bioRxiv Science⌕ Search

Biology subjects

Leung, Y. Y.

Publications and source records attributed to Leung, Y. Y..

14 recordsLinked to original sources

Evaluating sequence-to-function deep learning models for ancestry-stratified regulatory variant effect prediction using multi-ancestry blood eQTLs

BackgroundSequence-to-function (S2F) deep learning models are increasingly used to prioritize non-coding regulatory variants, but their behavior across ancestrally diverse populations remains unclear. Because both training data and reference resources are heavily European-centered, multi-ancestry benchmarks are needed to determine whether S2F scores capture regulatory effects consistently across populations with different allele-frequency and LD patterns. MethodsWe evaluated Borzoi and AlphaGenome using whole blood eQTL data from the MAGENTA cohort, including African American (AA; N = 224), Caribbean Hispanic (CH; N = 209), and Non-Hispanic White (NHW; N = 235) participants. Model predictions were benchmarked against sampled nominal eQTLs and ancestry-stratified SuSiE fine-mapped variants using Spearman correlation, direction concordance, inter-model convergence, and distance-matched AUROC, with sensitivity analyses for minor allele frequency and comparison-set definition. We also compared FILER functional annotation overlap among high-Posterior Inclusion Probability (PIP) variants across ancestries. ResultsBoth models showed weak agreement with nominal eQTL effect sizes across ancestries and TSS-distance bins ({rho} [&le;] 0.138), with direction concordance only marginally above chance. Agreement and discrimination improved for high-confidence fine-mapped variants, and Borzoi and AlphaGenome showed stronger inter-model convergence on fine-mapped variants than on nominal eQTLs, consistent with enrichment for regulatory variants whose effects are more apparent to sequence-based models. In distance-matched AUROC analyses at PIP [&ge;] 0.9 using PIP < 0.01 variants as low-PIP comparison variants, the AA high-PIP variant set yielded the highest discrimination for both Borzoi (0.837 [95% CI: 0.790-0.870]) and AlphaGenome (0.820 [0.793-0.845]). The CH-versus-NHW ordering was model-dependent: Borzoi yielded higher AUROC in NHW than CH, whereas AlphaGenome produced nearly identical CH and NHW estimates. AUROC values were lower when intermediate-PIP variants were used as comparison variants, but the AA set retained the highest discrimination. MAF-stratified sensitivity analyses attenuated some ancestry contrasts but did not eliminate the higher AA discrimination pattern. Functional annotation analysis showed that AA high-PIP variants more often overlapped chromatin accessibility and chromatin-contact annotations than NHW variants, despite lower overlap with prior eQTL and sQTL annotation catalogs. ConclusionsBorzoi and AlphaGenome showed limited agreement with nominal eQTL effect sizes, but better distinguished high-confidence fine-mapped eQTLs from low-PIP variants. These results support using S2F scores as prioritization evidence for fine-mapped regulatory variants, especially promoter-proximal high-PIP variants, rather than as standalone predictors of eQTL effect size. The strongest discrimination was observed for the AA high-PIP variant set. Overall, the AA result is best interpreted as stronger separation of high-PIP variants from lower-PIP comparison variants, shaped by fine-mapping resolution, LD, the choice of comparison variants, and annotation composition.

bioinformatics↗

A reference panel for linkage disequilibrium and genotype imputation using whole-genome sequencing data from 2,680 participants across India

India is the most populous country globally, yet genetic studies involving Indian individuals remain limited. The Indian population is composed of many founder groups and has a mixed genetic ancestry, including an ancestral component not observed anywhere outside of India. This presents a unique opportunity to uncover novel disease variants and develop more tailored medical interventions. To facilitate genetic research in India, a crucial first step is to create a foundational resource that serves as a benchmark for future population studies and methods development. To this end, we have constructed the largest and most nationally representative linkage disequilibrium and genotype imputation reference panels in India to date, using high-coverage whole-genome sequencing data of 2,680 Indian participants from the Longitudinal Aging Study in India-Harmonized Diagnostic Assessment of Dementia (LASI-DAD). As an LD reference panel, LASI-DAD includes 69.5 million variants, representing 170% and 213% increases relative to the 1000 Genomes Project (1000G) and TOP-LD panels, respectively. Besides serving as an LD lookup panel, LASI-DAD facilitates various statistical analyses that rely on precise LD estimates. In a polygenic risk score (PRS) analysis, LASI-DAD improved the predictive performance of PRS by 2.1% to 35.1% across traits and studies. As an imputation reference panel, LASI-DAD improved the imputation accuracy by 3% to 101% (mean = 38%) compared to the TOPMed panel (Version R3) and by 3% to 73% (mean = 27%) compared to the Genome Asia Pilot (GAsP) panel across different minor allele frequencies. The LASI-DAD reference panel is publicly available to benefit future studies.

genetics↗

CHARMER: detecting and harmonizing high-confidence chromatin interactions across tissues and Hi-C protocols

MotivationChromatin conformation capture experiments (CCC), such as Hi-C and Capture Hi-C (CHiC) work to elucidate the three-dimensional organization of the genome and the underlying epigenetic regulatory structures within. CCC experiments produce large amounts of FASTQ sequencing data with a substantial amount of technical noise and require sophisticated computational pipelines in order to extract meaningful results. Large-scale CCC data repositories like 4D Nucleome and ENCODE mostly provide raw contact information but lack annotated, statistically significant interaction data suitable for downstream genetic and genomic analyses. ResultsHere, we present CHARMER, an end-to-end pipeline integrated across multiple CCC assay types (HiC, CHiC) which generates statistically significant, harmonized, queryable, chromatin interactions in a consistent BED-like format across cell/tissue types and CCC assays. AvailabilityCHARMER is freely available at https://bitbucket.org/wanglab-upenn/CHARMER and harmonized chromatin interaction data will be available in the upcoming version of the FILER database (https://lisanwanglab.org/FILER).

bioinformatics↗

BTS: scalable Bayesian Tissue Score for prioritizing GWAS variants and their functional contexts across omics data

MotivationSummary statistics from genome-wide association studies (GWAS) are widely used in fine-mapping and colocalization analyses to identify causal variants and their enrichment in functional contexts, such as affected cell types and genomic features. With the expansion of functional genomic (FG) datasets, which now include hundreds of thousands of tracks across various cell and tissue types, it is critical to establish scalable algorithms integrating thousands of diverse FG annotations with GWAS results. ResultsWe propose BTS (Bayesian Tissue Score), a novel, highly efficient algorithm uniquely designed for 1) identifying affected cell types and functional elements (context-mapping) and 2) fine-mapping potentially causal variants in a context-specific manner using large collections of cell type-specific FG annotation tracks. BTS leverages GWAS summary statistics and annotation-specific Bayesian models to analyze genome-wide annotation tracks, including enhancers, open chromatin, and histone marks. We evaluated BTS on GWAS summary statistics for immune and cardiovascular traits, such as Inflammatory Bowel Disease (IBD), Rheumatoid Arthritis (RA), Systemic Lupus Erythematosus (SLE), and Coronary Artery Disease (CAD). Our results demonstrate that BTS is over 100x more efficient in estimating functional annotation effects and context-specific variant fine-mapping compared to existing methods. Importantly, this large-scale Bayesian approach prioritizes both known and novel annotations, cell types, genomic regions, and variants and provides valuable biological insights into the functional contexts of these diseases. Availability and implementationDocker image is available at https://hub.docker.com/r/wanglab/bts with pre-installed BTS R package (https://bitbucket.org/wanglab-upenn/BTS-R) and BTS GWAS summary statistics analysis pipeline (https://bitbucket.org/wanglab-upenn/bts-pipeline).

bioinformatics↗

Genetic, transcriptomic, histological, and biochemical analysis of progressive supranuclear palsy implicates glial activation and novel risk genes

Progressive supranuclear palsy (PSP) is a rare Parkinsonian disorder characterized by problems with movement, balance, cognition, and other symptoms. PSP differs from Alzheimers disease (AD) and other neurodegenerative diseases displaying abnormal forms of the microtubule-associated protein tau ("tauopathies") by the presence of pathology not only in neurons, but also in astrocytes and oligodendrocytes. Genetic contributors may mediate these differences, however much of PSP genetics remains unexplained. Here we conducted the largest genome-wide association study (GWAS) of PSP to date including 2,779 cases (2,595 neuropathologically-confirmed) and 5,584 controls and identified six independent PSP susceptibility loci with genome-wide significant (p < 5x10-8) associations including five known (MAPT, MOBP, STX6, RUNX2, SLCO1A2) and one novel locus (C4A). Integration with cell type-specific epigenomic annotations revealed a unique oligodendrocytic signature that distinguishes PSP from AD and Parkinsons disease. Candidate PSP risk gene prioritization using expression quantitative trait loci (eQTLs) identified oligodendrocyte-specific effects on gene expression in half of the genome-wide significant loci, as well as an association with elevated C4A expression in bulk brain tissue which may be driven by increased C4A copy number in PSP cases. Finally, histological studies demonstrated abnormal tau aggregates in oligodendrocytes that colocalize with C4 (complement) deposition. Integrating GWAS with functional studies including epigenomic and eQTL analyses, we identified potential causal roles for variation in MOBP, STX6, RUNX2, SLCO1A2, and C4A in the pathogenesis of PSP.

neuroscience↗

hipFG: High-throughput harmonization and integration pipeline for functional genomics data

SummaryPreparing functional genomic (FG) data with diverse assay types and file formats for integration into analysis workflows that interpret genome-wide association and other studies is a significant and time-consuming challenge. Here we introduce hipFG, an automatically customized pipeline for efficient and scalable normalization of heterogenous FG data collections into standardized, indexed, rapidly searchable analysis-ready datasets while accounting for FG datatypes (e.g., chromatin interactions, genomic intervals, quantitative trait loci). Availability and ImplementationhipFG is freely available at https://bitbucket.org/wanglab-upenn/hipFG. Docker container is available at https://hub.docker.com/r/wanglab/hipfg. Contactlswang@pennmedicine.upenn.edu Supplementary informationSupplementary data are available as BioRxiv supplemental files.

bioinformatics↗

Data Descriptor: Human whole exome genotype data for Alzheimer's Disease

Bigger sample size can help to identify new genetic variants contributing to an increased risk of developing Alzheimers disease. However, the heterogeneity of the whole-exome sequencing (WES) data generation methods presents a challenge to a joint analysis. Here we present a bioinformatics strategy for joint calling 20,504 WES samples collected across nine studies and sequenced using ten different capture kits in fourteen sequencing centers in the Alzheimers Disease Sequencing Project. gVCFs of samples were joint-called by the Genome Center for Alzheimers Disease into a single VCF, containing only positions within the union of capture kits. The VCF was then processed using specific strategies to account for the batch effects arising from the use of different capture kits from different studies. We identified 8.2 million autosomal variants. 96.82% of the variants are high-quality, and are located in 28,579 Ensembl transcripts. 41% of the variants are intronic and 15% are missense variants. 1.8% of the variants are with CADD>30. Our new strategy for processing these diversely generated WES samples has shown to generate high-quality data. The improved ability to combine data sequenced in different batches benefits the whole genomics research community. The WES data are accessible to the scientific community via https://dss.niagads.org/.

genetics↗

A comparative study of structural variant calling strategies using the Alzheimer's Disease Sequencing Project's whole genome family data

BackgroundReliable detection and accurate genotyping of structural variants (SVs) and insertion/deletions (indels) from whole-genome sequence (WGS) data is a significant challenge. We present a protocol for variant calling, quality control, call merging, sensitivity analysis, in silico genotyping, and laboratory validation protocols for generating a high-quality deletion call set from whole genome sequences as part of the Alzheimers Disease Sequencing Project (ADSP). This dataset contains 578 individuals from 111 families. MethodsWe applied two complementary pipelines (Scalpel and Parliament) for SV/indel calling, break-point refinement, genotyping, and local reassembly to produce a high-quality annotated call set. Sensitivity was measured in sample replicates (N=9) for all callers using in silico variant spike-in for a wide range of event sizes. We focused on deletions because these events were more reliably called. To evaluate caller specificity, we developed a novel metric called the D-score that leverages deletion sharing frequencies within and outside of families to rank recurring deletions. Assessment of overall quality across size bins was measured with the kinship coefficient. Individual callers were evaluated for computational cost, performance, sensitivity, and specificity. Quality of calls were evaluated by Sanger sequencing of predicted loss-of-function (LOF) variants, variants near AD candidate genes, and randomly selected genome-wide deletions ranging from 2 to 17,000 bp. ResultsWe generated a high-quality deletion call set across a wide range of event sizes consisting of 152,301 deletions with an average of 263 per genome. A total of 114 of 146 predicted deletions (78.1%) were validated by Sanger sequencing. Scalpel was more accurate in calling deletions [&le;]100 bp, whereas for Parliament, sensitivity was improved for deletions > 900 bp. We validated 83.0% (88/106) and 72.5% (37/51) of calls made by Scalpel and Parliament, respectively. Eleven deletions called by both Parliament and Scalpel in the 101-900 bin were tested and all were confirmed by Sanger sequencing. ConclusionsWe developed a flexible protocol to assess the quality of deletion detection across a wide range of sizes. We also generated a truth set of Sanger sequencing validated deletions with precise breakpoints covering a wide spectrum of sizes between 1 and 17,000 bp.

genetics↗

An Association Test of the Spatial Distribution of Rare Missense Variants within Protein Structures Improves Statistical Power of Sequencing Studies

Over 90% of variants are rare, and 50% of them are singletons in the Alzheimers Disease Sequencing Project Whole Exome Sequencing (ADSP WES) data. However, either single variant tests or unit-based tests are limited in the statistical power to detect the association between rare variants and phenotypes. To best utilize rare variants and investigate their biological effect, we exam their association with phenotypes in the context of protein. We developed a protein structure-based approach, POKEMON (Protein Optimized Kernel Evaluation of Missense Nucleotides), which evaluates rare missense variants based on their spatial distribution on the protein rather than allele frequency. The hypothesis behind this is that the three-dimensional spatial distribution of variants within a protein structure provides functional context and improves the power of association tests. POKEMON identified four candidate genes from the ADSP WES data, namely two known Alzheimers disease (AD) genes (TREM2 and SORL) and two novel genes (DUSP18 and CSF1R). For known AD genes, the signal from the spatial cluster is stable even if we exclude known AD risk variants, indicating the presence of additional low frequency risk variants within these genes. DUSP18 has a cluster of variants primarily shared by case subjects around the ligand-binding domain, and this cluster is further validated in a replication dataset with a larger sample size. POKEMON is an open-source tool available at https://github.com/bushlab-genomics/POKEMON.

bioinformatics↗

FILER: large-scale, harmonized FunctIonaL gEnomics Repository

MotivationQuerying massive collections of functional genomic and annotation data, linking and summarizing the query results across data sources and data types are important steps in high-throughput genomic and genetic analytical workflows. However, accomplishing these steps is difficult because of the heterogeneity and breadth of data sources, experimental assays, biological conditions (e.g., tissues, cell types), data types, and file formats. ResultsFunctIonaL gEnomics Repository (FILER) is a large-scale, harmonized functional genomics data catalog uniquely providing: 1) streamlined access to >50,000 harmonized, annotated functional genomic and annotation datasets across >20 integrated data sources, >1,100 biological conditions/tissues/cell types, and >20 experimental assays; 2) a scalable, indexing-based genomic querying interface; 3) ability for users to analyze and annotate their own experimental data against reference datasets. This rich resource spans >17 Billion genomic records for both GRCh37/hg19 and GRCh38/hg38 genome builds. FILER scales well with the experimental (query) data size and the number of reference datasets and data sources. When evaluated on large-scale analysis tasks, FILER demonstrated great efficiency as the observed running time for querying 1000x more genomic intervals (106 vs. 103) against all 7x109 hg19 FILER records increased sub-linearly by only a factor of 15x. Together, these features facilitate reproducible research and streamline querying, integrating, and utilizing large-scale functional genomics and annotation data. Availability and implementationFILER can be 1) freely accessed at https://lisanwanglab.org/FILER, 2) deployed on cloud or local servers (https://bitbucket.org/wanglab-upenn/FILER), and 3) integrated with other pipelines using provided scripts. Contactlswang@pennmedicine.upenn.edu

bioinformatics↗

NIAGADS Alzheimer's GenomicsDB: A resource for exploring Alzheimer's Disease genetic and genomic knowledge

INTRODUCTIONThe NIAGADS Alzheimers Genomics Database (GenomicsDB) is a public knowledgebase of Alzheimers disease (AD) genetic datasets and genomic annotations. METHODSIt uses a custom systems architecture to adopt and enforce rigorous standards that facilitate harmonization of AD-relevant GWAS summary statistics datasets with functional annotations, including a database of >230 million annotated variants from the AD Sequencing Projects joint-calling efforts. RESULTSThe knowledgebase generates genome browser tracks and interactive compiled from harmonized datasets and annotations in the underlying database. These facilitate data sharing and discovery, by contextualizing AD-risk associations in a broader functional genomic context or summarizing them in the context of functionally annotated genes and variants. DISCUSSIONCreated to make AD-genetics knowledge more accessible to AD-researchers, the GenomicsDB shares annotated AD-relevant summary statistics datasets via a web interface designed to guide users unfamiliar with genetic data in not only exploring, but also interpreting this ever-growing volume of data.

bioinformatics↗

SparkINFERNO: A scalable high-throughput pipeline for inferring molecular mechanisms of non-coding genetic variants

SummaryWe report SparkINFERNO (Spark-based INFERence of the molecular mechanisms of NOn-coding genetic variants), a scalable bioinformatics pipeline characterizing noncoding GWAS association findings. SparkINFERNO prioritizes causal variants underlying GWAS association signals and reports relevant regulatory elements, tissue contexts, and plausible target genes they affect. To achieve this, the SparkINFERNO algorithm integrates GWAS summary statistics with large-scale collection of functional genomics datasets spanning enhancer activity, transcription factor binding, expression quantitative trait loci, and other functional datasets across more than 400 tissues and cell types. Scalability is achieved by an underlying API implemented using Apache Spark and Giggle-based genomic indexing. We evaluated SparkINFERNO on large GWAS studies and show that SparkINFERNO is more than 60-times efficient and scales with data size and amount of computational resources. AvailabilitySparkINFERNO runs on clusters or a single server with Apache Spark environment, and is available at https://bitbucket.org/wanglab-upenn/SparkINFERNO or https://hub.docker.com/r/wanglab/spark-inferno. Contactlswang@pennmedicine.upenn.edu

bioinformatics↗

Inferring the molecular mechanisms of noncoding Alzheimer’s disease-associated genetic variants

Structured AbstractO_ST_ABSINTRODUCTIONC_ST_ABSWe set out to characterize the causal variants, regulatory mechanisms, tissue contexts, and target genes underlying noncoding late-onset Alzheimers Disease (LOAD)-associated genetic signals.\n\nMETHODSWe applied our INFERNO method to the IGAP genome-wide association study (GWAS) data, annotating all potentially causal variants with tissue-specific regulatory activity. Bayesian co-localization analysis of GWAS summary statistics and eQTL data was performed to identify tissue-specific target genes.\n\nRESULTSINFERNO identified enhancer dysregulation in all 19 tag regions analyzed, significant enrichments of enhancer overlaps in the immune-related blood category, and co-localized eQTL signals overlapping enhancers from the matching tissue class in ten regions (ABCA7, BIN1, CASS4, CD2AP, CD33, CELF1, CLU, EPHA1, FERMT2, ZCWPW1). We validated the allele-specific effects of several variants on enhancer function using luciferase expression assays.\n\nDISCUSSIONIntegrating functional genomics with GWAS signals yielded insights into the regulatory mechanisms, tissue contexts, and genes affected by noncoding genetic variation associated with LOAD risk.

bioinformatics↗

VCPA: genomic variant calling pipeline and data management tool for Alzheimer’s Disease Sequencing Project

Summary: We report VCPA, our SNP/Indel Variant Calling Pipeline and data management tool used for analysis of whole genome and exome sequencing (WGS/WES) for the Alzheimers Disease Sequencing Project. VCPA consists of two independent but linkable components: pipeline and tracking database. The pipeline is coded in Workflow Description Language and is fully optimized for the Amazon elastic compute cloud environment. This includes steps for processing raw sequence reads including read alignment, and all the way up to variant calling using GATK. The tracking database allows users to dynamically view the statuses of jobs running and the quality metrics reported by the pipeline. Users can thus monitor the production process and diagnose if any problem arises during the procedure. All quality metrics (>100 collected per processed genome) are stored in the database, thus facilitating users to compare, share and visualize the results. To summarize, VCPA is functional equivalent to the CCDG/TOPMed pipeline. Together with the dockerized database (also available as Amazon Machine Image), users can easily process any WGS/WES data on Amazon cloud with minimal installation.\n\nAvailability: VCPA is released under the MIT license and is available for academic and nonprofit use for free. The pipeline source code and step-by-step instructions are available from the National Institute on Aging Genetics of Alzheimers Disease Data Storage Site (http://www.niagads.org/VCPA).\n\nContact: yyee@pennmedicine.upenn.edu or lswang@pennmedicine.upenn.edu\n\nSupplementary information: Supplementary data are available at Bioinformatics online.

bioinformatics↗