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Vuckovic, D.

Publications and source records attributed to Vuckovic, D..

6 recordsLinked to original sources

Topology-Based Query Framework for Longitudinal Omics Trajectories

1 Abstract 1.1 Background Many longitudinal omics studies contain only a small number of repeated measurements collected before, during, or after an intervention. Existing approaches, including mixed-effects models and generalized additive models, estimate temporal effects but do not generally provide a discrete representation of trajectory topology that can be queried directly across experimental groups. 1.2 Methods We developed LongOmicsTraj, an open-source R package for topology-based representation and querying of short longitudinal omics trajectories. The framework encodes the direction of change between adjacent visits as up, down, or flat, with the ordered sequence defining an Ordinal Trajectory State (OTS). LongOmicsTraj operates downstream of trajectory estimation and can therefore be applied to empirical summaries or model-derived visit-level estimates, including those from linear mixed-effects models, generalized additive models, and polynomial regression, following a maSigPro-style time-course formulation [1]. OTS labels provide a common representation for topology-based querying, cross-group comparison, and evaluation of higherlevel representations such as trajectory clusters. We evaluated the framework using controlled simulations and bronchial biopsy transcriptomic data from the GLUCOLD corticosteroid intervention study (GEO accession GSE36221), measured at baseline, 6 months, and 30 months. The biological analysis compared continued inhaled corticosteroid (ICS) treatment, ICS withdrawal after 6 months, and placebo. 1.3 Results In simulations, LongOmicsTraj recovered predefined stable, monotonic, transient, rebound, and oscillatory trajectories with high accuracy when longitudinal signal was sufficiently clear, with performance declining under high-noise conditions and depending partly on the upstream estimator. In GLUCOLD, comparator-aware topology queries reduced 20,358 measured transcripts to 168 genes showing a corticosteroid response that was maintained during continued treatment, reversed following withdrawal, and was not reproduced under placebo. The selected genes included established corticosteroid-response genes and were enriched for immune-cell migration, chemotaxis, cell adhesion, and extracellular-matrix organisation. Topology-aware evaluation of FlexMix trajectory clusters additionally revealed substantial within-cluster temporal heterogeneity, with topology purities of approximately 46% to 60%. 1.4 Conclusions LongOmicsTraj provides a compact, directly queryable representation of temporal direction and order in short longitudinal omics studies. It complements existing longitudinal estimation and clustering methods by making trajectory structure explicit, enabling structured cross-group queries and quantification of temporal heterogeneity within trajectory clusters.

bioinformatics↗

Variant-to-function dissection of rare non-coding GWAS loci with high impact on blood traits

Understanding the function of genetic variants associated with human traits and diseases remains a significant challenge. Here we combined analyses based on natural genetic variation and genetic engineering to dissect the function of 94 non-coding variants associated with haematological traits. We describe 22 genetic variants impacting haematological variation through gene expression. Further, through in-depth functional analysis, we illustrate how a rare, non-coding variant near the CUX1 transcription factor impacts megakaryopoiesis through modulation of the CUX1 transcriptional cascade. Collectively, our findings enhance the functional interpretation of genetic association studies and advance understanding of how non-coding variants contribute to blood and immune system variation.

genetics↗

PIK3R3 is a candidate regulator of platelet count in people of Bangladeshi ancestry

Platelets are mediators of cardiovascular disease and are regulated by complex sets of interacting genes. To reveal new regulatory loci for platelet count (PLT), we performed genome-wide association studies (GWAS) in 20,218 Bangladeshi (BAN) and 9,198 Pakistani (PAK) individuals from the Genes and Health study. Most significantly associated loci (p <5 x10-8) replicated findings in prior transethnic GWAS. However, the BAN locus defined by rs946528 (chr1:46019890) did not associate with PLT in the PAK analysis but was in the same linkage disequilibrium block as PLT-associated variants in prior East Asian GWAS. The single independent association signal was refined to a 95% credible set of 343 variants spanning eight coding genes. Functional annotation, mapping to megakaryocyte regulatory regions and colocalization with whole blood eQTLs identified the most likely mediator of the PLT phenotype to be PIK3R3 encoding a regulator of phosphoinositol 3-kinase, widely linked elsewhere to adverse cardiovascular phenotypes.

genomics↗

Transcriptome-wide association study in UK Biobank Europeans identifies associations with blood cell traits.

Previous genome-wide association studies (GWAS) of hematological traits have identified over 10,000 distinct trait-specific risk loci, but the underlying causal mechanisms at these loci remain incompletely characterized. We performed a transcriptome-wide association study (TWAS) of 29 hematological traits in 399,835 UK Biobank (UKB) participants of European ancestry using gene expression prediction models trained from whole blood RNA-seq data in 922 individuals. We discovered 557 TWAS signals associated with hematological traits distinct from previously discovered GWAS variants, including 10 completely novel gene-trait pairs corresponding to 9 unique genes. Among the 557 associations, 301 were available for replication in a cohort of 141,286 participants of European ancestry from the Million Veteran Program (MVP). Of these 301 associations, 199 replicated at a nominal threshold ( = 0.05) and 108 replicated at a strict Bonferroni adjusted threshold ( = 0.05/301). Using our TWAS results, we systematically assigned 4,261 out of 16,900 previously identified hematological trait GWAS variants to putative target genes. Compared to coloc, our TWAS results show reduced specificity and increased sensitivity to assign variants to target genes.

genetics↗

Learning polygenic scores for human blood cell traits

Polygenic scores (PGSs) for blood cell traits can be constructed using summary statistics from genome-wide association studies. As the selection of variants and the modelling of their interactions in PGSs may be limited by univariate analysis, therefore, such a conventional method may yield sub-optional performance. This study evaluated the relative effectiveness of four machine learning and deep learning methods, as well as a univariate method, in the construction of PGSs for 26 blood cell traits, using data from UK Biobank (n=~400,000) and INTERVAL (n=~40,000). Our results showed that learning methods can improve PGSs construction for nearly every blood cell trait considered, with this superiority explained by the ability of machine learning methods to capture interactions among variants. This study also demonstrated that populations can be well stratified by the PGSs of these blood cell traits, even for traits that exhibit large differences between ages and sexes, suggesting potential for disease prevention. As our study found genetic correlations between the PGSs for blood cell traits and PGSs for several common human diseases (recapitulating well-known associations between the blood cell traits themselves and certain diseases), it suggests that blood cell traits may be indicators or/and mediators for a variety of common disorders via shared genetic variants and functional pathways.

genetics↗

Genetic Analyses of Blood Cell Structure for Biological and Pharmacological Inference

Thousands of genetic associations with phenotypes of blood cells are known, but few are with phenotypes relevant to cell function. We performed GWAS of 63 flow-cytometry phenotypes, including measures of cell granularity, nucleic acid content, and reactivity, in 39,656 participants in the INTERVAL study, identifying 2,172 variant-trait associations. These include associations mediated by functional cellular structures such as secretory granules, implicated in vascular, thrombotic, inflammatory and neoplastic diseases. By integrating our results with epigenetic data and with signals from molecular abundance/disease GWAS, we infer the hematopoietic origins of population phenotypic variation and identify the transcription factor FOG2 as a regulator of platelet -granularity. We show how flow cytometry genetics can suggest cell types mediating complex disease risk and suggest efficacious drug targets, presenting Daclizumab/Vedolizumab in autoimmune disease as positive controls. Finally, we add to existing evidence supporting IL7/IL7-R as drug targets for multiple sclerosis.

genetics↗