bioRxiv Science⌕ Search

bioRxiv · 10.1101/2024.09.24.614666

varCADD: large sets of standing genetic variation enable genome-wide pathogenicity prediction

Abstract

Machine learning and artificial intelligence are increasingly being applied to identify phenotypically causal genetic variation. These data-driven methods require comprehensive training sets to deliver reliable results. However, large unbiased datasets for variant prioritization and effect predictions are rare as most of the available databases do not represent a broad ensemble of variant effects and are often biased towards protein-coding genome, or even towards few well-studied genes. To overcome these issues, we propose several alternative training sets derived from subsets of human standing variation. Specifically, we use variants identified from whole-genome sequences of 71,156 individuals contained in gnomAD v3.0 and approximate the benign set with frequent and the deleterious set with rare standing variation. We apply the Combined Annotation Dependent Depletion framework (CADD) and train several alternative models using CADD v1.6. Using the NCBI ClinVar validation set, we demonstrate that the alternative models have state-of-the art accuracy, outperforming the widely used pathogenicity score CADD v1.6 in certain genomic regions. Being larger than conventional databases, including the evolutionary-derived training dataset of about 30 million variants in CADD, standing variation datasets cover a broader range of genomic regions and rare instances of the applied annotations. For example, they cover more recent evolutionary changes common in gene regulatory regions, which are more challenging to assess with conventional tools. Finally, datasets derived from standing variation better represent allelic changes in the human genome and do not require extensive simulations and adaptations to annotations of the evolutionary-derived sequence alterations used for CADD training. We provide datasets as well as trained models to the community for further development and application. Suggestion for a Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=82 SRC="FIGDIR/small/614666v1_ufig1.gif" ALT="Figure 1"> View larger version (22K): org.highwire.dtl.DTLVardef@191bf80org.highwire.dtl.DTLVardef@1b3975dorg.highwire.dtl.DTLVardef@1965d97org.highwire.dtl.DTLVardef@da8e59_HPS_FORMAT_FIGEXP M_FIG C_FIG Author s SummaryHere, we are presenting the varCADD approach for predicting variant deleteriousness. Throughout time, pathogenic allelic changes are selected against by purifying selection, while neutral or beneficial changes can be passed along to next generations. Consequently, the frequencies of pathogenic variants are decreasing, beneficial alleles are increasing and frequencies of neutral variants are subject to drift. For that, allele frequencies in standing variation can be used as a proxy for their deleteriousness. To train a machine learning model for variant prioritization, frequent variants from gnomAD 3.0 were used as proxy-benign set and rare variants as proxy-deleterious set. The resulting training set exceeds excisting data sets in their size and allows for genome-wide coverage of molecular effects. The training set was annotated with sequence conservation, epigenetic, sequence-based and other features using the CADD v1.6 framework, after which a logistic regression model was trained. The output of the model can be interpreted as a probability for a variant to have a deleterious effect on genetic function.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Nazaretyan, L., Rentzsch, P., Kircher, M.. 2024-09-25. varCADD: large sets of standing genetic variation enable genome-wide pathogenicity prediction. https://doi.org/10.1101/2024.09.24.614666

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Senescence-associated KRAS upregulation in peripheral T cells links to premature coronary artery disease

Aims: Premature coronary artery disease (PCAD) lacks specific molecular drivers, and the role of immunosenescence is unclear. We investigated whether aging-related gene dysregulation in T cells contributes to PCAD. Methods: We combined bulk transcriptomics of PBMCs from 12 PCAD patients and 21 controls, single-cell RNA sequencing of PBMCs and human atherosclerotic plaques, weighted gene co-expression network analysis, gene perturbation network analysis, and molecular docking. Results: KRAS was identified as a hub gene intersecting PCAD-associated genes and aging-related genes. Single-cell analysis showed KRAS upregulation predominantly in effector CD8+ T cells, which exhibited the highest senescence scores that were further elevated in disease. Network perturbation of KRAS strongly impacted the cell killing pathway. KRAS-high effector CD8+ T cells were detected in coronary and carotid plaques, displaying enhanced cytotoxicity, exhaustion, and senescence features. Additionally, a candidate small molecule was computationally predicted to bind inactive KRAS. Conclusions: Elevated KRAS expression in senescent, cytotoxic CD8+ T cells is associated with PCAD, bridging immunosenescence and premature atherosclerosis. This finding provides a novel biomarker candidate and potential therapeutic entry point, awaiting further functional validation.

bioinformatics↗

Targeted finetuning enables co-folding models to learn ligand-induced protein conformational states

Advances in protein structure prediction have enabled all-atom protein-ligand co-folding models that predict bound conformations directly from sequence and small-molecule structure. However, these models often fail to generalize to novel binding sites or alternative protein conformational states, limiting their utility for chemical biology and drug discovery. Here we show this limitation reflects training data bias rather than architectural constraints and can be overcome through targeted finetuning. Using ten previously unseen X-ray structures of Werner (WRN) helicase from a drug discovery program, we finetune Boltz-1 to learn both an allosteric binding site and a large conformational change locking the enzyme in an inactive state, while preserving accuracy on the ATP-bound state. The finetuned model generalizes to different chemical series and transfers the conformational logic across RecQ-family helicases in a binding-site sequence-dependent manner. This approach provides a blueprint for adapting foundation models as new structural and mechanistic data emerge, enabling co-folding networks to capture ligand-induced conformational switches and binding poses absent from their training data but central to biological regulation and therapeutic intervention.

bioinformatics↗

Benchmarking single-cell foundation models for aging biology

Single cell foundation models (scFMs) provide representations of cellular states, but their utility across biological questions in aging research remains unclear. We established a benchmark of cellular representations for aging research, evaluating ten general-purpose scFMs, three aging-specific models and conventional methods across five biological questions using more than 2.5 million single cell transcriptomes. Using frozen pretrained representations, Geneformer performed best among scFMs for chronological age prediction and age pseudotime concordance, although 2,000 highly variable genes achieved higher mean performance. Several scFMs captured positive molecular age shifts across three disease contexts, consistent with reported aging-associated changes. SCimilarity performed well for rare cellular state identification across out-of-distribution datasets, exceeding aging specific models and conventional baselines. At the gene level, scGPT showed the highest recovery of reference TF target interactions, including aging-related regulatory hubs. Overall, scFMs supported diverse aging analyses, but performance depended on the biological question, highlighting their utility for rare cellular state identification and regulatory analysis.

bioinformatics↗