bioRxiv Science⌕ Search

Biology subjects

Mi, H.

Publications and source records attributed to Mi, H..

13 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↗

Pathway Polygenic Risk Scores (pPRS) for the Analysis of Gene-environment Interaction

A polygenic risk score (PRS) is used to quantify the combined disease risk of many genetic variants. For complex human traits there is interest in determining whether the PRS modifies, i.e. interacts with, important environmental (E) risk factors. Detection of a PRS by environment (PRS x E) interaction may provide clues to underlying biology and can be useful in developing targeted prevention strategies for modifiable risk factors. The standard PRS may include a subset of variants that interact with E but a much larger subset of variants that affect disease without regard to E. This latter subset will water down the underlying signal in former subset, leading to reduced power to detect PRS x E interaction. We explore the use of pathway-defined PRS (pPRS) scores, using state of the art tools to annotate subsets of variants to genomic pathways. We demonstrate via simulation that testing targeted pPRS x E interaction can yield substantially greater power than testing overall PRS x E interaction. We also analyze a large study (N=78,253) of colorectal cancer (CRC) where E = non-steroidal anti-inflammatory drugs (NSAIDs), a well-established protective exposure. While no evidence of overall PRS x NSAIDs interaction (p=0.41) is observed, a significant pPRS x NSAIDs interaction (p=0.0003) is identified based on SNPs within the TGF-{beta} / gonadotropin releasing hormone receptor (GRHR) pathway. NSAIDS is protective (OR=0.84) for those at the 5th percentile of the TGF-{beta}/GRHR pPRS (low genetic risk, OR), but significantly more protective (OR=0.70) for those at the 95th percentile (high genetic risk). From a biological perspective, this suggests that NSAIDs may act to reduce CRC risk specifically through genes in these pathways. From a population health perspective, our result suggests that focusing on genes within these pathways may be effective at identifying those for whom NSAIDs-based CRC-prevention efforts may be most effective. Author SummaryThe identification of polygenic risk score (PRS) by environment (PRSxE) interactions may provide clues to underlying biology and facilitate targeted disease prevention strategies. The standard approach to computing a PRS likely includes many variants that affect disease without regard to E, reducing power to detect PRS x E interactions. We utilize gene annotation tools to develop pathway-based PRS (pPRS) scores and show by simulation studies that testing pPRS x E interaction can yield substantially greater power than testing PRS x E, while also integrating biological knowledge into the analysis. We apply our method to a large study of colorectal cancer to identify a significant pPRS x NSAIDs interaction (p=0.0003) based on SNPs within the TGF-{beta} / gonadotropin releasing hormone receptor (GRHR) pathway. Our findings suggest that focusing on genetic susceptibility within biologically informed pathways may be more sensitive for identifying exposures that can be considered as part of a precision prevention approach.

genetics↗

Spatial and Compositional Biomarkers in Tumor Microenvironment Predicts Clinical Outcomes in Triple-Negative Breast Cancer

Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited treatment options, which warrants identification of novel therapeutic targets. Deciphering nuances in the tumor microenvironment (TME) may unveil insightful links between anti-tumor immunity and clinical outcomes, yet such connections remain underexplored. Here we employed a dataset derived from imaging mass cytometry of 58 TNBC patient specimens at single-cell resolution and performed in-depth quantifications with a suite of multi-scale computational algorithms. We detected distinct cell distribution patterns among clinical subgroups, potentially stemming from different infiltration related to tumor vasculature and fibroblast heterogeneity. Spatial analysis also identified ten recurrent cellular neighborhoods (CNs) - a collection of local TME characteristics with unique cell components. Coupling of the prevalence of pan-immune and perivasculature immune hotspot CNs, enrichment of inter-CN interactions was associated with improved survival. Using a deep learning model trained on engineered spatial data, we can with high accuracy (mean AUC of 5-fold cross-validation = 0.71) how a separate cohort of patients in the NeoTRIP clinical trial will respond to treatment based on baseline TME features. These data reinforce that the TME architecture is structured in cellular compositions, spatial organizations, vasculature biology, and molecular profiles, and suggest novel imaging-based biomarkers for treatment development in the context of TNBC.

bioinformatics↗

Informing virtual clinical trials of hepatocellular carcinoma with spatial multi-omics analysis of a human neoadjuvant immunotherapy clinical trial

Human clinical trials are important tools to advance novel systemic therapies improve treatment outcomes for cancer patients. The few durable treatment options have led to a critical need to advance new therapeutics in hepatocellular carcinoma (HCC). Recent human clinical trials have shown that new combination immunotherapeutic regimens provide unprecedented clinical response in a subset of patients. Computational methods that can simulate tumors from mathematical equations describing cellular and molecular interactions are emerging as promising tools to simulate the impact of therapy entirely in silico. To facilitate designing dosing regimen and identifying potential biomarkers, we developed a new computational model to track tumor progression at organ scale while reflecting the spatial heterogeneity in the tumor at tissue scale in HCC. This computational model is called a spatial quantitative systems pharmacology (spQSP) platform and it is also designed to simulate the effects of combination immunotherapy. We then validate the results from the spQSP system by leveraging real-world spatial multi-omics data from a neoadjuvant HCC clinical trial combining anti-PD-1 immunotherapy and a multitargeted tyrosine kinase inhibitor (TKI) cabozantinib. The model output is compared with spatial data from Imaging Mass Cytometry (IMC). Both IMC data and simulation results suggest closer proximity between CD8 T cell and macrophages among non-responders while the reverse trend was observed for responders. The analyses also imply wider dispersion of immune cells and less scattered cancer cells in responders samples. We also compared the model output with Visium spatial transcriptomics analyses of samples from post-treatment tumor resections in the original clinical trial. Both spatial transcriptomic data and simulation results identify the role of spatial patterns of tumor vasculature and TGF{beta} in tumor and immune cell interactions. To our knowledge, this is the first spatial tumor model for virtual clinical trials at a molecular scale that is grounded in high-throughput spatial multi-omics data from a human clinical trial.

bioengineering↗

On the automatic annotation of gene functions using observational data and phylogenetic trees

MotivationGene function annotation is important for a variety of downstream analyses of genetic data. Yet experimental characterization of function remains costly and slow, making computational prediction an important endeavor. In this paper we use a probabilistic evolutionary model built upon phylogenetic trees and experimental Gene Ontology functional annotations that allows automated prediction of function for unannotated genes. ResultsWe have developed a computationally efficient model of evolution of gene annotations using phylogenies based on a Bayesian framework using Markov Chain Monte Carlo for parameter estimation. Unlike previous approaches, our method is able to estimate parameters over many different phylogenetic trees and functions. The resulting parameters agree with biological intuition, such as the increased probability of function change following gene duplication. The method performs well on leave-one-out validation, and we further validated some of the predictions in the experimental scientific literature. AvailabilityOur method has been implemented as an R package and it is available online at https://github.com/USCBiostats/aphylo. Code needed to reproduce the tables and figures can be found in https://github.com/USCbiostats/aphylo-simulations. Author summaryUnderstanding the individual role that genes play in life is a key issue in biomedical-sciences. While information regarding gene functions is continuously growing, the number of genes with unknown biological purpose is yet greater. Because of this, scientists have dedicated much of their time to build and design tools that automatically infer gene functions. In this paper, we present yet another attempt to do such. While very simple, our model of gene-function evolution has some key features that have the potential to generate an impact in the field: (a) compared to other methods, ours is highly-scalable, which means that it is possible to simultaneously analyze hundreds of what are known as gene-families, compromising thousands of genes, (b) supports our biological intuition as our models data-driven results coherently agree with what theory dictates regarding how gene-functions evolved, (c) notwithstanding its simplicity, the models prediction accuracy is comparable to other more complex alternatives, and (d) perhaps most importantly, it can be used to both support new annotations and to suggest areas in which existing annotations show inconsistencies that may indicate errors or controversies.

bioinformatics↗

The permeabilized SecY protein-translocation channel can serve as a nonspecific sugar transporter

As the initial step in carbohydrate catabolism in cells, the substrate-specific transporters via active transport and facilitated diffusion play a decisive role in passage of sugars through the plasma membrane into the cytoplasm. The SecY complex (SecYEG) in bacteria forms a membrane channel responsible for protein translocation. This work demonstrates that weakening the sealability of the SecY channel allowed free diffusion of sugars, including glucose, fructose, mannose, xylose, arabinose, and lactose, into the engineered cells, facilitating its rapid growth on a wide spectrum of monosaccharides and bypassing/reducing stereospecificity, transport saturation, competitive inhibition, and carbon catabolite repression (CCR), which are usually encountered with the specific sugar transporters. The SecY channel is structurally conserved in prokaryotes, thus it may be engineered to serve as a unique and universal transporter for bacteria to passage sugars as demonstrated in Escherichia coli and Clostridium acetobutylicum.

bioengineering↗

Resolving challenges in quantitative modeling of microbial community dynamics

Microbial communities can perform biochemical activities that monocultures cannot. Controlling communities requires an understanding of community dynamics. Here, we mathematically predict the growth rate of an engineered community consisting of two S. cerevisiae strains, each releasing a metabolite required and consumed by the partner. Initial model parameters were based on strain phenotypes measured in batch mono-cultures with zero or excess metabolite, and failed to quantitatively predict experimental results. To resolve model-experiment discrepancy, we chemically identified the correct exchanged metabolites, but this did not improve model performance. We then re-measured strain phenotypes in chemostats mimicking the metabolite-limited community environments, while mitigating or incorporating effects of rapid evolution. Almost all phenotypes we measured varied significantly with the metabolite environment. Once we used parameters measured in community-like chemostat environments, prediction agreed with experimental results. In summary, using a simplified community, we uncovered, and devised means to resolve, modeling challenges that are likely general.

microbiology↗

Intercellular signaling network underlies biological time across multiple temporal scales

MotivationCellular, physiological and molecular processes must be organized and regulated across multiple time domains throughout the lifespan of an organism. The technological revolution in molecular biology has led to the identification of numerous genes implicated in the regulation of diverse temporal biological processes. However, it is natural to question whether there is an underlying regulatory network governing multiple timescales simultaneously.\n\nResultsUsing queries of relevant databases and literature searches, a single dense multiscale temporal regulatory network was identified involving core sets of genes that regulate circadian, cell cycle, and aging processes. The network was highly enriched for genes involved in signal transduction (P = 1.82e-82), with p53 and its regulators such as p300 and CREB binding protein forming key hubs, but also for genes involved in metabolism (P = 6.07e-127) and cellular response to stress (P = 1.56e-93). These results suggest an intertwined molecular signaling network that affects biological time across multiple temporal scales in response to environmental stimuli and available resources.\n\nContactjoshua.millstein@usc.edu\n\nSupplementary informationSupplementary data are available online.

systems biology↗

BDQC: a general-purpose analytics tool for domain-blind validation of Big Data

Translational biomedical research is generating exponentially more data: thousands of whole-genome sequences (WGS) are now available; brain data are doubling every two years. Analyses of Big Data, including imaging, genomic, phenotypic, and clinical data, present qualitatively new challenges as well as opportunities. Among the challenges is a proliferation in ways analyses can fail, due largely to the increasing length and complexity of processing pipelines. Anomalies in input data, runtime resource exhaustion or node failure in a distributed computation can all cause pipeline hiccups that are not necessarily obvious in the output. Flaws that can taint results may persist undetected in complex pipelines, a danger amplified by the fact that research is often concurrent with the development of the software on which it depends. On the positive side, the huge sample sizes increase statistical power, which in turn can shed new insight and motivate innovative analytic approaches. We have developed a framework for Big Data Quality Control (BDQC) including an extensible set of heuristic and statistical analyses that identify deviations in data without regard to its meaning (domain-blind analyses). BDQC takes advantage of large sample sizes to classify the samples, estimate distributions and identify outliers. Such outliers may be symptoms of technology failure (e.g., truncated output of one step of a pipeline for a single genome) or may reveal unsuspected \" signal\" in the data (e.g., evidence of aneuploidy in a genome). We have applied the framework to validate real-world WGS analysis pipelines. BDQC successfully identified data outliers representing various failure classes, including genome analyses missing a whole chromosome or part thereof, hidden among thousands of intermediary output files. These failures could then be resolved by reanalyzing the affected samples. BDQC both identified hidden flaws as well as yielded new insights into the data. BDQC is designed to complement quality software development practices. There are multiple benefits from the application of BDQC at all pipeline stages. By verifying input correctness, it can help avoid expensive computations on flawed data. Analysis of intermediary and final results facilitates recovery from aberrant termination of processes. All these computationally inexpensive verifications reduce cryptic analytical artifacts that could seriously preclude clinical-grade genome interpretation. BDQC is available at https://github.com/ini-bdds/bdqc.

bioinformatics↗

A cortical pathway modulates sensory input into the olfactory striatum

Sensory cortices process stimuli in manners essential for perception. The piriform primary olfactory cortex (PCX) extends dense association fibers into the ventral striatums olfactory tubercle (OT), yet the function of this cortico-striatal pathway is unknown. We optically stimulated channelrhodopsin-transduced PCX glutamatergic neurons or their association fibers while recording OT neural activity in mice performing an olfactory task. Activation of PCX neurons or their association fibers within the OT controlled the firing of some OT neurons and bidirectionally modulated odor coding dependent upon the neurons intrinsic odor responsivity. Further, patch clamp recordings and retroviral tracing from D1 and D2 dopamine receptor-expressing OT medium spiny neurons revealed this input can be monosynaptic and that both cell types receive most of their input from a specific spatial zone localized within the ventro-caudal PCX. These results demonstrate that the PCX functionally accesses the direct and indirect pathways of the basal ganglia within the OT.

neuroscience↗