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ACMTF-R: supervised multi-omics data integration uncovering shared and distinct outcome-associated variation

The rapid growth of high-dimensional biological data has necessitated advanced data fusion techniques to integrate and interpret complex multi-omics and longitudinal datasets. Shared and unshared structure across such datasets can be identified in an unsupervised manner with Advanced Coupled Matrix and Tensor Factorization (ACMTF), but this cannot be related to an outcome. Conversely, N-way Partial Least Squares (NPLS) is supervised and captures outcome-associated variation but cannot identify shared and unshared structure. To bridge the gap between data exploration and prediction, we introduce ACMTF-Regression (ACMTF-R), an extension of ACMTF that incorporates a regression step, allowing for the simultaneous decomposition of multi-way data while explicitly capturing variation associated with a dependent variable. We present a detailed mathematical formulation of ACMTF-R, including its optimisation algorithm and implementation. Through extensive simulations, we systematically evaluate its ability to recover a small y-related component shared between multiple blocks, its robustness to noise, and the impact of the tuning parameter ({pi}) which controls the balance between data exploration and outcome prediction. Our results demonstrate that ACMTF-R can robustly identify the y-related component, correctly identifying outcome-associated shared and distinct variation, distinguishing it from existing approaches such as NPLS and ACMTF. The development of ACMTF-R was motivated by a real-world dataset investigating how maternal pre-pregnancy BMI affects the human milk microbiome, human milk metabolome, and infant faecal microbiome. Emerging evidence suggests that inter-generational transfer of maternal obesity may affect multiple omics layers, highlighting the need to identify outcome-associated variation. The applicability of ACMTF-R is therefore validated by applying it to this multi-omics dataset. ACMTF-R successfully identifies novel mother-infant relationships associated with maternal pre-pregnancy BMI, underscoring its utility in multi-omics research. Our findings establish ACMTF-R as a versatile tool for multi-way data fusion, offering new insights into complex biological systems by integrating common, local, and distinct variation in the context of a dependent variable. Author SummaryIn recent years, biological research has been transformed by the rise of high-throughput technologies, allowing us to simultaneously measure multiple different data (genes, microbes, and metabolites) within the same subject. While these datasets hold great promise, analysing them in an integrated way remains challenging. Existing tools either focus on uncovering patterns in the data or on predicting outcomes, but rarely both. In this study, we present a new method called ACMTF-Regression (ACMTF-R), which combines these aspects. ACMTF-R helps researchers identify shared and distinct biological patterns across different datasets while also relating these patterns to specific outcomes. Using simulated data, we show that ACMTF-R can detect subtle signals that would otherwise go unnoticed. We also apply it to a real-world study of mothers and their infants, revealing how maternal obesity influences breast milk and gut microbes in the baby. Our approach provides a powerful new tool for studying complex biological systems and can be especially valuable in fields like microbiome research, metabolomics, and personalized medicine.

systems biology↗

An AI-Cyborg System for Adaptive Intelligent Modulation of Organoid Maturation

Recent advancements in flexible bioelectronics have enabled continuous, long-term stable interrogation and intervention of biological systems. However, effectively utilizing the interrogated data to modulate biological systems to achieve specific biomedical and biological goals remains a challenge. In this study, we introduce an AI-driven bioelectronics system that integrates tissue-like, flexible bioelectronics with cyber learning algorithms to create a long-term, real-time bidirectional bioelectronic interface with optimized adaptive intelligent modulation (BIO-AIM). When integrated with biological systems as an AI-cyborg system, BIO-AIM continuously adapts and optimizes stimulation parameters based on stable cell state mapping, allowing for real-time, closed-loop feedback through tissue-embedded flexible electrode arrays. Applied to human pluripotent stem cell-derived cardiac organoids, BIO-AIM identifies optimized stimulation conditions that accelerate functional maturation. The effectiveness of this approach is validated through enhanced extracellular spike waveforms, increased conduction velocity, and improved sarcomere organization, outperforming both fixed and no stimulation conditions.

bioengineering↗

Multidimensional Boolean Patterns in Multi-omics Data

MotivationVirtually all biological systems are governed by a set of complex relations between their components. Identification of relations within biological systems involves a rigorous search for patterns among variables/parameters. Two-dimensional (involving two variables) patterns are identified using correlation, covariation, and mutual information approaches. However, these approaches are not suited to identify more complicated multidimensional relations, which simultaneously include 3, 4, and more variables. ResultsWe present a novel pattern-specific method to quantify the strength and estimate the statistical significance of multidimensional Boolean patterns in multiomics data. In contrast with dimensionality reduction and AI solutions, patterns identified by the proposed approach may provide a better background for meaningful mechanistic interpretation of the biological processes. Our preliminary analysis suggests that multidimensional patterns may dominate the landscape of multi-omics data, which is not surprising because complex interactions between components of biological systems are unlikely to be reduced to simple pairwise interactions.

bioinformatics↗

The Effects of Nonlinear Signal on Expression-Based Prediction Performance

Those building predictive models from transcriptomic data are faced with two conflicting perspectives. The first, based on the inherent high dimensionality of biological systems, supposes that complex non-linear models such as neural networks will better match complex biological systems. The second, imagining that complex systems will still be well predicted by simple dividing lines prefers linear models that are easier to interpret. We compare multi-layer neural networks and logistic regression across multiple prediction tasks on GTEx and Recount3 datasets and find evidence in favor of both possibilities. We verified the presence of non-linear signal for transcriptomic prediction tasks by removing the predictive linear signal with Limma, and showed the removal ablated the performance of linear methods but not non-linear ones. However, we also found that the presence of non-linear signal was not necessarily sufficient for neural networks to outperform logistic regression. Our results demonstrate that while multi-layer neural networks may be useful for making predictions from gene expression data, including a linear baseline model is critical because while biological systems are highdimensional, effective dividing lines for predictive models may not be.

bioinformatics↗

Analysis of Metabolic Network Disruption in Engineered Microbial Hosts due to Enzyme Promiscuity

BackgroundIncreasing understanding of metabolic and regulatory networks underlying microbial physiology has enabled creation of progressively more complex synthetic biological systems for biochemical, biomedical, agricultural, and environmental applications. However, despite best efforts, confounding phenotypes still emerge from unforeseen interplay between biological parts, and the design of robust and modular biological systems remains elusive. Such interactions are difficult to predict when designing synthetic systems and may manifest during experimental testing as inefficiencies that need to be overcome. Despite advances in tools and methodologies for strain engineering, there remains a lack of tools that can systematically identify incompatibilities between the native metabolism of the host and its engineered modifications. ResultsTransforming organisms such as Escherichia coli into microbial factories is achieved via a number of engineering strategies, used individually or in combination, with the goal of maximizing the production of chosen target compounds. One technique relies on suppressing or overexpressing selected genes; another involves on introducing heterologous enzymes into a microbial host. These modifications steer mass flux towards the set of desired metabolites but may create unexpected interactions. In this work, we develop a computational method, termed Metabolic Disruption Workflow (MDFlow), for discovering interactions and network disruption arising from enzyme promiscuity - the ability of enzymes to act on a wide range of molecules that are structurally similar to their native substrates. We apply MDFlow to two experimentally verified cases where strains with essential genes knocked out are rescued by interactions resulting from overexpression of one or more other genes. We then apply MDFlow to predict and evaluate a number of putative promiscuous reactions that can interfere with two heterologous pathways designed for 3-hydroxypropic acid (3-HP) production. ConclusionsUsing MDFlow, we can identify putative enzyme promiscuity and the subsequent formation of unintended and undesirable byproducts that are not only disruptive to the host metabolism but also to the intended end-objective of high biosynthetic productivity and yield. In addition, we show how enzyme promiscuity can potentially be responsible for the adaptability of cells to the disruption of essential pathways in terms of biomass growth.

systems biology↗

Exploring and explaining properties of motion processing in biological brains using a neural network

Visual motion perception underpins behaviours ranging from navigation to depth perception and grasping. Our limited access to biological systems constrain our understanding of how motion is processed within the brain. Here we explore properties of motion perception in biological systems by training a neural network ( MotionNetxy) to estimate the velocity image sequences. The network recapitulates key characteristics of motion processing in biological brains, and we use our complete access to its structure explore and understand motion (mis)perception at the computational-, neural-, and perceptual-levels. First, we find that the network recapitulates the biological response to reverse-phi motion in terms of direction. We further find that it overestimates the speed of slow reverse-phi motion while underestimating the speed of fast reverse-phi motion because of the correlation between reverse-phi motion and the spatiotemporal receptive fields tuned to motion in opposite directions. Second, we find that the distribution of spatiotemporal tuning properties in the V1 and MT layers of the network are similar to those observed in biological systems. We then show that compared to MT units tuned to fast speeds, those tuned to slow speeds primarily receive input from V1 units tuned to high spatial frequency and low temporal frequency. Third, we find that there is a positive correlation between the pattern-motion and speed selectivity of MT units. Finally, we show that the network captures human underestimation of low coherence motion stimuli, and that this is due to pooling of noise and signal motion. These findings provide biologically plausible explanations for well-known phenomena, and produce concrete predictions for future psychophysical and neurophysiological experiments.

neuroscience↗

BIOFORMERS: A SCALABLE FRAMEWORK FOR EXPLORING BIOSTATES USING TRANSFORMERS

AO_SCPLOWBSTRACTC_SCPLOWGenerative pre-trained models, such as BERT and GPT, have demonstrated remarkable success in natural language processing and computer vision. Leveraging the combination of large-scale, diverse datasets, transformers, and unsupervised learning, these models have emerged as a promising method for understanding complex systems like language. Despite the apparent differences, human language and biological systems share numerous parallels. Biology, like language, is a dynamic, interconnected network where biomolecules interact to create living entities akin to words forming coherent narratives. Inspired by this analogy, we explored the potential of using transformer-based unsupervised model development for analyzing biological systems and proposed a framework that can ingest vast amounts of biological data to create a foundational model of biology using BERT or GPT. This framework focuses on the concept of a biostate, defined as a high-dimensional vector encompassing various biological markers such as genomic, proteomic, transcriptomic, physiological, and phenotypical data. We applied this technique to a small dataset of single-cell transcriptomics to demonstrate its ability to capture meaningful biological insights into genes and cells, even without any pre-training. Furthermore, the model can be readily used for gene network inference and genetic perturbation prediction.

bioinformatics↗

MiBiOmics: An interactive web application for multi-omics data exploration and integration

BackgroundMulti-omics experimental approaches are becoming common practice in biological and medical sciences underlying the need to design new integrative techniques and applications to enable the holistic characterization of biological systems. The integrative analysis of heterogeneous datasets generally allows us to acquire additional insights and generate novel hypotheses about a given biological system. However, it can often become challenging given the large size of omics datasets and the diversity of existing techniques. Moreover, visualization tools for interpretation are usually non-accessible to biologists without programming skills. ResultsHere, we present MiBiOmics, a web-based and standalone application that facilitates multi-omics data visualization, exploration, integration, and analysis by providing easy access to dedicated and interactive protocols. It implements advanced ordination techniques and the inference of omics-based (multi-layer) networks to mine complex biological systems, and identify robust biomarkers linked to specific contextual parameters or biological states. ConclusionsThrough an intuitive and interactive interface, MiBiOmics provides easy-access to ordination techniques and to a network-based approach for integrative multi-omics analyses. MiBiOmics is currently available as a Shiny app at https://shiny-bird.univ-nantes.fr/app/Mibiomics and as a standalone application at https://gitlab.univ-nantes.fr/combi-ls2n/mibiomics.

bioinformatics↗

Novel Plasmodium falciparum metabolic network reconstruction identifies shifts associated with clinical antimalarial resistance

BACKGROUNDMalaria remains a major public health burden and resistance has emerged to every antimalarial on the market, including the frontline drug artemisinin. Our limited understanding of Plasmodium biology hinders the elucidation of resistance mechanisms. In this regard, systems biology approaches can facilitate the integration of existing experimental knowledge and further understanding of these mechanisms.\n\nRESULTSHere, we developed a novel genome-scale metabolic network reconstruction, iPfal17, of the asexual blood-stage P. falciparum parasite to expand our understanding of metabolic changes that support resistance. We identified 11 metabolic tasks to evaluate iPfal17 performance. Flux balance analysis and simulation of gene knockouts and enzyme inhibition predict candidate drug targets unique to resistant parasites. Moreover, integration of clinical parasite transcriptomes into the iPfal17 reconstruction reveals patterns associated with antimalarial resistance. These results predict that artemisinin sensitive and resistant parasites differentially utilize scavenging and biosynthetic pathways for multiple essential metabolites including folate and polyamines, and others within the mitochondria. Our findings are consistent with experimental literature, while generating novel hypotheses about artemisinin resistance and parasite biology. We detect evidence that resistance parasites maintain greater metabolic flexibility, perhaps representing an incomplete transition to the metabolic state most appropriate for nutrient-rich blood.\n\nCONCLUSIONUsing this systems biology approach, we identify metabolic shifts that arise with or in support of the resistant phenotype. This perspective allows us to more productively analyze and interpret clinical expression data for the identification of candidate drug targets for the treatment of resistant parasites.

systems biology↗

Intelligent Tool Orchestration for Rapid Mechanistic Model Prototyping: MCP Servers as AI-Biology Interfaces

The construction of multicellular mechanistic models in systems biology typically requires months of literature research, programming expertise, and deep knowledge of specialized computational tools. Here we present intelligent tool orchestration through Model Context Protocol (MCP) servers that enable Large Language Models (LLMs) agents to function as AI laboratory assistants for rapid model prototyping. We demonstrate this approach by constructing a multiscale model of cancer cell fate in response to TNF, entirely through natural language interactions, using an AI agent connected to MCP servers that interface with three complementary modeling software: NeKo for constructing gene regulatory networks from prior-knowledge databases, MaBoSS for simulating and analyzing Boolean models, and PhysiCell for setting up multicellular agent-based models. Our architecture encompasses more than 60 specialized tools, covering the entire workflow from data collection to multicellular simulation setup. From this use case we derived three key design principles for biological AI-tool integration: first, optimal tool granularity is best defined at biological decision points, where domain knowledge guides modeling choices; second, comprehensive session management is essential for tracking complex workflows and ensuring reproducibility across long interactions; and third, effective orchestration must be established from the start to let LLMs combine tools flexibly while maintaining biological coherence. In applying this framework across three different LLMs and scenarios, we observed consistent end-to-end orchestration as well as model-dependent differences in network size, dynamical behaviors, and integration details. This variability highlights both the portability of our approach and the importance of careful reporting and validation when deploying different LLMs in scientific contexts. While the resulting models require refinement, this work establishes the foundation for AI-assisted rapid prototyping in systems biology, enabling researchers to explore computational hypotheses at unprecedented speed while maintaining biological fidelity.

bioinformatics↗

Metatranscriptomics-based metabolic modeling of patient-specific urinary microbiome during infection

Urinary tract infections (UTIs) are a major health concern which incur significant socioeconomic costs in addition to substantial antibiotic prescriptions, thereby accelerating the emergence of antibiotic resistance. To address the challenge of antibiotic-resistant UTIs, our systems biology approach uncovers patient-specific uromicrobiome insights that are focused on community utilization of metabolites. By leveraging the distinct metabolic traits of patient-specific pathogens, we aim to identify metabolic dependencies of pathogens and provide suggestions for targeted interventions for future studies. Combining patient-specific metatranscriptomic data with genome-scale metabolic modeling and data from the Human Urine Metabolome, this study explores UTIs from a systems biology perspective through the reconstruction of tailored microbial community models to mirror the metabolic profiles of individual UTI patients urinary microbiomes. Delving into patient-specific bacterial gene expressions and microbial interactions, we identify metabolic signatures and propose mechanisms for UTI pathology. Our research underscores the potential of integrating metatranscriptomic data using systems biological approaches, providing insights into disease metabolic mechanisms and potential phenotypic manifestations. This contribution introduces a new method that could guide treatment options for antibiotic-resistant UTIs, aiming to lessen antibiotic use by combining the pathogens unique metabolic traits. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=113 SRC="FIGDIR/small/586446v2_ufig1.gif" ALT="Figure 1"> View larger version (30K): org.highwire.dtl.DTLVardef@1074251org.highwire.dtl.DTLVardef@192d45eorg.highwire.dtl.DTLVardef@b46927org.highwire.dtl.DTLVardef@638e2a_HPS_FORMAT_FIGEXP M_FIG Graphical Abstract Metatranscriptome sequencing was used to investigate the functional uromicrobiome across a cohort of 19 individuals; patient-specific microbiome community models were reconstructed and simulated in a virtual urine environment. Total RNA was extracted from patients urine and sequenced to assess the metatranscriptome, providing insights into patient-specific uromicrobiome microbial taxa and their associated gene expression during urinary tract infections (UTIs). These combinatory datasets derived from metatranscriptomics data were further expanded first to reconstruct species specific metabolic models that were conditioned with gene expression. Gene expression conditioned metabolic models were combined in an in silico environment with a defined urine media to construct patient-specific context-specific uromicrobiome models, enabling an understanding of each patients unique microbiome. Using this approach, we aimed to identify patient-specific microbiome dynamics and provide insight towards various metabolic features that can be utilized or validated in future studies for individualized intervention strategies. Created with www.biorender.com. C_FIG

systems biology↗

Representation and quantification Of Module Activity from omics data with rROMA

The efficiency of analyzing high-throughput data in systems biology has been demonstrated in numerous studies, where molecular data, such as transcriptomics and proteomics, offers great opportunities for understanding the complexity of biological processes. One important aspect of data analysis in systems biology is the shift from a reductionist approach that focuses on individual components to a more integrative perspective that considers the system as a whole, where the emphasis shifted from differential expression of individual genes to determining the activity of gene sets. Here, we present the rROMA software package for fast and accurate computation of the activity of gene sets with coordinated expression. The rROMA package incorporates significant improvements in the calculation algorithm, along with the implementation of several functions for statistical analysis and visualizing results. These additions greatly expand the packages capabilities and offer valuable tools for data analysis and interpretation. It is an open-source package available on github at: www.github.com/sysbio-curie/rROMA. Based on publicly available transcriptomic datasets, we applied rROMA to cystic fibrosis, highlighting biological mechanisms potentially involved in the establishment and progression of the disease and the associated genes. Results indicate that rROMA can detect disease-related active signaling pathways using transcriptomic and proteomic data. The results notably identified a significant mechanism relevant to cystic fibrosis, raised awareness of a possible bias related to cell culture, and uncovered an intriguing gene that warrants further investigation. Contact: loredana.martignetti@curie.fr

systems biology↗

Energy-based Modelling of Single Actin Filament Polymerisation Using Bond Graphs

Bond graphs provide an energy-based methodology for modelling complex systems in a hierarchical fashion; at the moment, the method allows biological system with both chemical and electrical subsystems to be modelled. Herein, the bond graph approach is extended to include chemomechanical transduction thus extending the range of biological systems to be modelled. Actin filament polymerisation and force generation is used as an example of chemo-mechanical transduction and it is shown that the TF (transformer) bond graph component provides a practical, and conceptually simple, alternative to the Brownian ratchet approach of Peskin, Odell, Oster & Mogilner. Furthermore it is shown that the bond graph approach leads to the same equation as the Brownian ratchet approach in the simplest case. The approach is illustrated by showing that flexibility and non-normal incidence can be modelled by simply adding additional bond graph components and that compliance leads to non-convexity of the force-velocity curve. Energy flows are fundamental to life; for this reason, the energy based approach is utilised to investigate the power transmission by the actin filament and its corresponding efficiency. The bond graph model is fitted to experimental data by adjusting model physical parameters.

systems biology↗

Multidimensional single-cell benchmarking of inducible promoters for precise dynamic control in budding yeast

For quantitative systems biology, simultaneous readout of multiple cellular processes as well as precise, independent control over different genes activities are essential. In contrast to readout systems such as fluorescent proteins, control systems such as inducible transcription-factor-promoter systems have only been characterized in an ad hoc fashion, impeding precise system-level manipulations of biological systems and reliable modeling. We designed and performed systematic benchmarks involving easy-to-communicate units to characterize and compare inducible transcriptional systems. We built a comprehensive single-copy library of inducible systems controlling standardized fluorescent protein expression in budding yeast, including GAL1pr, GALL, MET3pr, CUP1pr, PHO5pr, tetOpr, terminator-tetOpr, Z3EV system, the blue-light optogenetic systems El222-LIP, El222-GLIP and the red-light inducible PhyB-PIF3 system. To analyze these systems dynamic properties, we performed high-throughput time-lapse microscopy. The analysis of >100 000 cell images was made possible by the recently developed convolutional neural network YeaZ. We report key kinetic parameters, scaling of noise levels, impacts on growth, and, crucially, the fundamental leakiness of each system. Our multidimensional benchmarking additionally uncovers unexpected disadvantages of widely used tools, e.g., nonmonotonic activity of the MET3 and GALL promoters, slow off kinetics of the doxycycline and estradiol-inducible systems tetOpr and Z3EV, and high variability of PHO5pr and red-light activated PhyB-PIF3 system. We introduce two new tools for controlling gene expression: strongLOV, a more light-sensitive El222 mutant, and ARG3pr that functions as an OR gate induced by the lack of arginine or presence of methionine. To demonstrate the ability to finely control genetic circuits, we experimentally tuned the time between cell cycle Start and mitotic entry in budding yeast, artificially simulating near-wild-type timing. The characterizations presented here define the compromises that need to be made for quantitative experiments in systems and synthetic biology. To calibrate perturbations across laboratories and to allow new inducible systems to be benchmarked, we deposited single-copy reporter yeast strains, plasmids, and computer analysis code in public repositories. Furthermore, this resource can be accessed and expanded through the website https://promoter-benchmark.epfl.ch/.

synthetic biology↗

Dynamic compensation, parameter identifiability, and equivariances

A recent paper by Karin, Swisa, Glaser, Dor, and Alon introduced the mathematical notion of dynamical compensation (DC) in biological circuits, arguing that DC helps explain important features of glucose homeostasis as well as other key physiological regulatory mechanisms. The present paper establishes a connection between DC and two well-known notions in systems biology: system equivalence and parameter (un)identifiability. This recasting leads to effective tests for verifying DC in mathematical models.

systems biology↗

Conclusions about Neural Network to Brain Alignment are Profoundly Impacted by the Similarity Measure

Deep neural networks are widely used to model biological perception and behavior, making the similarities and differences between artificial and biological systems consequential. If a principle (e.g. self-supervised learning) produces a model resembling biology, this is taken as evidence the same principle shapes the biological system. But what it means for an artificial system to be similar to a biological one is complex. A popular approach compares representations of identical stimuli using a similarity measure like Representational Similarity Analysis. Yet scientific questions rarely specify which measure is appropriate, raising a key question: do conclusions depend on this choice? Focusing on vision, we show that measure choice influences both hierarchical correspondence between systems and the ranking of which artificial systems are most biological. Reanalyzing prior studies, we find the choice hugely consequential: models best under one measure are often worst under another, and prior conclusions can flip or dissolve. Different metrics capture fundamentally different aspects of similarity, warranting healthy skepticism toward such comparisons.

neuroscience↗

Quasineutral dynamics shape coexistence and clearance in a model ofin vitro phage-bacteria interactions

Phage therapy, which uses viruses that infect bacteria to target and lyse specific bacterial pathogens, has re-emerged as a promising strategy to combat antibiotic-multiresistant bacteria. Advances in metagenomics and synthetic biology, together with systems biology approaches combining mathematical modeling with experimental data, provide excellent opportunities to understand phage-bacteria dynamics. Here we analyze a mathematical model successfully calibrated using in vitro data on the multidrug-resistant bacterium Klebsiella pneumoniae in the presence of the phage vB Kpn 2-P4. The model describes a system with a susceptible bacterial population that can generate phage-resistant mutants. By analyzing the equilibria and bifurcations of the model, we identify a coexistence scenario between phage-resistant bacteria and phages governed by a quasineutral line of equilibria with both stable and unstable segments. Biologically, this quasineutral structure implies that phage-resistant bacteria can persist across a wide range of phage densities without selective pressure favoring a unique outcome, making clearance highly sensitive to additional mortality mechanisms. The clearance of phage-resistant bacteria can be achieved by combining phage activity with an increased death rate of the resistant strains. This process is governed by a global transcritical bifurcation of the quasineutral line. Our model offers mechanistic insight into potential scenarios leading to the complete elimination of phage-resistant bacteria. Author summaryBacteriophages--viruses that infect bacteria--are being reconsidered as alternatives to antibiotics, but bacterial resistance to phages often emerges rapidly. Understanding when phages and bacteria coexist and when resistant bacteria can be eliminated remains a major challenge. In this study, we analyze a mathematical model calibrated with in vitro data describing interactions between bacteria, bacteriophages, and phage-resistant mutants. Using tools from dynamical systems theory, we show that coexistence between phages and resistant bacteria is organized by a quasineutral line of equilibrium states rather than a single stable outcome. This structure explains why long-term dynamics can be highly sensitive to initial conditions without being chaotic. We further identify a bifurcation that leads to the extinction of resistant bacteria when their effective mortality exceeds a critical threshold. Our results provide a mechanistic framework for interpreting resistance-driven outcomes in phage-bacteria systems and highlight how mathematical structure can constrain therapeutic strategies, even in simple experimental settings.

systems biology↗

Force sensing on cells and tissues by atomic force microscopy

Biosensors are aimed to detect tiny physical and chemical stimuli in biological systems. Physical forces are ubiquitous, being implied in all cellular processes, including cell adhesion, migration, and differentiation. Given the strong interplay between cells and their microenvironment, the extracellular matrix (ECM), the structural and mechanical properties of the ECM play an important role in the transmission of external stimuli to single cells within the tissue. Vice versa, also cells themselves use self-generated forces to probe the biophysical properties of the ECM. ECM mechanics influences cell fate, regulates tissue development and show peculiar features in health and disease conditions of living organisms. Force sensing in biological systems is therefore crucial to dissect and understand complex biological processes, such as mechanotransduction. Atomic Force Microscopy (AFM), which can both sense and apply forces at the nanoscale, with sub-nanoNewton sensitivity, represents an enabling technology and a crucial experimental tool in biophysics and mechanobiology. In this work, we report on the application of AFM to study of biomechanical fingerprints of different components of biological systems, such as the ECM, the whole cell, and cellular components, like the nucleus and the glycocalyx. We show that physical observables like the (spatially resolved) Youngs modulus of elasticity of ECMs or cells, and the effective thickness and stiffness of the glycocalyx, can be quantitatively characterised by AFM. Their modification can be correlated to changes of the microenvironment, physio-pathological conditions, or gene regulation.

biophysics↗