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Leveraging data from multiple ancestries can greatly improve fine-mapping power due to differences in linkage disequilibrium and allele frequencies. We propose MultiSuSiE, an extension of the sum of single effects model (SuSiE) to multiple ancestries that allows causal effect sizes to vary across ancestries based on a multivariate normal prior informed by empirical data. We evaluated MultiSuSiE via simulations and analyses of 14 quantitative traits leveraging whole-genome sequencing data in 47k African-ancestry and 94k European-ancestry individuals from All of Us. In simulations, MultiSuSiE applied to Afr47k+Eur47k was well-calibrated and attained higher power than SuSiE applied to Eur94k; interestingly, higher causal variant PIPs in Afr47k compared to Eur47k were entirely explained by differences in the extent of LD quantified by LD 4th moments. Compared to very recently proposed multi-ancestry fine-mapping methods, MultiSuSiE attained higher power and/or much lower computational costs, making the analysis of large-scale All of Us data feasible. In real trait analyses, MultiSuSiE applied to Afr47k+Eur94k identified 579 fine-mapped variants with PIP > 0.5, and MultiSuSiE applied to Afr47k+Eur47k identified 44% more fine-mapped variants with PIP > 0.5 than SuSiE applied to Eur94k. We validated MultiSuSiE results for real traits via functional enrichment of fine-mapped variants. We highlight several examples where MultiSuSiE implicates well-studied or biologically plausible fine-mapped variants that were not implicated by other methods.
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http://dx.doi.org/10.1101/2024.05.13.24307291 | DOI Listing |
Cell Genom
August 2025
Department of Genome Informatics, Graduate School of Medicine, the University of Tokyo, Tokyo, Japan; Department of Statistical Genetics, Osaka University Graduate School of Medicine, Suita, Japan; Laboratory for Systems Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan; Labor
Psoriasis vulgaris (PsV) is an immune-mediated inflammatory skin disorder with complex genetic architecture. Most genome-wide association studies (GWASs) of PsV have been limited to analyzing common single-nucleotide variants in Europeans, lacking diversity in the variant spectrum and ancestral background. To investigate the contribution of rare variants (RVs) and structural variants (SVs), we perform a whole-genome sequencing study involving 1,415 PsV cases and 3,968 controls in Japanese.
View Article and Find Full Text PDFNucleic Acids Res
August 2025
National Genomics Data Center, China National Center for Bioinformation, Beijing 100101, China.
A systematic dissection of the functional impacts of non-coding variations across diverse tissues and cell types is essential for deciphering the molecular architecture underlying complex traits. Given the significance of chickens as both a key livestock species and a fundamental model organism, the development of an integrative genomics resource is imperative. Leveraging SNP-to-gene-to-trait linking strategies-including molecular quantitative trait loci (molQTL), regulatory elements, and context- or environment-dependent regulatory heterogeneity-we developed the ChickenGTEx portal (http://chicken.
View Article and Find Full Text PDFNat Commun
August 2025
Centre for Neuropsychiatric Genetics and Genomics, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University, Cardiff, UK.
Rare coding variants across many genes contribute to schizophrenia liability, but they have only been implicated in 12 genes at exome-wide levels of significance. To increase power for gene discovery, we analyse exome-sequencing data for rare coding variants in a new sample of 4650 schizophrenia cases and 5719 controls, and combine these with published sequencing data for a total of 28,898 cases, 103,041 controls and 3444 proband-parent trios. We identify associations for STAG1 and ZNF136 at exome-wide significance, genes that were previously implicated in schizophrenia by the SCHEMA study at a false discovery rate of 5%.
View Article and Find Full Text PDFPancreatology
August 2025
Department of Internal Medicine I, Martin Luther University (MLU), Halle (Saale), Germany. Electronic address:
Background/objectives: Enhancers are key drivers of tissue-specific gene expression and can contain variants associated with pancreatic diseases. Enhancer-target gene assignment remains challenging, with the Activity-By-Contact (ABC) model, integrating open-chromatin, histone modification and chromatin interaction data, consistently outperforming other approaches. Recently an advanced version, the generalized ABC (gABC) model was published, yet lacking a clear and unique promoter definition impairing interpretability.
View Article and Find Full Text PDFNat Genet
July 2025
Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Methods that analyze single-cell paired RNA sequencing (RNA-seq) and assay for transposase-accessible chromatin using sequencing (ATAC-seq) multiome data have shown promise in linking regulatory elements to genes. However, existing methods exhibit low concordance and do not capture the effects of genomic distance. We propose pgBoost, an integrative modeling framework that trains a non-linear combination of existing linking strategies (including genomic distance) on expression quantitative trait locus (eQTL) data to assign a probabilistic score to each candidate single-nucleotide polymorphism-gene link.
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