bioRxiv Science⌕ Search

bioRxiv · 10.64898/2026.11.03.763980

RAPTORGraph: graph-based pathway modeling for causal discovery in single-cell perturbations

Abstract

Experiments involving the perturbation of individual cells are central to understanding cellular mechanisms and can accelerate drug discovery. Causal representation learning allows us to uncover the latent factors that regulate biological systems and predict the impact of novel perturbations. Unfortunately, existing methods fail to address intervention spillover in a closed-world setting where intervention targets are known a priori, such as in Perturb-seq experiments, due to their reliance on dense encoders. Furthermore, incorporating curated biological pathways into the model imposes a confirmatory bias, forcing it to explain the data through preexisting pathways and reducing the set of hypotheses the model can explore, while discarding novel signals that lie outside the annotated pathways. In this work, we introduce RAPTORGraph, a {beta}-variational autoencoder with a GraphPathway encoder that explicitly models complex gene-to-gene interactions within learned pathways. Moreover, our model's preconditioning isolates the influence of perturbed genes, yielding clean, single-node latent interventions required for identifiable causal discovery and eliminating spillover. Finally, we train the model on data preprocessed with optimal-transport alignment, which guarantees a well-defined mapping between control and perturbed samples and further stabilizes the learned latent representations. We demonstrate that RAPTORGraph improves state-of-the-art performance on downstream analyses of unseen perturbations, such as non-additive interactions, while performing competitively on objective metrics, such as mean squared error and maximum mean discrepancy. The source code is available at https://github.com/sXperfect/RAPTORGraph.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Adhisantoso, Y. G., Schröder, S. K., Gress, M., Hernaez, M., Voges, J.. 2026-11-04. RAPTORGraph: graph-based pathway modeling for causal discovery in single-cell perturbations. https://doi.org/10.64898/2026.11.03.763980

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

KEEP EXPLORING

Related preprints

StableProt: Structure-Aware Deep Learning for Protein Thermostability (Tm) and Environmental Adaptation (OGT) Prediction

Predicting protein melting temperature (Tm) and organismal optimal growth temperature (OGT) is essential for enzyme engineering, biocatalyst design, and metagenomic bioprospecting, yet computational prediction faces several fundamental bottlenecks: sequence-only representations miss tertiary packing; dual-task coupling induces destructive gradient conflict; natural database skew (>87% mesophiles) drives mesophilic collapse; and existing tools produce uncalibrated point predictions. To address these challenges, we present StableProt, a structure-aware framework that couples amino acid sequences with Foldseek 3Di structural tokens via a frozen SaProt backbone to capture 3D contacts. Disjoint heads condition thermodynamic stability on ecological context without gradient conflict, while targeted 14% mesophilic subsampling expands thermophile representation to eliminate mesophilic collapse. Calibrated ensemble modeling reduces calibration error to 1.92%, providing dependable 95% confidence intervals. Evaluating models across 10{degrees}C temperature intervals reveals severe baseline collapse at thermal extremes, whereas StableProt maintains robust accuracy across regimes. On ProThermDB and zero-shot FireProtDB, StableProt achieves state-of-the-art probabilistic accuracy (CRPS = 4.52{degrees}C and 8.71{degrees}C) while recovering 92.0% of hyperthermophiles ([≥]80{degrees}C), and in prospective validation, its calibrated intervals capture both enzyme stability (75.3% coverage) and host environmental growth temperatures (78.1% coverage). StableProt is freely accessible as an interactive web server at https://stableprot.dixitlab.org/.

bioinformatics↗

RoDPAA: A Robust Dissimilarity-Based Principal Angle Analysis Framework for Multi-View Microbiome Data Integration

Multiview microbiome studies profile the same participants across body sites or molecular layers, but integration is hampered by sparse, compositional data, modest sample sizes and methods that recognize only exact sharing. We present RoDPAA (Robust Dissimilarity-based Principal Angle Analysis), a framework that represents each view through any data-appropriate dissimilarity, such as Bray--Curtis, without log-ratio transformation or likelihood assumptions. RoDPAA aligns view-specific signal subspaces through principal angles, captures complete and partial sharing, and tests by permutation how many components are shared, using only eigendecomposition and little tuning. In Gaussian simulations, RoDPAA matched JIVE and MOFA given true ranks, ran faster and alone recovered the shared dimension in every replicate. In two inflammatory bowel disease (IBD) cohorts with sparse, zero-inflated data, Bray--Curtis-based RoDPAA recovered shared structure that was stable to prevalence filtering, whereas log-ratio-based alternatives were not. Its leading microbiome--metabolome factors, learned without disease labels, were the only ones associated with IBD.

bioinformatics↗

Deducing splicing events from transcript sets with splicelogic

Long-read RNA sequencing captures a greater proportion of full-length transcripts, enabling more accurate isoform identification, discovery of novel isoforms, and more precise differential transcript usage analysis. However, comparing transcripts, whether between conditions or between sets such as novel and annotated isoforms, yields complex isoform changes that are hard to manipulate, summarize, and visualize. This is compounded by vertical integration of some tools, where downstream analysis depends on the specific output of a particular upstream tool. To address this gap, we have developed splicelogic, an R/Bioconductor package that makes transcript-set comparisons biologically interpretable by turning them into discrete splicing events, such as exon skipping, alternative splice sites, intron retention, and alternative transcription start and end sites. We designed splicelogic to integrate easily with existing RNA-seq workflows and tools. The splicelogic functions are modular, readable, and extensible, making it easy for users to adapt core logic to their own custom scientific questions or novel splicing definitions. By obtaining interpretable splicing events from transcript changes, splicelogic enables downstream analyses, including annotation of RNA-binding protein recognition sites, alongside summary statistics and visualization. The splicelogic package is publicly available and distributed through Bioconductor.

bioinformatics↗