Biology Direct最新文献

{"title":"Redox imbalance in urology: mechanistic insights into the development and progression of selected urological conditions.","authors":"Nadine Gelbrich, Matthias B Stope","doi":"10.1186/s13062-026-00885-2","DOIUrl":"10.1186/s13062-026-00885-2","url":null,"abstract":"<p><p>Reactive oxygen species (ROS) are key mediators of cellular signalling and play a vital role in regulating both physiological and pathological processes. In urologically relevant tissues, particularly the prostate, bladder and kidneys, redox processes influence vascular function, immune responses, cell proliferation, metabolic adaptations and programmed cell death. A disruption of redox homeostasis contributes significantly to the development and progression of urological diseases, including prostate cancer, urothelial carcinoma of the bladder and renal cell carcinoma. This review article examines the mechanisms underlying the transition from physiological redox regulation to pathological dysregulation, as well as their significance for tumourigenesis, the tumour microenvironment, therapeutic resistance and disease progression. Finally, diagnostic and therapeutic perspectives of redox-based strategies, including innovative approaches such as medical gas plasma, are discussed.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"21 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13670583/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Post-translational modifications in Neuroimmune cells during neuroinflammation: integrated regulatory networks and therapeutic opportunities.","authors":"Wei Li, Yaqi Liu, Haoling Zhang, Haolong Zhang, Wenwen Shao, Ting Hu, Yan Liao, Wangzheqi Zhang, Xiaohong Kang","doi":"10.1186/s13062-026-00974-2","DOIUrl":"10.1186/s13062-026-00974-2","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Neuroinflammation represents a common pathological mechanism underlying a wide range of central nervous system (CNS) disorders, encompassing neurodegenerative disorders (NDDs), ischemic stroke (IS), traumatic brain injury (TBI), and demyelinating diseases such as multiple sclerosis (MS). This process is initiated by the orchestrated responses of microglia, astrocytes, oligodendrocyte-lineage cells, neurons, brain endothelial cells, and infiltrating peripheral immune cells. Neuroinflammation can facilitate tissue repair or, conversely, perpetuate chronic inflammation and neural damage. Post-translational modifications (PTMs) serve as critical mediators linking extracellular danger signals and intracellular metabolic conditions to alterations in protein activity, stability, localization, interactions, and degradation. Notably, the biological impact of a PTM cannot be solely deduced from its classification; rather, it is contingent upon factors such as the specific enzyme responsible for its addition or removal, the identity of the substrate, the modified residue or ubiquitin-chain architecture, the subcellular localization, the cellular context, and the stage of the disease. In this review, we synthesize evidence on various PTMs such as phosphorylation, ubiquitination, SUMOylation, acetylation, methylation, glycosylation, S-nitrosylation (SNO), and metabolite-coupled modifications, including lactylation and succinylation. We analyze their convergent and divergent roles across different neuroimmune cell types, disease-related stimuli, and temporal contexts, and investigate the mechanisms by which intercellular communication propagates PTM-dependent inflammatory signals. Special emphasis is placed on the ordered and competitive crosstalk among PTMs that modulate nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), NOD-like receptor protein 3 (NLRP3) inflammasome, and JAK-STAT signaling pathways, as well as the integrity of the blood-brain barrier (BBB), oligodendrocyte differentiation, and remyelination processes. Additionally, we assess PTM-regulating enzymes as potential therapeutic targets, while highlighting current limitations such as uneven cell-specific evidence, extrapolation from non-neural systems, low modification stoichiometry, rapid turnover, tissue-processing artifacts, and the insufficiency of transcriptomic data alone to demonstrate site-specific protein modifications. The integration of single-cell and spatial multi-omics with PTM-enrichment proteomics, quantitative site-occupancy assessments, and orthogonal mechanistic validation is anticipated to facilitate the generation of PTM maps that are resolved at the cellular, site-specific, and developmental stage levels. This evidence-based framework has the potential to enhance biomarker-guided disease stratification and inform the development of more selective, brain-targeted therapeutic interventions for neuroinflammatory disorders. CLINICAL TRIAL NUMBER: Not a","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"21 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13563871/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148954987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated analysis of single-cell transcriptome identifies a glial-neurovascular signaling trajectory in brain repair after ischemia.","authors":"Hanyou Liu, Zhenwei Li, Ruxu Geng, Lingui Gu, Xinjie Bao","doi":"10.1186/s13062-026-00912-2","DOIUrl":"10.1186/s13062-026-00912-2","url":null,"abstract":"<p><strong>Background: </strong>Ischemic stroke triggers complex multicellular responses across neurons, glia, and the neurovascular unit, but the temporal coordination among these cell types remains incompletely understood. In this study, we integrated five publicly available mouse single-cell RNA sequencing datasets spanning the acute, subacute, and recovery phases after middle cerebral artery occlusion (MCAO), together with complementary rat single-nucleus RNA-seq data, to establish a time-resolved transcriptomic framework of post-ischemic brain repair.</p><p><strong>Results: </strong>Integrative single-cell analysis identified candidate multicellular communication patterns linking microglia, astrocytes, oligodendrocyte lineage cells, endothelial cells, and neurons during post-ischemic remodeling. Microglia exhibited an early transition from inflammatory activation toward lipid metabolic and neuroprotective programs. Astrocytes shifted from injury-associated reactive states to reparative phenotypes and emerged as central coordinators of intercellular communication. Oligodendrocyte progenitor cells activated maturation programs associated with remyelination, while the neurovascular unit underwent coordinated remodeling characterized by dynamic signaling interactions among astrocytes, microglia, endothelial cells, and neurons. Selected glial and neurovascular signaling patterns were also detectable in the complementary rat snRNA-seq data.</p><p><strong>Conclusions: </strong>Our analysis suggests that post-ischemic brain repair involves time-associated multicellular programs integrating inflammation resolution, astrocyte-mediated repair, oligodendrocyte maturation, and neurovascular remodeling. These findings provide a hypothesis-generating transcriptomic framework for understanding stage-associated brain repair after ischemic stroke and may inform the development of time-aware therapeutic strategies targeting cell-state transitions and intercellular communication.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"21 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13548491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148905016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: The B7 family subgroup reflects tumor cell heterogeneity and patient post-operative prognosis in gallbladder cancer.","authors":"Chuhan Ma, Huixin Hu, Yang Li, Chongli Zhong, YunHao Dong, Zhanhao Chang, Shuo Xu, Yuyang Zhang, Hangqi Hu, Chao Lv, Yu Tian","doi":"10.1186/s13062-026-00925-x","DOIUrl":"10.1186/s13062-026-00925-x","url":null,"abstract":"","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"21 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heart failure may promote breast cancer progression through a Col10a1-associated Tgf-β/Smad-EMT pathway.","authors":"Danfeng Zhang, Man Wang, LiHua Wu, Bo Gao, Yongbiao Ai, Ziyang Wang, Ming Xu, Fengmei Yang","doi":"10.1186/s13062-026-00964-4","DOIUrl":"10.1186/s13062-026-00964-4","url":null,"abstract":"<p><strong>Background: </strong>Heart failure (HF) is clinically associated with aggravated breast cancer (BC) progression; however, the integrative genomic mechanisms underlying this cardio-oncological crosstalk remain poorly understood.</p><p><strong>Methods: </strong>We conducted integrative bioinformatics analyses combining weighted gene co-expression network analysis (WGCNA) and machine learning algorithms to screen key hub genes involved in HF and BC progression. The candidate gene Col10a1 was further validated using myocardial infarction (MI)-induced HF xenograft mouse models, paired clinical plasma and tumor specimens, and comprehensive in vitro functional assays.</p><p><strong>Results: </strong>COL10A1 expression was higher in breast cancer patients with CVD than in BC-only patients. Given the limited sample size, these findings were considered exploratory. Mechanistically, elevated Col10a1 was associated with activation of the transforming growth factor‑β (Tgf-β)/Smad signaling pathway and induction of epithelial-mesenchymal transition (EMT). In vivo, the HF microenvironment markedly accelerated BC tumor growth and was accompanied by enhanced Col10a1 expression and Tgf-β signaling activation. In vitro, cardiomyocyte-derived Col10a1 significantly promoted the proliferation, migration, and invasion of BC cells, whereas Col10a1 knockdown significantly attenuated these malignant phenotypes.</p><p><strong>Conclusions: </strong>Our study identifies a potential regulatory link between HF and BC and provides preliminary mechanistic insights into the role of Col10a1 in BC progression under cardiac injury conditions. Col10a1 may serve as a candidate mediator in the interaction between cardiac injury and BC progression.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"21 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13621664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149073647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of satellite DNAs in repeatome organization and sex chromosome evolution in the owl monkey Aotus infulatus and congeneric species.","authors":"Gustavo Akira Toma, Edivaldo Herculano Corrêa de Oliveira, Klebson Demelas Maurício, Liliane Almeida Carneiro, Thomas Liehr, Marcelo de Bello Cioffi","doi":"10.1186/s13062-026-00948-4","DOIUrl":"10.1186/s13062-026-00948-4","url":null,"abstract":"<p><strong>Background: </strong>Multiple sex chromosome systems provide exceptional models for investigating the genomic mechanisms underlying sex chromosome evolution. In Neotropical primates, owl monkeys (Aotus) are notable for their extensive karyotypic diversity and recurrent emergence of complex sex chromosome systems. Here, we present a comprehensive cytogenomic analysis of the repeatome of Aotus infulatus, a species exhibiting an X₁ × ₂Y sex chromosome system. Using low-coverage whole-genome sequencing from males and females, combined with comparative analyses of three congeneric species (A. nancymaae, A. vociferans, and A. trivirgatus), we characterized the composition, abundance, and evolutionary dynamics of their repeatomes across the genus.</p><p><strong>Results: </strong>Repetitive sequences account for approximately 37% of the A. infulatus genome, with satellite DNAs (satDNAs) representing the most variable component among species. Nine satDNA families were identified in A. infulatus, most of which show high sequence conservation across Aotus, consistent with a shared ancestral repeat library followed by lineage-specific amplification. Comparative analyses between sexes revealed a modest enrichment of satDNAs in the male genome. Fluorescence in situ hybridization uncovered differential chromosomal distributions of several satellites, including sex-biased accumulation on the X₁ and Y chromosomes. In contrast, comparative genomic hybridization revealed extensive sharing of repetitive sequences between sexes, indicating limited genomic divergence between the X₁ and Y chromosomes.</p><p><strong>Conclusions: </strong>Our results demonstrate that repetitive DNA, particularly satDNAs, has played a central role in reshaping the sex chromosome architecture of A. infulatus. This study establishes Aotus as a compelling primate model for investigating the genomic consequences of sex chromosome fusion and highlights the importance of repeatome dynamics in the evolution of multiple sex chromosome systems.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"21 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13520323/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CUDC-907 attenuates pulmonary fibrosis by reversing HDAC1-mediated SMAD4 deacetylation at lysine 45.","authors":"Yu Li, Yuan Cui, Haoyu Qiu, Kai Fu, Chenye Shao, Zhike Chen, Jian Yang, Jiawei Chen, Xin Lv, Xiumin Zhou, Xin Tong, Chang Li, Jun Zhao","doi":"10.1186/s13062-026-00951-9","DOIUrl":"10.1186/s13062-026-00951-9","url":null,"abstract":"<p><p>Pulmonary fibrosis is characterized by the persistent activation of fibroblasts into myofibroblasts, a process largely driven by TGF-β/SMAD signaling. Acetylation has emerged as a fundamental regulatory mechanism in cellular homeostasis and tissue fibrosis, yet whether and how the acetylation of core SMAD transcription factors at specific residues orchestrates this process remains entirely unknown. Here, through a screen of FDA-approved epigenetic modulators, we identify CUDC-907, a dual HDAC and PI3K inhibitor, as a potent suppressor of fibroblast activation and lung fibrosis. CUDC-907 attenuates TGF-β1-induced myofibroblast differentiation, contractile activity, and extracellular matrix deposition in human lung fibroblasts. Mechanistically, we demonstrate that TGF-β1 triggers the recruitment of HDAC1 to deacetylate SMAD4 at lysine 45 (K45), a modification that is essential for SMAD complex assembly and nuclear translocation. CUDC-907 targets this pathway by inhibiting HDAC1, thereby restoring SMAD4 K45 acetylation and sterically hindering the formation of the heteromeric SMAD signaling complex. Notably, mutation of K45 (K45R) or HDAC1 inactivation renders fibroblasts refractory to the anti-fibrotic effects of CUDC-907, establishing the HDAC1-SMAD4 K45 axis as the primary therapeutic target. Furthermore, therapeutic administration of CUDC-907 significantly ameliorates lung injury and collagen deposition in a bleomycin-induced mouse model. Collectively, our findings identify SMAD4 K45 acetylation as a critical molecular switch in fibrogenesis and position CUDC-907 as a promising epigenetic strategy for the treatment of fibrotic lung diseases.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"21 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540917/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148872934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CHFR drives gastric cancer stemness and hepatic metastasis by suppressing ITCH-mediated ubiquitination and degradation of OCT4.","authors":"Mugen Dai, Jianbo Wang, Qing Xu, Yixiu Shao, Han Wang, Xiaomeng Wu, Jundi Pan, Bin Ye","doi":"10.1186/s13062-026-00920-2","DOIUrl":"https://doi.org/10.1186/s13062-026-00920-2","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer (GC) is one of the most lethal malignancies worldwide, and hepatic metastasis is a major cause of its poor clinical prognosis. The stemness regulator octamer-binding transcription factor 4 (OCT4) drives the migration, invasion and metastasis of GC cells. As a RING-type E3 ubiquitin ligase, Checkpoint with Forkhead-associated and RING finger domains (CHFR) has been identified as a key promoter of metastasis in advanced GC. However, the precise molecular mechanisms underlying CHFR-mediated modulation of GC metastasis remain unclear.</p><p><strong>Results: </strong>This study systematically explored the biological functions and molecular mechanism of CHFR in GC via public data analysis, in vitro cell experiments and in vivo hepatic metastasis models. Functional assays revealed that CHFR overexpression enhanced the stemness and metastatic capacity of GC cells but inhibited cell proliferation. Mechanistically, CHFR stabilized OCT4 protein by blocking itchy E3 ubiquitin-protein ligase (ITCH)-mediated ubiquitination and proteasomal degradation of OCT4. Molecular docking predicted a direct interaction between CHFR and ITCH, and site mutation studies showed that their binding interface was essential for CHFR-induced OCT4 stabilization. DynaMut2 and FoldX mutagenesis confirmed Tyr530 (CHFR) and Thr222 (ITCH) as critical interfacial residues, whose alanine substitution weakened complex binding. Biochemical Co-IP ubiquitination assays verified CHFR targets ITCH for proteasomal degradation to suppress ITCH-dependent OCT4 breakdown. OCT4 knockdown rescue experiments further validated OCT4 as the essential downstream mediator of CHFR-induced glycolytic reprogramming, stemness and invasion in GC cells. Importantly, in vivo xenograft assays demonstrated that CHFR overexpression significantly promoted GC liver metastasis, whereas simultaneous overexpression of CHFR and ITCH reversed this metastatic phenotype.</p><p><strong>Conclusion: </strong>CHFR enhances the stemness and metastatic progression of advanced GC cells by antagonizing ITCH-dependent OCT4 degradation, highlighting the CHFR/ITCH/OCT4 axis as a therapeutic target for GC treatment.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"21 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13487966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA HNF1A-AS1 promotes prostate cancer progression via the miR-138-5p/KDM6B axis.","authors":"Tingxuan Lv, Kexiang Wang, Weicai Chang, Feng Feng","doi":"10.1186/s13062-026-00934-w","DOIUrl":"10.1186/s13062-026-00934-w","url":null,"abstract":"<p><strong>Background: </strong>Prostate cancer (PCa) is a widespread malignancy with poor prognosis in advanced stages. However, the role of long non-coding RNA (lncRNA) HNF1A-AS1 in PCa progression and its underlying mechanisms remain largely unclear. This study aims to explore the expression trends and clinical associations of HNF1A-AS1 in PCa, and to reveal the potential functional networks by which it regulates the malignant progression of PCa.</p><p><strong>Methods: </strong>Expression of HNF1A-AS1 was detected in 113 pairs of PCa and adjacent tissues by quantitative real-time PCR (qRT-PCR). Cell Counting Kit-8 (CCK-8), Transwell, Western blot, and Fe²⁺ concentration assays were performed to assess cell proliferation, migration, invasion, and ferroptosis. Dual-luciferase reporter assays validated targeting relationships.</p><p><strong>Results: </strong>HNF1A-AS1 was markedly upregulated in PCa tissues and cells. High expression of HNF1A-AS1 correlated with advanced tumor progression, poor differentiation, higher Gleason grade, and reduced recurrence-free survival. Silencing of HNF1A-AS1 suppressed PCa cell proliferation, migration, and invasion, and triggered biochemical events consistent with ferroptosis. Mechanistically, HNF1A-AS1 directly sponged miR-138-5p, which in turn targeted KDM6B. Rescue experiments confirmed that the HNF1A-AS1/miR-138-5p/KDM6B axis regulates malignant phenotypes and ferroptosis in PCa cells.</p><p><strong>Conclusions: </strong>HNF1A-AS1 represents a potential independent prognostic factor for PCa. HNF1A-AS1 drives PCa progression through suppression of ferroptosis via the miR-138-5p/KDM6B axis, representing a promising therapeutic candidate.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"21 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13660208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synthetic horizontal gene transfer for ecosystem restoration.","authors":"Victor Maull, Guim Aguadé-Gorgorió, Victor de Lorenzo, Ricard Solé","doi":"10.1186/s13062-026-00919-9","DOIUrl":"10.1186/s13062-026-00919-9","url":null,"abstract":"<p><p>Restoring endangered ecosystems has become a pressing issue as the effects of global warming continue to harm existing communities. During the last decade, several studies have suggested the use of synthetic biology as a tool to protect these biodiverse communities by increasing their functionality. A critical example concerns soil microbiome communities in drylands, where increasing water retention by some of the constituent species could effectively protect the ecosystem from abrupt degradation. However, how to effectively deploy a functional synthetic construct that can scale its impact to the community level remains an open question. Recent experimental research has designed recombinant gene plasmids with the capacity to horizontally transfer across soil microbial communities. Here, we explore the impacts of synthetic horizontal gene transfer in models of ecological consortia. We define a consumer-resource model in which species can share an engineered plasmid that reduces resource loss, effectively coupling multispecies dynamics and gene spreading. By doing so, we identify a wide range of parameters and the optimal gene transfer conditions for which the intervention promotes biodiversity and biomass gains, while regulating gene propagation and the spread of engineered organisms. Our work provides a first step toward understanding the mechanisms and opportunities of engineered plasmid transfer in multispecies ecological communities.</p>","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"21 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}