PLoS genetics · 2020
Adiponectin GWAS loci harboring extensive allelic heterogeneity exhibit distinct molecular consequences.
СтатьяПоддержка NIH: внешняя программаResearch Support, N.I.H., IntramuralПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Spracklen Cassandra N, Iyengar Apoorva K, Vadlamudi Swarooparani, Raulerson Chelsea K, Jackson Anne U, Brotman Sarah M, Wu Ying, Cannon Maren E, Davis James P, Crain Aaron T, Currin Kevin W, Perrin Hannah J, Narisu Narisu, Stringham Heather M, Fuchsberger Christian, Locke Adam E, Welch Ryan P, Kuusisto Johanna K, Pajukanta Päivi, Scott Laura J, Li Yun, Collins Francis S, Boehnke Michael, Laakso Markku, Mohlke Karen L
Аннотация
Loci identified in genome-wide association studies (GWAS) can include multiple distinct association signals. We sought to identify the molecular basis of multiple association signals for adiponectin, a hormone involved in glucose regulation secreted almost exclusively from adipose tissue, identified in the Metabolic Syndrome in Men (METSIM) study. With GWAS data for 9,262 men, four loci were significantly associated with adiponectin: ADIPOQ, CDH13, IRS1, and PBRM1. We performed stepwise conditional analyses to identify distinct association signals, a subset of which are also nearly independent (lead variant pairwise r2<0.01). Two loci exhibited allelic heterogeneity, ADIPOQ and CDH13. Of seven association signals at the ADIPOQ locus, two signals colocalized with adipose tissue expression quantitative trait loci (eQTLs) for three transcripts: trait-increasing alleles at one signal were associated with increased ADIPOQ and LINC02043, while trait-increasing alleles at the other signal were associated with decreased ADIPOQ-AS1. In reporter assays, adiponectin-increasing alleles at two signals showed corresponding directions of effect on transcriptional activity. Putative mechanisms for the seven ADIPOQ signals include a missense variant (ADIPOQ G90S), a splice variant, a promoter variant, and four enhancer variants. Of two association signals at the CDH13 locus, the first signal consisted of promoter variants, including the lead adipose tissue eQTL variant for CDH13, while a second signal included a distal intron 1 enhancer variant that showed ~2-fold allelic differences in transcriptional reporter activity. Fine-mapping and experimental validation demonstrated that multiple, distinct association signals at these loci can influence multiple transcripts through multiple molecular mechanisms.
Предметные рубрики MeSH
AdiponectinAdipose TissueAllelesCadherinsDNA-Binding ProteinsGene FrequencyGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansInsulin Receptor Substrate ProteinsMaleMetabolic SyndromePhenotypePolymorphism, Single NucleotideQuantitative Trait LociRegulatory Sequences, Nucleic AcidTranscription Factors