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首页> 外文期刊>Circulation. Genomic and precision medicine. >Genetic Control of Left Atrial Gene Expression Yields Insights into the Genetic Susceptibility for Atrial Fibrillation
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Genetic Control of Left Atrial Gene Expression Yields Insights into the Genetic Susceptibility for Atrial Fibrillation

机译：左心室基因表达的基因控制收益率见解遗传易感性对心房颤动

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BACKGROUND: Genome-wide association studies have identified 23 loci for atrial fibrillation (AF), but the mechanisms responsible for these associations, as well as the causal genes and genetic variants, remain undefined. METHODS: To identify the effect of common genetic variants on gene expression that might explain the mechanisms linking genome-wide association loci with AF risk, we performed RNA sequencing of left atrial appendages from a biracial cohort of 265 subjects. RESULTS: Combining gene expression data with genome-wide single nucleotide polymorphism data, we found that approximately two-thirds of the expressed genes were regulated in cis by common genetic variants at a false discovery rate of <0.05, defined as cis-expression quantitative trait loci. Twelve of 23 reported AF genome-wide association loci displayed genome-wide significant cis-expression quantitative trait loci, at PRRX1 (chromosome 1q24), SNRNP27 (1q24), CEP68 (2p14), FKBP7 (2q31), KCNN2 (5q22), FAM13B (5q31), CAV1 (7q31), ASAH1 (8p22), MYOZ1 (10q22), C11ORF45 (11q24), TBX5 (12q24), and SYNE2 (14q23), suggesting that altered expression of these genes plays a role in AF susceptibility. Allelic expression imbalance was used as an independent method to characterize the cis-control of gene expression. One thousand two hundred forty-eight of 5153 queried genes had cis-single nucleotide polymorphisms that significantly regulated allelic expression at a false discovery rate of <0.05. CONCLUSIONS: We provide a genome-wide catalog of the genetic control of gene expression in human left atrial appendage. These data can be used to confirm the relevance of genome-wide association loci and to direct future functional studies to identify the genes and genetic variants responsible for complex diseases such as AF.
机译：背景:全基因组关联研究确定23个位点为心房纤颤(房颤),但负责这些机制协会、以及因果基因和基因变异,仍然是未定义的。识别常见的遗传变异的影响基因表达可能解释机制全基因组关联位点与房颤风险,我们进行RNA序列的左心房从265年一个混血的附属物科目。全基因组单核苷酸多态性数据,我们发现,大约三分之二的表达的基因在独联体的监管常见的错误发现率的遗传变异< 0.05,定义为cis-expression定量特征位点。协会位点显示全基因组重大cis-expression定量特征位点,PRRX1(染色体1抓起)SNRNP27(1抓起)(5问),CAV1(7问),ASAH1(8第22位),MYOZ1(10的时候),(14 q23处),这表明表达的改变这些基因在房颤易感性中发挥作用。等位基因表达失衡是用作独立的方法来描述cis-control基因表达。几百5153年48查询基因cis-single核苷酸多态性,显著调节在一个等位基因的表达错误发现率< 0.05。提供一个全基因组基因的目录控制基因表达在人类左心房肢。全基因组关联位点和之间的相关性直接未来功能的研究来确定基因和遗传变异负责复杂的疾病,如房颤。

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