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Inecik, K.

Publications and source records attributed to Inecik, K..

8 recordsLinked to original sources

An integrated single cell and spatial omics atlas of human prenatal development

Single cell genomics has enabled analysis of human prenatal development at unprecedented resolution. However, most studies have relied on dissociated tissues during restricted windows of development, limiting insights into how spatially distributed networks of cells, and multicellular niches emerge and adapt to distinct organ microenvironments in situ. Moreover, existing human developmental atlases have not yet been harmonised, and we thus lack a comprehensive catalogue of known cell types in the developing human body. Here, we introduce the Human Developmental Cell Atlas (HDCA), a unified structural, cellular and molecular resource for prenatal human development. The HDCA integrates published and unpublished single cell/nucleus RNAseq atlases across prenatal organs, and includes a newly generated, spatially resolved, multimodal cell atlas of intact human embryos. Spanning 4-22 post conceptional weeks, capturing embryonic and early to mid fetal stages, the HDCA contains [~]4.6 million cells/nuclei which resolve into [~]450 cell types, explorable with a bespoke web portal. For a global overview of the human embryos multicellular communities, we applied unsupervised deep learning to our intact human embryo spatial data, charting 114 tissue niches that are structural and signalling hubs for the cellular interactions of the embryo. Guided by these niches, we profiled cellular networks over space and time, not examinable using single-organ atlases. In so doing, we revealed tissue-specific fibroblast patterning from previously undescribed mesenchyme progenitors, early diversification of organ-specific blood capillaries and lymphatic vasculature, emergence of neural crest cell fates, the formation of placode-and neural crest-derived peripheral sensory neurons, and how tissue niches guide peripheral neuron maturation and axonal migration. The HDCA thus serves as a comprehensive step towards a comprehensive understanding of human prenatal development, and a template towards unravelling the biology of congenital disorders.

developmental biology↗

IDTrack: Time- and Namespace-Aware Identifier Harmonization for Reproducible Workflows

MotivationReproducibility in computational biology fails silently when gene identifiers drift beneath unchanged analysis code: the same frozen pipeline, rerun months later, yields different results not because biology evolved but because identifier semantics shifted with upstream annotation releases--a failure mode invisible to version control and containerization because the mapping layer itself constitutes an undeclared coordinate system whose time axis advances independently of downstream workflows. Gene identifiers occupy positions in a joint space of namespace, annotation release, genome assembly, and entity layer that evolves through retirements, merges, splits, and nomenclature reassignments, so atlas integration, retrospective reanalysis, and perturbation screens inherit temporal dependencies that existing utilities cannot surface: current mappers answer what an identifier resolves to now rather than under what declared contract the feature space was constructed. ResultsIDTrack reconceptualizes identifier harmonization as a time-indexed coordinate transformation by materializing annotation release history into a snapshot-bounded identifier graph and solving conversions through a time-traveling, contract-constrained pathfinder that pins release boundaries, assembly contexts, and ambiguity policies as explicit parameters rather than implicit endpoint state. This architecture surfaces reachability and ambiguity as interpretable outcome classes--unmapped, uniquely resolved, or ambiguously multi-target--enables atlas-scale harmonization with explicit collision handling, and records every mapping decision in a provenance ledger that transforms invisible preprocessing into citable methodological infrastructure whose coordinate choices can be inspected, compared, and reproduced rather than lost as ephemeral preprocessing. Availability and ImplementationCode: https://github.com/theislab/idtrack; package: pip install idtrack. Contactkemal.inecik@helmholtz-munich.de; erkmenerken22@ku.edu.tr; fabian.theis@helmholtz-munich.de. Supplementary InformationSupplementary material elaborates on architectural decisions and implementation details.

bioinformatics↗

Beyond Visual Inspection: Principled Benchmarking of Single-Cell Trajectory Representations with scTRAM

Single-cell representation learning aims to construct low-dimensional embeddings that preserve biologically salient manifold structures. Yet current evaluation protocols remain inadequate for assessing trajectory fidelity--essential for studying cell differentiation, immune responses, disease progression and perturbation--relying on heuristic visualizations or scalar surrogates that overlook multiscale trajectory geometry. To address this gap, we present scTRAM--single-cell trajectory representation metrics--a principled benchmarking framework that quantitatively evaluates how well single-cell embeddings retain groundtruth trajectories across complementary failure modes, from local neighborhood scrambling to global branch mis-ordering. Through our experiments, we show that scTRAM reveals modelspecific trade-offs in preserving distinct aspects of trajectory structure, with edge-specific decomposition exposing localized representational biases at high resolution. Systematic validation across diverse biological contexts confirms that the metric suite is sensitive to genuine structural properties rather than statistical artifacts. By shifting from qualitative, ad-hoc judgments to quantitative, principled approach, scTRAM enables rigorous comparison of embedding methods and informs downstream analyses where trajectory integrity is essential for biological interpretation.

bioinformatics↗

TarDis: Achieving Robust and Structured Disentanglement of Multiple Covariates

Addressing challenges in domain invariance within single-cell genomics necessitates innovative strategies to manage the heterogeneity of multi-source datasets while maintaining the integrity of biological signals. We introduce TarDis, a novel deep generative model designed to disentangle intricate covariate structures across diverse biological datasets, distinguishing technical artifacts from true biological variations. By employing tailored covariate-specific loss components and a self-supervised approach, TarDis effectively generates multiple latent space representations that capture each continuous and categorical target covariate separately, along with unexplained variation. Our extensive evaluations demonstrate that TarDis outperforms existing methods in data integration, covariate disentanglement, and robust out-of-distribution predictions. The models capacity to produce interpretable and structured latent spaces, including its pioneering work in ordered latent representations for continuous covariates, markedly enhances its utility in hypothesis-driven research. Consequently, TarDis offers a promising analytical platform for advancing scientific discovery, providing insights into cellular dynamics, and enabling targeted therapeutic interventions. Progress and potentialModern single-cell genomics provides an unprecedented view into cellular heterogeneity, yet the very richness that propels new discoveries also complicates downstream analysis. Gene-expression patterns emerge from overlapping biological processes (e.g., differentiation programs, disease progression) and extrinsic factors (e.g., laboratory protocols, technical artifacts). Disentanglement, in this context, aims to parse these intertwined influences into interpretable latent representations, a crucial step for elucidating how complex covariates shape cellular states. While methods that correct for batch effects have become standard, these strategies often fall short in achieving the deeper objective of capturing subtle, high-dimensional biological dynamics. In single-cell experiments, cells navigate intricate developmental trajectories, respond nonlinearly to environmental or pharmaceutical perturbations, and exhibit myriad context-specific behaviors. Without disentanglement, these diverse signals frequently remain intermingled, limiting biological interpretability and hindering hypothesis-driven research. Disentangling biological covariates is particularly vital for addressing nuanced questions in single-cell research. For example, in a disease model involving multiple genetic variants and variable drug dosing, researchers may wish to examine the effect of each variant independently or investigate how dosage influences a specific mutant background. Similarly, in developmental biology, uncovering how cells evolve across a continuum of pseudotime (e.g., from pluripotent to fully differentiated states) is critical for identifying the genes that orchestrate fate decisions while isolating the influence of developmental time from tissue-specific contexts, along with other confounding factors such as culture conditions, sample preparation, or donor genetic characteristics. Alternatively, disentangling lineage commitment signals from spatial patterning cues enables the identification of master regulators driving fate decisions. Moreover, by explicitly isolating and representing each covariate as an independent latent dimension, one can systematically navigate and interrogate a rich multidimensional covariate space. This approach extends beyond merely observing biological states, it enables exploration of novel or unmeasured cellular conditions through latent-space manipulations. For instance, disentangled latent spaces could allow researchers to computationally predict cellular responses at drug dosages or developmental stages that were never experimentally observed, significantly broadening the scope and predictive power of experimental datasets. Such analyses yield testable hypotheses for unexplored biological phenomena and enable informed planning of subsequent experimental validations. The challenge of covariate disentanglement stems fundamentally from the complexity of modeling joint distributions of gene expression conditioned simultaneously on multiple covariates, both categorical (e.g., tissue type, disease condition) and continuous (e.g., pseudotime, dosage). This is inherently an underdetermined problem because single-cell measurements represent only sparse snapshots within a vast combinatorial space of covariate conditions. Conventional modeling approaches often conflate correlated covariates, collapsing biological variability into ambiguous latent factors, and typically fail to explicitly create separate latent representations for disentangled covariates. Moreover, continuous covariates introduce an additional layer of complexity; yet discretizing them artificially imposes arbitrary boundaries, obscuring subtle transitions and hindering accurate capture of biological gradients. Therefore, preserving the continuous nature of such covariates in disentangled representations is critical, as it maintains their intrinsic ordering and enables researchers to discern nuanced biological shifts--such as identifying thresholds in dose-response relationships or characterizing gradual developmental transitions--in a naturally interpretable manner. The key idea in this paper is to devise a tailored deep generative model for systematically separating both categorical and continuous covariates into independent latent dimensions, while still ensuring coherent integration of the underlying gene-expression data. By explicitly targeting these covariates and preserving continuous variables as smooth, ordered latent axes, our approach clarifies complex interactions and uncovers nuanced patterns that remain concealed under standard analyses. The resulting disentangled representations can then support robust out-of-distribution generalizations, refined differential analyses, and more principled hypotheses about how diverse factors interact to drive cellular variation.

bioinformatics↗

flowVI: Flow Cytometry Variational Inference

Single-cell flow cytometry stands as a pivotal instrument in both biomedical research and clinical practice, not only offering invaluable insights into cellular phenotypes and functions but also significantly advancing our understanding of various patient states. However, its potential is often constrained by factors such as technical limitations, noise interference, and batch effects, which complicate comparison between flow cytometry experiments and compromise its overall impact. Recent advances in deep representation learning have demonstrated promise in overcoming similar challenges in related fields, particularly in the context of single-cell transcriptomic sequencing data analysis. Here, we propose flowVI, a multimodal deep generative model, tailored for integrative analysis of multiple massively parallel cytometry datasets from diverse sources. By effectively modeling noise variances, technical biases, and batch-specific heterogeneity using probabilistic data representation, we demonstrate that flowVI not only excels in the imputation of missing protein markers but also seamlessly integrates data from distinct cytometry panels. FlowVI thus emerges as a potent tool for constructing comprehensive flow cytometry atlases and enhancing the precision of flow cytometry data analyses. The source code for replicating these findings is hosted on GitHub, theislab/flowVI

bioinformatics↗

scARE: Attribution Regularization for Single Cell Representation Learning

Single-cell data generation techniques have provided valuable insights into the intricate nature of cellular heterogeneity. However, effectively unraveling subtle variations within a specific gene set of interest, while mitigating the confounding presence of higher-order variability, remains challenging. To address this, we propose scARE, a novel end-to-end generative deep learning model, amplifies model sensitivity to a preselected subset of features while minimizing others. scARE incorporates an auxiliary attribution loss term during model training, which empowers researchers to manipulate the models behavior robustly and flexibly. In this study, we showcased scAREs applicability in two concrete scenarios: uncovering subclusters associated with the expression patterns of two cellular pathway genes, and its ability to optimize the model training procedure by leveraging time-points metadata, resulting in improved downstream performance.

bioinformatics↗

High-throughput profiling of drug interactions in Gram-positive bacteria

Drug combinations present a powerful strategy to tackle antimicrobial resistance, but have not been systematically tested in many bacterial species. Here, we used an automated high-throughput setup to profile [~] 8000 combinations between 65 antibacterial drugs in three Gram-positive species: the model species, Bacillus subtilis and two prominent pathogens, Staphylococcus aureus and Streptococcus pneumoniae. Thereby, we recapitulate previously known drug interactions, but also identify ten times more interactions than previously reported in the pathogen S. aureus, including two synergies that were also effective in multi-drug resistant clinical S. aureus isolates in vitro and in vivo. Interactions were largely species-specific and mostly synergistic for drugs targeting the same cellular process, as observed also for Gram-negative species1. Yet, the dominating synergies are clearly distinct between Gram-negative and Gram-positive species, and are driven by different bottlenecks in drug uptake and vulnerabilities of their cell surface structures. To further explore interactions of commonly prescribed non-antibiotic drugs with antibiotics, we tested 2728 of such combinations in S. aureus, detecting a plethora of unexpected antagonisms that could compromise the efficacy of antimicrobial treatments in the age of polypharmacy. We uncovered even more synergies than antagonisms, some of which we could demonstrate as effective combinations in vivo against multi-drug resistant clinical isolates. Among them, we showed that the antiaggregant ticagrelor interferes with purine metabolism and changes the surface charge of S. aureus, leading to strong synergies with cationic antibiotics. Overall, this exemplifies the untapped potential of approved non-antibacterial drugs to be repurposed as antibiotic adjuvants. All data can be browsed through an interactive interface (https://apps.embl.de/combact/).

microbiology↗

MultiCPA: Multimodal Compositional Perturbation Autoencoder

Single-cell multimodal profiling provides a high-resolution view of cellular information. Recently, multimodal profiling approaches have been coupled with CRISPR technologies to perform pooled screens of single or combinatorial perturbations. This opens the possibility of exploring the massive space of combinatorial perturbations and their regulatory effects computationally from the extrapolation of a few experimentally feasible combinations. Here, we propose MultiCPA, an end-to-end generative architecture to predict multimodal perturbation response at single cell level. Two mixing strategies to integrate multiple modalities are introduced and compared with existing methods. MultiCPA was also shown to accurately predict unseen combinatorial perturbation responses for multiple modalities. The code to reproduce the results is available on GitHub, theislab/multicpa.

systems biology↗