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Queme, B.

Publications and source records attributed to Queme, B..

6 recordsLinked to original sources

Annotation-Based Gene-Peak Links Improve Regulatory Network Prediction of Gene Expression in Human Kidney Multi-Omics

BackgroundLinking distal regulatory elements to their target genes is a central problem for interpreting chromatin accessibility and other non-coding genomic data. Proximity-based mapping is convenient but ignores three-dimensional enhancer-promoter architecture and can misassign long-range regulatory effects. Correlation-based approaches can also miss regulatory links because of limited statistical power and restrictive distance or significance thresholds. Single-cell and single-nucleus multi-omic datasets, such as 10x Multiome profiles that jointly measure chromatin accessibility and gene expression in the same cells or nuclei, now provide a way to evaluate gene-peak linkage strategies by testing how well linked accessibility features predict gene expression. Existing methods often focus on scoring individual enhancer-gene pairs. In this study, we proposed and constructed a fast annotation-based candidate gene-peak network and tested whether it improves downstream prediction of gene expression. MethodsWe first built a unified gene-peak regulatory network by integrating enhancer-based, promoter-based, and proximity-based linkage strategies. We then used single-cell multiome data from the Kidney Precision Medicine Project (KPMP) 10x Multiome cohort to evaluate whether the proposed links captured regulatory signals. We aggregated RNA expression and ATAC accessibility at the cell-type cluster level and trained predictive models to evaluate how well different linkage strategies could explain gene expression based on accessibility. Model performance was compared between annotation-based (including both enhancer- and promoter-based links) and proximity-based gene-peak links using testing R{superscript 2} and mean squared error (MSE) in a strict set of 1,704 genes and an adaptive set of 7,973 genes with more relaxed requirements. ResultsIn the strict regime (1,704 genes with [≥]20 peaks assigned by the nearest-TSS rule and [≥]10 annotated enhancer-based peaks), the annotation-based model consistently achieved higher testing R{superscript 2} and lower testing MSE than the proximity-based model. In the larger adaptive regime (7,973 genes with [≥]5 proximity-based and [≥]2 enhancer-based peaks), we defined for each gene a balanced number of selected peaks based on its available closest and enhancer links; the annotation-based model again showed globally higher testing R{superscript 2} and lower testing MSE. These improvements were observed over a broad range of candidate-linked peak numbers. ConclusionsUsing human kidney 10x Multiome data, we show that a fast annotation-based gene-peak linkage framework can improve prediction of gene expression from chromatin accessibility compared with conventional approaches. These results support the use of biologically informed enhancer and promoter annotations when constructing candidate gene regulatory networks. Our framework also showed concordance with the correlation-based Signac LinkPeaks method while providing broader coverage and greater computational efficiency. We have implemented these annotation-based linkage methods in the GPlinksR R package, providing a fast and scalable tool for constructing regulatory networks.

genomics↗

Beyond Pathway Boundaries: A Degree-Aware Network Clustering Test for Gene Sets

Over-representation analysis (ORA) is the most commonly used interpretation tool for gene lists despite well-documented limitations: pathway boundaries are fixed, genes are assumed independent, and results depend on the background set. Network-based methods address these using interaction-network modularity, but introduce hub bias: highly connected genes appear clustered under naive nulls because curated networks overrepresent well-studied genes. Existing corrections are imperfect: edge permutation destroys the topology the test should condition on, and propagation methods hide the confound in parameter tuning. We introduce MANGO (Morans Autocorrelation for Network Gene Over-representation), which asks one conditional question: does a gene sets spatial autocorrelation on a fixed biological network exceed what its degree composition alone would predict? MANGO computes Global Morans I under a null that conditions on both the network and the binned degree distribution of the gene set, then decomposes significant signals at the component and gene level. In benchmarks, uniform nulls produce a false positive rate of 1.0 on hub-enriched gene sets with no real clustering; ten-bin degree-stratified nulls bring that to 0.0 with no power loss (AUC [&ge;] 0.98; on degree-typical signals, |{Delta}AUC| [&le;] 0.004). Pathway-spiking simulations confirm detection of real biological clustering across diverse pathway sizes and degree profiles. Applied to the FIGI colorectal cancer GWAS (204 SNPs), the set is degree-typical (KS p = 0.83), yet Morans I is highly significant (p < 0.001). Component-level jackknife localizes the entire signal to a single 24-gene module spanning TGF-{beta}, Wnt/cadherin, and related pathways, with four bottlenecks (SMAD3, MYC, CTNNB1, PTPN1) matching established CRC driver biology. eTOC blurbMANGO tests whether a gene sets spatial autocorrelation on a biological network exceeds what its degree composition predicts, by conditioning Global Morans I on the binned degree distribution with the network held fixed. Significant signals are decomposed to modules, bottleneck genes, and statistical drivers through component jackknife, articulation-point, and gene-jackknife analysis.

bioinformatics↗

SNPWay: streamlined SNP-to-function and pathway over-representation analysis

MotivationPost-GWAS interpretation frequently requires translating variant lists (e.g., lead SNPs, clumped loci, credible sets, or curated panels) into pathway and functional hypotheses. In practice, obtaining pathway and functional over-representation results from SNP inputs often requires stitching together multiple tools for variant annotation, regulatory annotation, gene identifier handling, and statistical testing. This integration burden can reduce reproducibility and restrict end-to-end analysis to groups with dedicated bioinformatics support. SummaryWe present SNPWay, a web server and R package that performs end-to-end SNP-to-function and pathway over-representation analysis in a single standardized workflow. SNPWay accepts rsIDs, VCF files, or hg19/GRCh37 genomic coordinates. It queries Annotation Query (AnnoQ) to obtain SNP-to-gene mappings from ANNOVAR, SnpEff, and VEP under both Ensembl and RefSeq gene models, and incorporates enhancer-gene links via PEREGRINE to augment mappings for noncoding variants. SNPWay aggregates mapped genes into a single, non-redundant, combined gene list and submits it to PANTHER for over-representation testing against the Homo sapiens reference list, returning over-represented pathways and functional categories (e.g., Gene Ontology) with direct links for interactive exploration in PANTHER. SNPWays modular architecture is designed for extensibility, enabling incorporation of additional analysis methods in future releases. A step-by-step walkthrough is provided in Supplementary Data. Availability and implementationWeb server: https://snpway.annoq.org/. R package and source code: https://github.com/USCbiostats/Annoq_Overrepr_Workflow. Documentation: https://snpway.annoq.org/about. Examples: The website contains Sample files for the input formats, also provided in Supplementary Data. SNPWay is free to use with no mandatory login. Contacthuaiyumi@usc.edu Supplementary informationSupplementary data are available at Bioinformatics online

bioinformatics↗

From SNPs to Pathways: A genome-wide benchmark of annotation discrepancies and their impact on protein- and pathway-level inference

BackgroundAccurate single-nucleotide polymorphism (SNP) annotation is central to genomic research yet widely used tools and gene models often yield divergent results. Prior studies have shown such discrepancies in small datasets, but the extent of genome-wide variation and its impact on downstream pathway analysis remain unclear. ResultsWe conducted a comprehensive comparison of three commonly used SNP annotation tools, ANNOVAR, SnpEff, and VEP, using both Ensembl and RefSeq gene models to evaluate more than 40 million SNPs from the Haplotype Reference Consortium. At the protein level, annotation output differed significantly across tools and gene models (p-adj < 0.001), with discrepancies present in both genic and intergenic regions. RefSeq produced broader annotation coverage, particularly for intergenic SNPs, while Ensembl showed greater internal consistency. SnpEff provided the most complete coverage overall, whereas no single tool or model configuration achieved full annotation recovery of the union reference. Integration across tools and models maximized coverage and reduced annotation loss. In a case study of 204 colorectal cancer-associated SNPs from the FIGI GWAS, pathway enrichment results varied depending on annotation strategy. The fully integrated approach identified all four significant pathways, whereas several single-tool or single-model strategies missed one or more. ConclusionSNP annotation outcomes are influenced by both the tool and gene model used, and relying on a single approach may result in incomplete coverage. A multi-tool, multi-model strategy provides the most comprehensive annotation and preserves enriched pathways, supporting more robust and reproducible genomic interpretation.

bioinformatics↗

In vivo quantitative high-throughput screening for drug discovery and comparative toxicology

Quantitative high-throughput screening (qHTS) evaluates the pharmacology of drug and investigational agent libraries for potential therapeutic uses, toxicological risk assessment, and increasingly for academic chemical tool discovery. Phenotypic HTS assays aim to interrogate molecular pathways and networks, often relying on cell culture systems, historically with less emphasis on multicellular organisms. C. elegans has served as a powerful eukaryotic model organism for human biology and disease by virtue of genetic conservation and experimental tractability. Here we describe a paradigm to enable C. elegans in qHTS using 384-well microtiter plate laser scanning cytometry. GFP-expressing organisms are used to reveal phenotype-modifying structure-activity relationships to guide subsequent life stages and proteomic analysis. E. coli bacterial ghosts, a non-replicating nutrient source, allow compound exposures over 7-days spanning two life cycles to mitigate complications from bacterial overgrowth. We demonstrate the method with a library composed of anti-infective agents, or molecules of general toxicological concern. Each was tested in 7-point titration to assess the feasibility of nematode-based in vivo qHTS, and examples of follow-up strategies were provided to study organism-based chemotype selectivity and subsequent network perturbations having a physiological impact. We anticipate a broader application of this qHTS-coupled proteomics approach will enable the analysis of C. elegans orthologous transgenic phenotypes of human pathologies to facilitate drug and probe profiling from high-impact chemical libraries for a range of therapeutic indications and study of potential toxicological signatures. Graphic Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=159 SRC="FIGDIR/small/505462v1_ufig1.gif" ALT="Figure 1"> View larger version (52K): org.highwire.dtl.DTLVardef@7ef320org.highwire.dtl.DTLVardef@8bc35corg.highwire.dtl.DTLVardef@1c6f446org.highwire.dtl.DTLVardef@cf56f1_HPS_FORMAT_FIGEXP M_FIG C_FIG

pharmacology and toxicology↗

qHTSWaterfall: 3-dimensional visualization software for quantitative high-throughput screening (qHTS) data

High throughput screening (HTS) is widely used in drug discovery and chemical biology to identify and characterize agents having pharmacologic properties often by evaluation of large chemical libraries. Standard HTS data can be simply plotted as an x-y graph usually represented as % activity of a compound tested at a single concentration vs compound ID, whereas quantitative HTS (qHTS) data incorporates a third axis represented by concentration. By virtue of the additional data points arising from the compound titration and the incorporation of logistic fit parameters that define the concentration-response curve, such as EC50 and Hill slope, qHTS data has been challenging to display on a single graph. Here we provide a flexible solution to the rapid plotting of complete qHTS data sets to produce a 3-axis plot we call qHTS Waterfall Plots. The software described here can be generally applied to any 3-axis dataset and is available as both an R package and an R shiny application.

bioinformatics↗