Frontiers in systems biology最新文献

{"title":"Biophysics-informed computational framework for predicting antisense oligonucleotide knockdown efficacy under small-data constraints.","authors":"Risha Guha, Shawn Kim, Anwita Bandaru, Nithika Vivek","doi":"10.3389/fsysb.2026.1921636","DOIUrl":"https://doi.org/10.3389/fsysb.2026.1921636","url":null,"abstract":"<p><p>A central strategy in treating neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS), is lowering levels of disease-driving proteins. Antisense oligonucleotides (ASOs) offer a direct RNA-targeted approach to reduce protein expression, but experimental discovery and optimization are constrained by small, heterogeneous datasets and target-specific variability. Computational models that predict ASO knockdown efficacy directly from sequence and context could improve candidate selection, yet generalization across gene families and experimental settings remains challenging. In this study, we present a biophysics-based computational framework for predicting RNase H-active ASO knockdown efficacy under small-data constraints. We curate and integrate heterogeneous literature-derived ASO efficacy measurements into a unified dataset and evaluate model transfer using independently generated experimental ASOs targeting ALS-relevant genes DAZAP1 and FAM69C. Knockdown efficacy is defined at the transcript level (%KD), providing a mechanistic measure of RNase H-mediated activity. To our knowledge, this is the first framework that combines ASO feature engineering with one-shot family calibration for prediction under realistic small-data conditions. We integrate sequence representations with physics-based features capturing RNA-DNA hybridization thermodynamics, targeting RNA accessibility. Compared to sequence-only baselines, this mechanistic feature augmentation reduces external wet-lab prediction error, improving generalization to independent experimental data. Despite these gains, uncalibrated predictions exhibit systematic target-family-specific scale bias. We address this challenge by using a minimal one-shot family calibration strategy that applies an additive offset derived from a single experimentally measured reference ASO per new target family. We further assess the model's behavior using a leave-one-family-out simulation on literature-derived ASO families, repeatedly applying one-shot calibration to quantify its expected benefit and variability under controlled small-n conditions. One-shot calibration markedly improves absolute prediction accuracy while preserving within-family ranking, without retraining or increasing model complexity. Out-of-distribution evaluation shows stable performance for DAZAP1 and increased uncertainty for FAM69C, consistent with the expected effects of very small sample sizes. Permutation-based interpretability analyses show that predictive signal is dominated by global sequence architecture, with thermodynamic and accessibility features providing correlated, secondary contributions. Together, these results establish a computational workflow in which literature-trained models can be transferred to new target genes using minimal experimental input, supporting systematic ASO prioritization in small-data models.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1921636"},"PeriodicalIF":2.6,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13713387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149302693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"One health perspectives on pharmaceutical and clinical effluents driving multidrug resistance in aquatic ecosystems: a comprehensive review.","authors":"Anshnu Tyagi, Minakshi Rajput, Sudhanshu Mishra","doi":"10.3389/fsysb.2026.1890380","DOIUrl":"https://doi.org/10.3389/fsysb.2026.1890380","url":null,"abstract":"<p><p>Antimicrobial resistance (AMR) has emerged as one of the most pressing global health challenges, yet the contribution of environmental reservoirs to the spread of multidrug resistance (MDR) remains insufficiently integrated into mainstream discussions. This systematic review synthesizes evidence from 167 peer-reviewed studies published between 2000 and 2026 to examine how pharmaceutical manufacturing effluents and clinical waste drive the dissemination of antibiotic resistance genes (ARGs) and multidrug-resistant bacteria in aquatic ecosystems. The literature was systematically identified and selected from major scientific databases using predefined inclusion and exclusion criteria. The reviewed evidence consistently shows that aquatic environments receiving inadequately treated pharmaceutical and healthcare waste which creates environmental hotspots characterized by elevated antibiotic residues, mobile genetic elements, and resistant microbial communities. Sub-inhibitory antibiotic concentrations, biofilm-mediated horizontal gene transfer and quorum-sensing dynamics collectively accelerate resistance gene dissemination beyond what direct selective killing alone would predict. Heavy metals, including copper, zinc, mercury, cadmium, and arsenic, further reinforce resistance through co-selection mechanisms, sustaining clinically important determinants such as <i>blaNDM-1</i>, <i>blaKPC</i>, and <i>mcr-1</i> even in environments with limited antibiotic exposure. The review also highlights the role of non-pathogenic environmental bacteria as genetic reservoirs that facilitate the movement of resistance traits into pathogenic microorganisms. Metagenomic evidence confirms bidirectional exchange of resistance determinants between environmental and clinical bacterial populations, firmly situating the environmental resistome within a One Health framework. Despite growing evidence, important knowledge gaps remain regarding environmental-to-clinical transmission pathways, long-term ecological impacts, and the effectiveness of current mitigation strategies under diverse environmental conditions. Future research should prioritize longitudinal surveillance, multi-omics and systems biology approaches, metagenomic resistome profiling, and machine-learning-based predictive frameworks to better understand resistance dynamics across interconnected ecosystems. The findings support the integration of ARG monitoring into environmental management programs and underscore the need for advanced wastewater treatment technologies, harmonized discharge regulations, and coordinated One Health policies to curb the environmental amplification of antimicrobial resistance. These insights also contribute directly to achieving multiple Sustainable Development Goals, particularly SDG 1, 2, 3, 6, 9, 12, and 17 by fostering sustainable and integrated approaches to AMR mitigation.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1890380"},"PeriodicalIF":2.6,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13714260/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149302698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ELM-CLAIM: a claim-calibration framework for adaptive, memory-like, learning-like, and goal-directed claims in engineered living materials.","authors":"Jordi Vallverdú","doi":"10.3389/fsysb.2026.1905585","DOIUrl":"https://doi.org/10.3389/fsysb.2026.1905585","url":null,"abstract":"<p><p>Engineered Living Materials (ELMs) combine living cells with matrices, interfaces, environmental fields, and sometimes electronic or computational controllers. Their multicomponent architecture creates an attribution problem: the same observed output may reflect passive material physics, active cellular regulation, interface or morphological change, environmental gradients, controller adaptation, or coupled-system dynamics. This article proposes ELM-CLAIM (Engineered Living Materials-Controls for Learning, Adaptation, Intelligence, and Memory), an author-proposed claim-calibration and reporting framework for matching adaptive vocabulary to measurable state variables, temporal criteria, attribution targets, and evidence classes. The framework classifies specific behaviors from passive responsiveness (L0) through active responsiveness (L1), adaptation (L2), memory-like behavior (L3), learning-like behavior (L4), and autonomous goal-directedness (L5). It also provides an evidence-tiered claim-to-control matrix, proportional substitution rules for experimentally intractable controls, component- and controller-level attribution logic, model-transparency requirements, and a reviewer-oriented reporting checklist. Essential entries denote evidential functions rather than a single mandatory assay, allowing justified orthogonal controls while requiring claims to be lowered when major alternatives remain unresolved. Published cases are used illustratively to stress-test interpretability rather than to validate the framework statistically. ELM-CLAIM calibrates language; it does not by itself validate an experiment, define cognition, or constitute a community standard. Community testing, inter-reviewer reliability assessment, and prospective experimental use remain necessary next steps.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1905585"},"PeriodicalIF":2.6,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13713307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149302724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Coherence, transformation, and breakdown in living systems: part II - predictions and implications for systemic health.","authors":"Andreas Nicolaides","doi":"10.3389/fsysb.2026.1910994","DOIUrl":"10.3389/fsysb.2026.1910994","url":null,"abstract":"<p><p>Part I of this two-part series advanced the CHORA Hypothesis as a candidate account of biological coherence: how organised biological function is sustained, transformed, and lost within the organism and across the lineage over deep time. The hypothesis holds that a Common Higher-Order Regulatory Architecture (CHORA) operates as an integrated, hierarchically structured level of organisation across cells, tissues, organisms, and generations, sustaining within-organism coherence and evolutionary coherence alike. It holds further that the germline is the principal conduit through which the architecture is propagated, that the same architectural features which sustain biological coherence underlie the characteristic modes of its failure, and that disruption of the architecture at the organism level underlies the convergent signatures of systemic disease. This paper develops the empirical predictions and the systemic health implications that follow. Section 1 sets out six predictions under the commitments from which they follow. The first three follow from the architecture's integrated operation: catastrophic rather than graded failure at architecturally central components; the concentration of lineage transitions at mid-hierarchical regulatory levels; and the bidirectional intergenerational consequences of perturbation at germline-soma coupled components. The fourth derives from germline priority in propagation and concerns intergenerational erosion under partial germline compromise, with somatic analogues at architecturally shared components. The fifth derives from the coherence-breakdown relationship and concerns the entrenchment of pathological regimes through feedback architectures repurposed under displaced upstream conditions. The sixth derives from disruption of the architecture at the organism level and concerns the convergence of systemic pathologies on shared signatures of architectural breakdown. Each prediction is examined against alternative accounts and the postdictive and prospective evidence bearing on it. Several predictions organise existing evidence under a single architectural account; others are mainly prospective. Section 2 draws out the implications for systemic health. Health and entrenched systemic disease are not opposing states but alternative regimes of the same biological-coherence-sustaining architecture. On this account, developmental origins, ageing, and intergenerational transmission are intelligible as expressions of a shared architectural logic. The deeper ontological question of what kind of thing this architecture is, together with the framework's broader conceptual implications, is addressed in a forthcoming publication.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1910994"},"PeriodicalIF":2.6,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13713253/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149290324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phylogenetic tree inference with tropical axial attention.","authors":"Chris Teska, Kurt Pasque, Ruriko Yoshida, Baran Hashemi","doi":"10.3389/fsysb.2026.1886918","DOIUrl":"10.3389/fsysb.2026.1886918","url":null,"abstract":"<p><p>In this work, we introduce a Tropical Axial Attention neural reasoning architecture that replaces vanilla softmax dot-product attention with max-plus operators, inducing a piecewise-linear structure aligned with dynamic programming formulations. From multi-species sequence alignments, our model learns all possible pairwise distances and is trained using a combination of <math> <mrow> <msub><mrow><mi>ℓ</mi></mrow> <mrow><mn>1</mn></mrow> </msub> </mrow> </math> and tropical symmetric distance metric losses with an ultrametric violation penalty. We leverage the well known isomorphic relationship between the space of all phylogenetic trees with <math><mrow><mi>n</mi></mrow> </math> species and tropical Grassmannian to show that tropical attention provides a natural geometric framework for phylogenetic inference. On empirical <math><mrow><mi>D</mi> <mi>S</mi> <mn>1</mn> <mo>-</mo> <mi>D</mi> <mi>S</mi> <mn>11</mn></mrow> </math> alignments, where true trees are unknown, the tropical model achieves the lowest MAE to its FastME-induced tree metric on every dataset, with a MAE reductions averaging 81.5% relative to Phyloformer and 98.4% relative than Phyloformer 2. These results suggest that tropical attention is a useful geometric inductive bias for neural phylogenetic inference, especially under distribution shift and when tree-metric consistency is important.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1886918"},"PeriodicalIF":2.6,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13696944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149278054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bridging communication gaps across the biomedical ecosystem.","authors":"Elizabeth A Burke, Samantha N Schumm, Amy Jobe, Kara Whelply, Ishita Das","doi":"10.3389/fsysb.2026.1939110","DOIUrl":"10.3389/fsysb.2026.1939110","url":null,"abstract":"<p><p>The current landscape of science communication is undergoing rapid transformation, shaped by profound societal shifts including the COVID-19 pandemic, the rise of social media, the decline of traditional news media, and the growing influence of large language models. These changes have fundamentally altered how the biomedical community and the public share, consume, and trust scientific information. This article contextualizes these changes, explains why redesigning the science communication ecosystem is urgent, and offers recommendations to improve accuracy, strengthen trust, and deepen public engagement. Specifically, philanthropy can play a key role by driving momentum and optimizing the flow of scientific information across three stages: (1) scientific discovery to publication, (2) interpretation and distribution, and (3) public engagement.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1939110"},"PeriodicalIF":2.6,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13696191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149278076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Addressing biomedical complexity using the energy systems language.","authors":"Federico Surra, Francesco Gonella, Luigi Conte, Alessandra Romano","doi":"10.3389/fsysb.2026.1903662","DOIUrl":"10.3389/fsysb.2026.1903662","url":null,"abstract":"<p><p>Biological complex systems self-organize and evolve through feedback-driven interactions not adequately captured by linear cause-effect models. To address this gap, we propose a novel approach grounded in Energy Systems Language (ESL). It provides a description of how resource availability, carrying capacity and feedback networks shape the system trajectories. ESL is rooted in open systems Thermodynamics, shifting the focus from the biology of events to their systemic structure. Models are built on biomedical knowledge, with parameters determined by empirical observation and biophysical constraints, producing simulators that address \"what if\" exploratory questions. We applied this approach to the antigen-specific adaptive immune response as a proof-of-concept of the framework designed to investigate system-level dynamic regime stability and qualitative response to external driving forces. We developed a computational simulator reproducing hallmark features of humoral immunity at daily, monthly and decadal time-scales, including germinal-center dynamics, establishment of long-lived plasma cells, antibody secretion, and long-term decline in the absence of antigen re-exposure. Using this approach, future investigations of complex pathologies, e.g., lymphoid malignancies and autoimmune diseases, can be developed, providing computational tools for testing hypotheses on patient-specific therapeutic strategies.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1903662"},"PeriodicalIF":2.6,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13683192/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149240590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"On matrix-analytic Markov modulated models for evolution: application potential and future directions required to advance the field.","authors":"Małgorzata M O'Reilly, Barbara R Holland","doi":"10.3389/fsysb.2026.1906462","DOIUrl":"10.3389/fsysb.2026.1906462","url":null,"abstract":"<p><p>Markov modulated (MM) models in the theory of matrix-analytic methods (MAMs) are a class of probabilistic models whose key feature is an underlying Markov environment that drives the evolution of some complex and unpredictable system. Our goal in this paper is to emphasise their great potential for understanding evolution and the need for close multidisciplinary collaborations between probabilists and evolutionary biologists to advance the field. We give an overview of the fundamental MM models in MAMs, namely quasi-birth-and-death processes (QBDs) and stochastic fluid models (SFMs), in which the fluctuations in the level variable are modulated by fluctuations in the phase variable. We illustrate their application potential in evolution through an example of phylogenetic inference, state a general tree likelihood formula applicable to a wide range of MM models, and discuss future directions required to advance the theory of MM models as well as in the applications of the existing theory to evolutionary contexts.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1906462"},"PeriodicalIF":2.6,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13682963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149240637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Coherence, transformation, and breakdown in living systems: part I - the common higher-order regulatory architecture (CHORA) hypothesis.","authors":"Andreas Nicolaides","doi":"10.3389/fsysb.2026.1910966","DOIUrl":"10.3389/fsysb.2026.1910966","url":null,"abstract":"<p><p>The coherence of living systems extends beyond the lifespan of the individual organism: it persists across biological lineages, through the turnover of organisms and change across deep evolutionary time. This paper terms this phenomenon evolutionary coherence, the lineage-scale expression of a more general property, biological coherence, whose organism-scale expression systems biology has characterised while its evolutionary counterpart has not. Biological coherence is analysed through four aspects - stability, transformation, connectivity, and coordination - each expressed at both the lineage and the organism scale. Their lineage-level manifestations appear in familiar but unreconciled patterns: persistent morphologies, punctuated transformation, structured hybridisation, and the channelled forms evolutionary change repeatedly takes. At the organism scale the same aspects govern the maintenance of organised function and its breakdown, including the convergence of distinct systemic diseases on shared signatures of regulatory dysfunction. Such patterns are not readily accommodated by the foundational ideas of evolutionary biology and biomedicine, which engage auxiliary hypotheses to account for them; some point toward higher-order organisation but stop short of articulating it as primary. Proceeding by abductive inference, the paper specifies the requirements a unifying account must meet, then surveys the molecular evidence and develops a systems model of their operation. The architectures examined are hierarchical gene regulatory networks, bow-tie physiological regulation, germline regulatory systems, the regulation of repetitive DNA, and centromere identity. The framework is articulated as the CHORA Hypothesis: that a Common Higher-Order Regulatory Architecture, common to the organism and the lineage, operates as an integrated level across organisms and generations; that the germline is its principal conduit; that the features sustaining coherence also underlie its failure; and that its disruption at the organism level underlies these convergent signatures of dysfunction. The architecture is not a further agency but the largely conserved higher-order organisation realised by established molecular processes - transposable-element activity foremost among them - and through which coherence is sustained. These processes are its molecular signatures; the architecture's own nature is left open. Health and entrenched disease are, on this account, alternative regimes of the one architecture. Part II develops the discriminating predictions and systemic-health implications.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1910966"},"PeriodicalIF":2.6,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149217522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The archibiome: extending engineered living materials to multiscale built environments.","authors":"A Sandak, W Pajerski, A Gubenšek, K Butina Ogorelec, A Černoša","doi":"10.3389/fsysb.2026.1943876","DOIUrl":"10.3389/fsysb.2026.1943876","url":null,"abstract":"<p><p>The integration of living systems into architecture is advancing rapidly through developments in biotechnology, materials science, and design approaches grounded in regenerative principles. Engineered Living Materials (ELMs) and living artefacts demonstrate how microbial systems can be embedded within materials to enable responsiveness, metabolic activity, and adaptive functionality. However, current applications remain largely confined to discrete material components, overlooking the complex and dynamic microbial ecosystems already present within buildings. This opinion paper introduces the concept of the archibiome as a framework for extending ELMs from isolated systems to interconnected architectural environments. The archibiome conceptualizes buildings as dynamic microbial ecosystems in which engineered systems, material interfaces, and native microbial communities interact across spatial and temporal scales. While this shift offers opportunities for adaptive and regenerative design, it also introduces challenges related to system stability, environmental variability, biosafety, and regulatory constraints. Addressing these challenges requires interdisciplinary approaches that integrate microbial ecology, materials engineering, architectural design, and regulatory science. Ultimately, the archibiome positions microbial life as a design variable, enabling a transition toward predictive, systems-level strategies for living architecture.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1943876"},"PeriodicalIF":2.6,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13654977/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149168158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}