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Sharapov, S. Z.

Publications and source records attributed to Sharapov, S. Z..

4 recordsLinked to original sources

A novel framework for analysis of the shared genetic background of correlated traits

We propose a novel effective framework for analysis of the shared genetic background for a set of genetically correlated traits using SNP-level GWAS summary statistics. This framework called SHAHER is based on the construction of a linear combination of traits by maximizing the proportion of its genetic variance explained by the shared genetic factors. SHAHER requires only full GWAS summary statistics and matrices of genetic and phenotypic correlations between traits as inputs. Our framework allows both shared and unshared genetic factors to be to effectively analyzed. We tested our framework using simulation studies, compared it with previous developments, and assessed its performance using three real datasets: anthropometric traits, psychiatric conditions and lipid concentrations. SHAHER is versatile and applicable to summary statistics from GWASs with arbitrary sample sizes and sample overlaps, allows incorporation of different GWAS models (Cox, linear and logistic) and is computationally fast.

bioinformatics↗

Same role but different actors: genetic regulation of post-translational modification of two distinct proteins

Post-translational modifications (PTMs) diversify protein functions and dynamically coordinate their signalling networks, influencing most aspects of cell physiology. Nevertheless, their genetic regulation or influence on complex traits is not fully understood. Here, we compare for the first time the genetic regulation of the same PTM of two proteins - glycosylation of transferrin and immunoglobulin G (IgG). By performing genome-wide association analysis of transferrin glycosylation, we identified 10 significantly associated loci, all novel. Comparing these with IgG glycosylation-associated genes, we note protein-specific associations with genes encoding glycosylation enzymes (transferrin - MGAT5, ST3GAL4, B3GAT1; IgG - MGAT3, ST6GAL1) as well as shared associations (FUT6, FUT8). Colocalisation analyses of the latter suggest that different causal variants in the FUT genes regulate fucosylation of the two proteins. We propose that they affect the binding of different transcription factors in different tissues, with fucosylation of IgG being regulated by IKZF1 in B-cells and of transferrin by HNF1A in liver.

genomics↗

Varicose veins of lower extremities: insights from the first large-scale genetic study

Varicose veins of lower extremities (VVs) are a common multifactorial vascular disease. Genetic factors underlying VVs development remain largely unknown. Here we report the first large-scale study of VVs performed on a freely available genetic data of 408,455 European-ancestry individuals. We identified 7 reliably associated loci that explain 10% of the SNP-based heritability, and prioritized the most likely causal genes CASZ1, PPP3R1, EBF1, STIM2, and HFE. Genetic correlation analysis confirmed known epidemiological associations and found genetic overlap with various traits including fluid intelligence score, educational attainment, smoking, and pain. Finally, we observed causal effects of height, weight, both fat and fat-free mass, and plasma levels of MICB and CD209 proteins.

genomics↗

Network based conditional genome wide association analysis of human metabolomics

BackgroundGenome-wide association studies (GWAS) have identified hundreds of loci influencing complex human traits, however, their biological mechanism of action remains mostly unknown. Recent accumulation of functional genomics ( omics) including metabolomics data opens up opportunities to provide a new insight into the functional role of specific changes in the genome. Functional genomic data are characterized by high dimensionality, presence of (strong) statistical dependencies between traits, and, potentially, complex genetic control. Therefore, analysis of such data asks for development of specific statistical genetic methods.\n\nResultsWe propose a network-based, conditional approach to evaluate the impact of genetic variants on omics phenotypes (conditional GWAS, cGWAS). For each trait of interest, based on biological network, we select a set of other traits to be used as covariates in GWAS. The network could be reconstructed either from biological pathway databases or directly from the data. We evaluated our approach using data from a population-based KORA study (n=1,784, 1.7 M SNPs) with measured metabolomics data (151 metabolites) and demonstrated that our approach allows for identification of up to five additional loci not detected by conventional GWAS. We show that this gain in power is achieved through increased precision of genetic effect estimates, and in presence of specific contra-intuitive pleiotropic scenarios (when genetic and environmental sources of covariance are acting in opposite manner). We justify existence of such scenarios, and discuss possible applications of our method beyond metabolomics.\n\nConclusionsWe demonstrate that in context of metabolomics network-based, conditional genome-wide association analysis is able to dramatically increase power of identification of loci with specific contra-intuitive pleiotropic architecture. Our method has modest computational costs, can utilize summary level GWAS data, and is applicable to other omics data types. We anticipate that application of our method to new and existing data sets will facilitate progress in understanding genetic bases of control of molecular and complex phenotypes.\n\nShort abstractWe propose a network-based, conditional approach for genome-wide analysis of multivariate omics phenotypes. Our methods can incorporate prior biological knowledge about biological pathways from external sources. We evaluated our approach using metabolomics data and demonstrated that our approach has bigger power and allows for identification of additional loci. We show that gain in power is achieved through increased precision of genetic effect estimates, and in presence of specific contra-intuitive pleiotropic scenarios (when genetic and environmental sources of covariance are acting in opposite manner). We justify existence of such scenarios, and discuss possible applications of our method beyond metabolomics.

genomics↗