Search bioRxiv⌕ Search

bioRxiv · 10.1101/077636

Managing Uncertainty in Metabolic Network Structure and Improving Predictions Using EnsembleFBA

Abstract

Genome-scale metabolic network reconstructions (GENREs) are repositories of knowledge about the metabolic processes that occur in an organism. GENREs have been used to discover and interpret metabolic functions, and to engineer novel network structures. A major barrier preventing more widespread use of GENREs, particularly to study non-model organisms, is the extensive time required to produce a high-quality GENRE. Many automated approaches have been developed which reduce this time requirement, but automatically-reconstructed draft GENREs still require curation before useful predictions can be made. We present a novel ensemble approach to the analysis of GENREs which improves the predictive capabilities of draft GENREs and is compatible with many automated reconstruction approaches. We refer to this new approach as Ensemble Flux Balance Analysis (EnsembleFBA). We validate EnsembleFBA by predicting growth and gene essentiality in the model organism Pseudomonas aeruginosa UCBPP-PA14. We demonstrate how EnsembleFBA can be included in a systems biology workflow by predicting essential genes in six Streptococcus species and mapping the essential genes to small molecule ligands from DrugBank. We found that some metabolic subsystems contribute disproportionately to the set of predicted essential reactions in a way that is unique to each Streptococcus species. These species-specific network structures lead to species-specific outcomes from small molecule interactions. Through these analyses of P. aeruginosa and six Streptococci, we show that ensembles increase the quality of predictions without drastically increasing reconstruction time, thus making GENRE approaches more practical for applications which require predictions for many non-model organisms. All of our functions and accompanying example code are available in an open online repository.\n\nAuthor SummaryMetabolism is the driving force behind all biological activity. Genome-scale metabolic network reconstructions (GENREs) are representations of metabolic systems that can be analyzed mathematically to make predictions about how a biochemical system will behave as well as to design biochemical systems with new properties. GENREs have traditionally been reconstructed manually, which can require extensive time and effort. Recent software solutions automate the process (drastically reducing the required effort) but the resulting GENREs are of lower quality and produce less reliable predictions than the manually-curated versions. We present a novel method (\"EnsembleFBA\") which overcomes uncertainties involved in automated reconstruction by pooling many different draft GENREs together into an ensemble. We tested EnsembleFBA by predicting the growth and essential genes of the common pathogen Pseudomonas aeruginosa. We found that when predicting growth or essential genes, ensembles of GENREs achieved much better precision or captured many more essential genes than any of the individual GENREs within the ensemble. By improving the predictions that can be made with automatically-generated GENREs, we open the door to studying systems which would otherwise be infeasible.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Matthew Biggs, Jason A Papin. 2016-09-26. Managing Uncertainty in Metabolic Network Structure and Improving Predictions Using EnsembleFBA. https://doi.org/10.1101/077636

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

KEEP EXPLORING

Related preprints

Personalized Immunotherapy via Multiscale Tumor-Immune Modeling and Optimal Control

Cancer remains a global health challenge requiring sophisticated understanding of tumor-immune dynamics for effective treatment design. Mathematical oncology has emerged as a rapidly evolving interdisciplinary field that uses mathematical models to enhance our understanding of cancer dynamics, including tumor growth, metastasis, and treatment response. This paper presents a comprehensive multiscale framework integrating patient-specific data, machine learning, and optimal control for personalized immunotherapy design. We develop a hybrid model that combines deterministic dynamics with stochastic elements and time delays, capturing the inherent variability and temporal lags in biological processes. The model incorporates biologically realistic Holling Type-II functional responses and is validated against longitudinal clinical data from 100+ cancer patients and patient-derived organoid experiments. Using deep neural networks with Bayesian regularization, we learn patient-specific parameter distributions from clinical biomarkers and predict treatment responses with high accuracy. Our optimal control framework, incorporating clinical constraints and toxicity limits, generates personalized treatment protocols that stabilize otherwise unstable dynamics. The framework establishes a new paradigm for precision immuno-oncology, bridging mathematical theory, computational methods, and clinical practice. Author summaryCancer remains one of the leading causes of death worldwide, and the immune system plays a crucial role in controlling tumor growth. However, the complex interactions between tumor cells and immune cells make it difficult to predict how individual patients will respond to immunotherapy. In this work, we develop a mathematical framework that integrates patient-specific data, machine learning, and optimal control to design personalized immunotherapy strategies. Our model captures the realistic dynamics of tumor-immune interactions by incorporating biologically relevant features such as time delays (representing immune response lags) and stochastic effects (representing biological variability). Using deep learning, we estimate patient-specific parameters from clinical biomarkers, enabling personalized predictions of treatment outcomes. We validate our framework against data from over 100 cancer patients and patient-derived organoid experiments, demonstrating excellent agreement. Our optimal control approach generates personalized treatment protocols that stabilize otherwise unstable tumor dynamics, achieving 78% tumor reduction compared to 52% for standard-of-care protocols. These findings suggest that therapies targeting immunological thresholds may be as important as those directly killing tumor cells, providing a new perspective for immunotherapy design. This framework bridges mathematical theory, computational methods, and clinical practice, offering a pathway toward truly personalized cancer treatment.

Systems Biology↗

Reversible Opto-Chemical activation of KRASG12V signaling with near single-cell precision

KRAS mutations drive some of the most lethal carcinomas, and genomic and inducible systems have established many of the cellular and tissue-level consequences. However, these approaches operate at the level of oncogene expression, allowing for cellular adaptation that masks the individual role of KRAS oncoprotein signaling. Here, we developed a reversible Opto-Chemical system to activate KRAS signaling by chemically translocating a cytosolic mutant KRASG12V G-domain to the plasma membrane upon light or small-molecule input. In MDCK cells, the G-domain plasma membrane recruitment activated downstream signaling and reduced collective migration. In mouse small Intestinal Organoids, G-domain recruitment promoted increased crypt size and number under Epidermal Growth Factor-deprived conditions. We further showed that the increased number of crypts depended on continuous KRASG12V signaling. Finally, under the same deprived conditions, localized activation in just one budding crypt promoted crypt formation compared to controls. This system decouples oncoprotein activity from oncogene expression, allowing to investigate the KRAS signaling contribution to early epithelial transformation.

Systems Biology↗

Mammalian aging involves genome-wide splicing degeneration leading to functional decline

Alternative splicing exhibits significant changes during development and aging, affecting the composition and variance in the transcriptome. However, it is unclear whether and how age-associated splicing dysregulation leads to functional consequences. Here, an integrative analysis of transcriptome data across mouse and human tissues revealed that aging is characterized by systematic deterioration of the fidelity of RNA splicing, here termed splicing degeneration, a measure of functional alteration of reading frame and domain configuration of protein products. Genes with higher aging-associated splicing degeneration were more conserved and enriched for processes such as RNA metabolism and antigen presentation. By assessing alternative splicing events associated with functional deterioration, we quantified the degree of splicing degeneration. Its level increased with age but was alleviated following calorie restriction or rapamycin treatment, indicating that it can serve as a new molecular hallmark of aging. Mechanistically, through a comprehensive meta-data analysis, we discovered that splicing degeneration is associated with age-associated changes in specific splicing factors, which in turn showed a strong association with age-related transcriptome changes. Overall, our study demonstrates the intricate relationship between aging and genome-wide splicing degeneration, revealing a promising target for aging interventions acting to reverse splicing degeneration.

Systems Biology↗