of these prioritized SNPs. The resulting data analysis identified 141 SNPs with allelic enhancer activity. Further analysis of allelic transcription factor (TF) binding prioritized 20 key TFs mediating the central-obesity-relevant genetic regulatory network. Finally, as an example, we illustrate the molecular mechanisms of how rs8079062 acts as an allele-specific enhancer to regulate the expression of its targeted RNF157. We also evaluated the role of RNF157 in the adipogenic differentiation process. In conclusion, our results provide an important resource for understanding the genetic regulatory mechanisms underlying central obesity.
中心性肥胖与多种疾病的发生风险增加相关,且独立于总体肥胖。全基因组关联研究(GWAS)已鉴定出300多个与中心性肥胖相关的易感位点。然而,由于大多数位点位于非编码区,对这些位点的功能理解有限。为了解决这一问题,我们的研究首先基于精细定位和表观基因组注释分析,对2034个单核苷酸多态性(SNP)进行了优先级排序。随后,我们采用自转录活性调控区测序(STARR-seq)系统评估这些优先级SNP的增强子活性。数据分析确定了141个具有等位基因增强子活性的SNP。对等位基因转录因子(TF)结合的进一步分析确定了20个介导与中心性肥胖相关的基因调控网络的关键TF。最后,作为一个例子,我们阐述了rs8079062如何作为等位基因特异性增强子来调控其靶向的RNF157表达的分子机制。我们还评估了RNF157在脂肪生成分化过程中的作用。总之,我们的结果为理解中心性肥胖潜在的遗传调控机制提供了重要资源。