探讨体重指数与脑形态性状遗传相关性的分子基础。

IF 4 2区 生物学 Q1 GENETICS & HEREDITY
PLoS Genetics Pub Date : 2025-04-10 eCollection Date: 2025-04-01 DOI:10.1371/journal.pgen.1011658
Daniela Fusco, Camilla Marinelli, Mathilde André, Lucia Troiani, Martina Noè, Fabrizio Pizzagalli, Davide Marnetto, Paolo Provero
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引用次数: 0

摘要

一些研究已经证明了结构磁共振成像(sMRI)得出的身体质量指数(BMI)和脑形态特征之间存在显著的表型和遗传相关性。我们使用英国生物银行收集的sMRI、BMI和遗传数据,系统地计算了数百个大脑结构的面积、体积和厚度测量与BMI之间的遗传相关性。与先前的文献一致,我们发现许多此类测量与BMI具有负遗传相关性。然后,我们利用脑eQTL数据和基于摘要的孟德尔随机化分析了这种相关性背后的分子机制,从而产生了一个基因图谱,这些基因在脑组织中的基因调控表达与脑形态和BMI呈多向性。在一些情况下,精细定位之后的共定位分析允许确定可信的变异集,这些变异集可能是宏观表型和基因表达的因果关系。特别是,表观遗传精细定位鉴定了TUFM基因5' UTR中的rs7187776变异可能是BMI增加和尾状体体积减少的原因,可能是通过替代等位基因产生的ETS结合位点导致染色质可及性增加,特别是在小胶质细胞中。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Exploring the molecular basis of the genetic correlation between body mass index and brain morphological traits.

Several studies have demonstrated significant phenotypic and genetic correlations between body mass index (BMI) and brain morphological traits derived from structural magnetic resonance imaging (sMRI). We use the sMRI, BMI, and genetic data collected by the UK Biobank to systematically compute the genetic correlations between area, volume, and thickness measurements of hundreds of brain structures on one hand, and BMI on the other. In agreement with previous literature, we find many such measurements to have negative genetic correlation with BMI. We then dissect the molecular mechanisms underlying such correlations using brain eQTL data and summary-based Mendelian randomization, thus producing an atlas of genes whose genetically regulated expression in brain tissues is pleiotropic with brain morphology and BMI. Fine-mapping followed by colocalization analysis allows, in several cases, the identification of credible sets of variants likely to be causal for both the macroscopic phenotypes and for gene expression. In particular, epigenetic fine mapping identifies variant rs7187776 in the 5' UTR of the TUFM gene as likely to be causal of increased BMI and decreased caudate volume, possibly through the creation, by the alternate allele, of an ETS binding site leading to increased chromatin accessibility, specifically in microglial cells.

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来源期刊
PLoS Genetics
PLoS Genetics GENETICS & HEREDITY-
自引率
2.20%
发文量
438
期刊介绍: PLOS Genetics is run by an international Editorial Board, headed by the Editors-in-Chief, Greg Barsh (HudsonAlpha Institute of Biotechnology, and Stanford University School of Medicine) and Greg Copenhaver (The University of North Carolina at Chapel Hill). Articles published in PLOS Genetics are archived in PubMed Central and cited in PubMed.
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