Life Sci. 2025 Aug 5:123893. doi: 10.1016/j.lfs.2025.123893. Online ahead of print.

NO ABSTRACT

PMID:40769822 | DOI:10.1016/j.lfs.2025.123893

Genes Dev. 2025 Aug 6. doi: 10.1101/gad.352747.125. Online ahead of print.

ABSTRACT

Regulators of chromatin accessibility play key roles in cell fate transitions, triggering the onset of novel transcription programs as cells differentiate. In the Drosophila male germline stem cell lineage, tMAC, a master regulator of spermatocyte differentiation that binds thousands of loci, is required for local opening of chromatin, allowing activation of spermatocyte-specific promoters. Here we show that a cell type-specific surveillance system involving the multiple zinc finger protein Kmg and the pipsqueak domain protein Dany dampens transcriptional output from weak tMAC-dependent promoters and counteracts tMAC binding at thousands of additional cryptic promoters, thus preventing massive expression of aberrant protein-coding transcripts. ChIP-seq showed Kmg enriched at the tMAC-bound promoters that it repressed, consistent with direct action. In contrast, Kmg and Dany did not repress highly expressed tMAC-dependent genes, where they colocalized with their binding partner, the chromatin remodeler Mi-2 (NuRD), along the transcribed regions rather than at the promoter. We discuss a model where Kmg, together with Dany and Mi-2, dampens expression from weak or ectopic promoters while allowing robust transcription from highly expressed Aly-dependent genes.

PMID:40769719 | DOI:10.1101/gad.352747.125

J Theor Biol. 2025 Aug 4:112231. doi: 10.1016/j.jtbi.2025.112231. Online ahead of print.

ABSTRACT

Colorectal cancer (CRC) poses a major public health challenge due to its increasing prevalence, particularly among younger populations. Microsatellite instability-high (MSI-H) CRC and deficient mismatch repair (dMMR) CRC constitute 15% of all CRC and exhibit remarkable responsiveness to immunotherapy, especially with PD-1 inhibitors. Despite this, there is a significant need to optimise immunotherapeutic regimens to maximise clinical efficacy and patient quality of life. To address this, we employ a novel framework driven by delay integro-differential equations to model the interactions among cancer cells, immune cells, and immune checkpoints in locally advanced MSI-H/dMMR CRC (laMCRC). Several of these components are being modelled deterministically for the first time in cancer, paving the way for a deeper understanding of the complex underlying immune dynamics. We consider two compartments: the tumour site and the tumour-draining lymph node, incorporating phenomena such as dendritic cell (DC) migration, T cell proliferation, and CD8+ T cell exhaustion and reinvigoration. Parameter values and initial conditions are derived from experimental data, integrating various pharmacokinetic, bioanalytical, and radiographic studies, along with deconvolution of bulk RNA-sequencing data from the TCGA COADREAD and GSE26571 datasets. We finally optimised neoadjuvant treatment with pembrolizumab, a widely used PD-1 inhibitor, to balance efficacy, efficiency, and toxicity in laMCRC patients. We mechanistically analysed factors influencing treatment success and improved upon currently FDA-approved therapeutic regimens for metastatic MSI-H/dMMR CRC, demonstrating that a single medium-to-high dose of pembrolizumab may be sufficient for effective tumour eradication while being efficient, safe and practical.

PMID:40769472 | DOI:10.1016/j.jtbi.2025.112231

Nature. 2025 Aug 6. doi: 10.1038/s41586-025-09461-6. Online ahead of print.

ABSTRACT

Migration of transplanted allogeneic myeloid cells into the brain following systemic hematopoietic stem and progenitor cells transplantation (HCT) holds great promise as a therapeutic modality to correct genetic deficiencies in the brain such as lysosomal storage diseases.1-3 However, the toxic myeloablation required for allogeneic HCT can cause serious, life-threatening side effects limiting its applicability. Moreover, transplanted allogeneic myeloid cells are highly vulnerable to rejection even in an immune-privileged organ like the brain. Here we report a brain-restricted, high-efficiency microglia replacement approach without myeloablative preconditioning. Unlike previous assumptions, we found that hematopoietic stem cells are not required to repopulate the myeloid compartment of the brain environment. In contrast, Sca1- committed progenitor cells were highly efficient to replace microglia following intracerebral injection. This finding enabled the development of brain-restricted preconditioning and avoided long-term peripheral engraftment thus eliminating complications such as graft-vs-host disease. Evaluating its therapeutic potential, we found that our allogeneic microglia replacement method rescues the murine model of Sandhoff disease, a lysosomal storage disease caused by hexosaminidase B deficiency. In support of the translational relevance of this approach, we discovered that human induced pluripotent stem cell-derived myeloid progenitor cells display a similar engraftment potential following brain-restricted conditioning. Our results overcome current limitations of conventional HCT and may pave the way for the development of allogeneic microglial cell therapies for the brain.

PMID:40769206 | DOI:10.1038/s41586-025-09461-6

Sci Transl Med. 2025 Aug 6;17(810):eadt1452. doi: 10.1126/scitranslmed.adt1452. Epub 2025 Aug 6.

ABSTRACT

Each year in the United States, ~50% of adults ≥18 years old are vaccinated against influenza viruses, with protective efficacy averaging 40.5% over the past 20 years. To model annual seasonal influenza, a cohort of 74 adults, who were unscreened for preexisting A/H1N1 immunity and half of whom were recently immunized with licensed QIV (mean of 64 days), were challenged with A/H1N1 influenza virus. Transcriptomic, proteomic, and VDJ repertoire analyses were performed on nasal and peripheral blood samples from participants to identify nasal mucosal and systemic immune responses that correlated with viral shedding and immune correlates of protection. Viral-shedding participants showed increased T cell, but not B cell, VDJ diversity with expansion of low-frequency B cell clones postchallenge, including broadly neutralizing motifs. Nonshedding participants demonstrated decreased clonality and increased richness of B and T cell VDJ clones, increased preinoculation nasal mucosal immune gene and serum protein expression, and increased ex vivo peripheral blood mononuclear cell responses. Nasal mucosal responses in participants shedding virus for 2 or more days showed higher early viral loads and exhibited stronger induction of antiviral responses compared with those in participants who shed virus for 1 day. Last, participants with a single day of viral shedding were three times more likely to be female. These data shed light on the complex immune responses in the nasal mucosa and the periphery after influenza vaccination and infection, which will be critical for next-generation vaccine development.

PMID:40768601 | DOI:10.1126/scitranslmed.adt1452

Plant Biotechnol J. 2025 Aug 6. doi: 10.1111/pbi.70289. Online ahead of print.

ABSTRACT

Nitrogen availability remains a principal constraint to crop productivity. Plants cannot directly assimilate the abundant nitrogen available in our atmosphere; instead, they rely on the uptake of inorganic forms of nitrogen, such as ammonium and nitrate from the soil. Nitrogen is a limiting nutrient in wheat production, and wheat yields are very responsive to nitrogen fertilisation. Only diazotrophic bacteria can convert atmospheric nitrogen to ammonia via biological nitrogen fixation (BNF), and although improving BNF in wheat has been a longstanding objective, there have been no descriptions of successful modification of wheat crops showing increased BNF in the literature. Here we describe the use of polycistronic multiplexed CRISPR to modify the flavone biosynthetic pathway of hexaploid wheat (Triticum aestivum) plants, generating DNA-edited plants with increased apigenin content. The apigenin-enriched plants exude apigenin into the soil, inducing the colonisation of the roots and subsequent formation of biofilms in soil by diazotrophic bacteria. The low permeability of the biofilm to oxygen protected the bacterial nitrogenase and stimulated BN. Under nitrogen-limiting conditions, apigenin-enriched wheat lines exhibited increased nitrogen content, improved photosynthetic performance, and higher grain yield relative to wild-type controls. This work demonstrates the feasibility of engineering associative BNF in cereals via metabolic reprogramming of root exudation, offering a sustainable route to reduce dependence on synthetic nitrogen fertilisers.

PMID:40768387 | DOI:10.1111/pbi.70289

Appl Biochem Biotechnol. 2025 Aug 6. doi: 10.1007/s12010-025-05322-0. Online ahead of print.

ABSTRACT

Hydrothermal processing is known to influence the nutritional and functional properties of cereals; however, its effects on the bioactive metabolite composition of traditional Indian brown rice varieties remain underexplored. In this study, we investigated the impact of hydrothermal treatment on four indigenous rice varieties, Seeraga samba, Kattu ponni, Kuzhiyadichaan, and Poongar, focusing on the compositional changes in lipophilic bioactive compounds. Using GC-MS/MS analysis, we quantified the alterations in fatty acids, phytosterols, triterpenes, and tocopherols before and after processing. Significant varietal responses were also observed. Seeraga samba exhibited a 20.38% increase in total fatty acid post-treatment, whereas Kuzhiyadichaan showed a 13.72% increase in β-sitosterol (p < 0.01). Poongar displayed an 18.92% increase in polyunsaturated fatty acids, whereas Kattu ponni showed a 2.13% increase in squalene content. Notably, vitamin E and γ-tocopherol were detected exclusively in hydrothermally processed Kuzhiyadichaan and Poongar, indicating enhanced micronutrient release. Statistical analysis revealed significant compositional differences (p < 0.05) between the raw and processed samples with distinct clustering patterns. These findings suggest that hydrothermal processing can be strategically optimized to enhance the nutraceutical value of traditional brown rice, thereby offering a promising approach for dietary biofortification and functional food development.

PMID:40768180 | DOI:10.1007/s12010-025-05322-0

Forensic Sci Med Pathol. 2025 Aug 6. doi: 10.1007/s12024-025-01044-1. Online ahead of print.

NO ABSTRACT

PMID:40767910 | DOI:10.1007/s12024-025-01044-1

Front Pharmacol. 2025 Jul 22;16:1606914. doi: 10.3389/fphar.2025.1606914. eCollection 2025.

ABSTRACT

INTRODUCTION: Prostate cancer (PCa) remains a significant global health challenge despite advancements in treatment strategies. There is a need to explore the molecular heterogeneity of PCa to facilitate the development of personalized treatment approaches. This study investigates the molecular heterogeneity of PCa by combining genomic and transcriptomic data using a systems biology approach.

METHODS: By utilising whole-genome sequencing and differentially expressed genes from "The Cancer Genome Atlas Prostate Adenocarcinoma (TCGA-PRAD)" patient samples, we identified 357 intersecting genes. From protein-protein interaction network analysis, 22 hub genes were identified as critical regulators associated with PCa prognosis and pathogenesis. Furthermore, these hub genes were subjected to functional and pathway enrichment analysis via gene ontology (GO) and the Kyoto Encyclopaedia of Genes and Genomes (KEGG).

RESULTS: Notably, the PI3K/Akt signalling pathway was significantly enriched with eight of these hub genes, with significant clinical relevance. Dipeptidyl Peptidase 4 (DPP4) emerged as a promising therapeutic target. Further, in vitro assays were performed to investigate and validate the molecular role of DPP4 through pharmacological inhibition using Linagliptin, a selective DPP4 inhibitor. Inhibition of DPP4 led to the induction of apoptosis, G1/S phase cell cycle arrest, and significant suppression of cell proliferation and migration in PC3 and DU145 cell lines.

DISCUSSION: These experiments revealed novel downstream regulatory effects of DPP4, demonstrating that its inhibition results in the transcriptional downregulation of FGF17, PDGFRA, COL4A1, and COL9A2, thereby contributing to the inactivation of the PI3K/Akt signaling pathway. Collectively, these findings highlight DPP4 as a potential therapeutic target for the treatment of PCa.

PMID:40766751 | PMC:PMC12321844 | DOI:10.3389/fphar.2025.1606914

bioRxiv [Preprint]. 2025 Jul 31:2025.07.29.667408. doi: 10.1101/2025.07.29.667408.

ABSTRACT

Mass spectrometry (MS)-based proteomics remains technically demanding and prohibitively expensive for many large-scale or routine applications, with per-sample costs of hundreds of dollars or more. To democratize access to proteomics and facilitate its integration into more high-throughput multi-omic studies, we present a robust analytical framework for achieving in-depth, quantitative proteome profiling at a cost of approximately $10 per sample, termed the "$10 proteome." Using the Thermo Fisher Orbitrap Astral and Bruker timsTOF Ultra 2 mass spectrometers, we evaluated performance across sample inputs ranging from 200 pg to 100 ng and active gradient lengths from 5 to 60 minutes. Proteome coverage saturated within the low-nanogram input range, with ∼8000 protein groups quantified from as little as 10 ng of input and nearly 6000 protein groups from 200 pg. With already demonstrated low-cost one-pot sample preparation workflows that are appropriate for this sample input range, standardized MS acquisition settings, and high-throughput nanoLC operated at ∼10 min per sample, the $10 proteome becomes feasible. This study establishes a practical, scalable, and cost-effective foundation for global proteome profiling, paving the way for routine, large-scale applications in systems biology, clinical research and beyond.

PMID:40766599 | PMC:PMC12324313 | DOI:10.1101/2025.07.29.667408

Res Sq [Preprint]. 2025 Jul 29:rs.3.rs-7077811. doi: 10.21203/rs.3.rs-7077811/v1.

ABSTRACT

Multiple mechanisms of immunity must be coordinated to defend against a comprehensive range of pathogens; however, the mechanisms by which broad-spectrum antipathogens act remain largely elusive. Here, we employed systems biology approaches to understand the organization of human immune cells at the single-cell level, as well as their reorganization in response to K21, a silane derivative effective against viral, bacterial, and fungal infections. K21 induced pro-inflammatory pathways in M1 and M2c macrophages without altering cytokine secretion, decreased a specific subtype of M1 macrophages and CXCL4-induced M2-like macrophages, and improved mitochondrial health by enhancing mitochondrial recycling via mitophagy. Similar treatment of the in vivo model organism C. elegans induced mitophagy and extended lifespan, suggesting evolutionary conservation of mechanism. Our work demonstrates that a drug that remodels mitochondria and metabolism can shape the immune cell repertoire, which could aid the development of more effective antimicrobials and prevent the emergence of drug-resistant pathogens.

PMID:40766249 | PMC:PMC12324592 | DOI:10.21203/rs.3.rs-7077811/v1

Blood Vessel Thromb Hemost. 2025 May 26;2(3):100077. doi: 10.1016/j.bvth.2025.100077. eCollection 2025 Aug.

ABSTRACT

We developed a platform to measure the oxygen-dependent mechanical properties and oxygen saturation of individual irreversibly sickled cells (ISCs). We identified and measured ISCs from a cohort of 10 individuals with sickle cell disease. ISCs were found to have an average shear surface modulus 20 times that of nonsickled cells and a sixth that of red blood cells (RBCs) with detectable hemoglobin polymer. We found that the number of ISCs was significantly reduced at 53 mm Hg oxygen compared with ≥91 mm Hg oxygen, suggesting that these RBCs can still form polymer under hypoxia. We also found that the fraction of ISCs present in a blood sample had a negative correlation with donor fetal hemoglobin (HbF) fraction, suggesting that HbF could play a role in mitigating occurrence of ISCs.

PMID:40765910 | PMC:PMC12320412 | DOI:10.1016/j.bvth.2025.100077

Front Plant Sci. 2025 Jul 22;16:1624335. doi: 10.3389/fpls.2025.1624335. eCollection 2025.

ABSTRACT

INTRODUCTION: Areca catechu is a widely cultivated palm species with significant economic and medicinal value. However, A. catechu is a tropical plant that is particularly susceptible to low temperatures.

METHODS: This study integrates physiological profiling with transcriptomic sequencing to systematically investigate the cold-response mechanisms of A. catechu.

RESULTS: Multivariate variance analysis revealed that peroxidase (POD) activity and chlorophyll content are significant biomarkers strongly correlated with cold tolerance. A comprehensive investigation into the temporal expression of genes in response to 24 hours of cold stress was conducted, using RNA-seq analysis. This analysis yielded a substantial number of differentially expressed genes (DEGs), amounting to 20,870, which were found to be subject to temporal regulation. KEGG pathway enrichment analysis revealed substantial activation in three metabolic pathways: phytohormone signaling, alkaloid biosynthesis (tropane/piperidine/pyridine), and flavonoid biosynthesis. The application of Weighted Gene Co-expression Network Analysis (WGCNA), in conjunction with a dynamic tree-cutting algorithm, resulted in the identification of 25 co-expression modules. Eigenvector centrality analysis identified six hub genes responsive to cold stress: ZMYND15, ABHD17B, ATL8, WNK5, XTH3 and TPS. The findings of this study delineate three key aspects: (1) temporal dynamics of cold-responsive physiological processes, (2) pathway-level characterization of DEG enrichment patterns, and (3) genetic determinants underlying cold stress adaptation.

DISCUSSION: These findings clarify the time series and core physiological indicators of A. catechu during various physiological processes, identify pivotal genes associated with cold stress, and provide a gene-to-phenotype framework for optimizing cold-resilient cultivation protocols and molecular marker-assisted breeding strategies.

PMID:40765861 | PMC:PMC12321864 | DOI:10.3389/fpls.2025.1624335

Int J Biol Sci. 2025 Jul 11;21(10):4586-4603. doi: 10.7150/ijbs.109973. eCollection 2025.

ABSTRACT

Bladder cancer poses severe threats to human health due to its aggressive nature and resistance to drug treatment; however, the underlying mechanisms have not been fully investigated. In the present study, we identify SBSPON (Somatomedin B and Thrombospondin Type 1 Domain Containing) as a novel tumor suppressor. The expression of SBSPON was downregulated in bladder cancer and correlated with poor overall survival. SBSPON suppressed the proliferation and migration ability of bladder cancer cells in vitro, and inhibited tumor growth of bladder cancer cells in vivo. Genetic ablation of Sbspon in mice significantly accelerated the progression of N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN) induced bladder cancer. Mechanistically, SBSPON is a novel HSPA5 binding glycoprotein. SBSPON functioned through binding to HSPA5 and inhibiting its membrane translocation, resulting in an inactivated AKT signaling pathway. More importantly, SBSPON inhibited the cisplatin resistance of bladder cancer cells by reducing the inhibitory effect of HSPA5 on apoptosis. In summary, the novel glycoprotein SBSPON functions as a tumor suppressor and inhibits resistance to cisplatin in bladder cancer. This may provide novel therapeutic strategies for bladder cancer treatment.

PMID:40765821 | PMC:PMC12320502 | DOI:10.7150/ijbs.109973

Int J Biol Sci. 2025 Jul 11;21(10):4683-4700. doi: 10.7150/ijbs.113805. eCollection 2025.

ABSTRACT

Colorectal cancer (CRC) metastasis continues to account for a substantial proportion of cancer-related deaths worldwide. Calcium-binding protein S100A4 is a known executor of CRC metastasis. S100A4 has been correlated to metastasis formation in the past, and therefore pharmaceutical intervention reduces the metastatic phenotype. Herein, a high-throughput screen (HTS) of 105,600 compounds from the EMBL screening library using an S100A4 promoter-driven luciferase construct transfected into HCT116 cells identified novel compounds for S100A4 transcriptional inhibition. The most promising inhibitors identified were tested for S100A4 transcriptional inhibition, their impact on wound healing, migration, proliferation and viability of cancer cells. Subsequently, the leading candidate E12 was tested in vivo in a xenograft mouse model (HCT116/CMVp- Luc). After several testing rounds, E12 a 2-(4-fluorobenzenesulfonamido)benzamide-based compound showed the strongest inhibition of S100A4 expression at mRNA (EC50 < 1 µM; 48 h) and protein level and concomitant restriction of metastatic abilities in two CRC cell lines with a tolerable viability reduction. In vivo, a reduction in metastasis formation was demonstrated, displayed by reduced overall bioluminescence of tumors and human satellite DNA in the liver of treated mice. This study exhibited E12's promising potential for S100A4 targeted metastasis inhibition therapy to improve the outcome of metastasized CRC patients.

PMID:40765817 | PMC:PMC12320493 | DOI:10.7150/ijbs.113805

J Drug Target. 2025 Aug 5:1-29. doi: 10.1080/1061186X.2025.2544786. Online ahead of print.

ABSTRACT

Vascular diseases such as atherosclerosis, aneurysms, and peripheral arterial disease remain leading causes of morbidity and mortality, with current treatments primarily managing symptoms rather than addressing underlying molecular drivers. Gene therapy offers a promising avenue for targeted intervention, and recent advances in multi-omics approaches-including genomics, transcriptomics, and epigenetics-are enhancing the precision and efficacy of these therapies. High-throughput sequencing and integrative omics analyses have facilitated the identification of causal genes, non-coding RNAs, and epigenetic regulators involved in vascular pathology. This review examines how multi-omics frameworks inform gene therapy design, from genomic editing of cardiovascular disease loci to transcriptome-guided RNA therapies and epigenetic modulation of disease states. We highlight emerging applications such as CRISPR-based interventions, RNA therapeutics, and individualized precision medicine strategies. Additionally, we address analytical challenges, implementation hurdles, and ethical considerations in translating multi-omics-driven gene therapies into clinical practice. By integrating systems biology and advanced computational methods, the convergence of multi-omics and gene therapy holds transformative potential for vascular medicine, offering new avenues for disease modification and patient-specific therapeutic solutions.

PMID:40765035 | DOI:10.1080/1061186X.2025.2544786

Mol Syst Biol. 2025 Aug 5. doi: 10.1038/s44320-025-00134-0. Online ahead of print.

ABSTRACT

Generating longitudinal and multi-layered big biological data is crucial for effectively implementing artificial intelligence (AI) and systems biology approaches in characterising whole-body biological functions in health and complex disease states. Big biological data consists of multi-omics, clinical, wearable device, and imaging data, and information on diet, drugs, toxins, and other environmental factors. Given the significant advancements in omics technologies, human metabologenomics, and computational capabilities, several multi-omics studies are underway. Here, we first review the recent application of AI and systems biology in integrating and interpreting multi-omics data, highlighting their contributions to the creation of digital twins and the discovery of novel biomarkers and drug targets. Next, we review the multi-omics datasets generated worldwide to reveal interactions across multiple biological layers of information over time, which enhance precision health and medicine. Finally, we address the need to incorporate big biological data into clinical practice, supporting the development of a clinical decision support system essential for AI-driven hospitals and creating the foundation for an AI and systems biology-based healthcare model.

PMID:40764831 | DOI:10.1038/s44320-025-00134-0

Sci Rep. 2025 Aug 5;15(1):28599. doi: 10.1038/s41598-025-13419-z.

ABSTRACT

From cellular mechanotransduction to the formation of embryonic tissues and organs, mechanics has been shown to play an important role in the control of cell behavior and embryonic development. Most of our existing knowledge of how mechanics affects cell behavior comes from in vitro studies, mainly because measuring cell and tissue mechanics in 3D multicellular systems, and especially in vivo, remains challenging. Oil microdroplet sensors, and more recently gel microbeads, use surface deformations to directly quantify mechanical stresses within developing tissues, in vivo and in situ, as well as in 3D in vitro systems like organoids or multicellular spheroids. However, an automated analysis software able to quantify the spatiotemporal evolution of stresses and their characteristics from particle deformations is lacking. Here we develop STRESS (Surface Topography Reconstruction for Evaluation of Spatiotemporal Stresses), an analysis software to quantify the geometry of deformable particles of spherical topology, such as microdroplets or gel microbeads, that enables the automatic quantification of the temporal evolution of stresses in the system and the spatiotemporal features of stress inhomogeneities in the tissue. As a test case, we apply these new code to measure the temporal evolution of mechanical stresses using oil microdroplets in developing zebrafish tissues. Starting from a 3D timelapse of a droplet, the software automatically calculates the statistics of local anisotropic stresses, decouples the deformation modes associated with tissue- and cell-scale stresses, obtains their spatial features on the droplet surface and analyzes their spatiotemporal variations using spatial and temporal stress autocorrelations. We provide fully automated software in Matlab/Python and also in Napari (napari-STRESS), which allows the visualization of mechanical stresses on the droplet surface together with the microscopy images of the biological systems. The automated nature of the analysis will help users obtain quantitative information about mechanical stresses in a wide range of 3D multicellular systems, from developing embryos or tissue explants to organoids.

PMID:40764636 | DOI:10.1038/s41598-025-13419-z

Sci Rep. 2025 Aug 5;15(1):28596. doi: 10.1038/s41598-025-05085-y.

ABSTRACT

The Scorpaeniformes order encompasses a diverse array of teleost fish, including commercially important and venomous species. Fish venoms offer significant pharmacological potential, but incomplete phylogenetic understanding has hindered research. Resolving relationships among venomous fish families is crucial for studying venom evolution and discovering novel bioactive compounds. To address these phylogenetic uncertainties, we generated and assembled the complete mitochondrial genomes of Paracentropogon rubripinnis (Tetrarogidae) and Inimicus japonicus (Synanceiidae), two representative venomous species. The circular mitogenomes, 16,465 bp and 16,676 bp in length, respectively, contain the typical vertebrate mitochondrial gene complement. Comparative analyses revealed a highly conserved gene order and orientation across Scorpaeniformes, with slight variations in the Notothenioidei outgroups. We identified three novel conserved sequence blocks in the control regions and characterized structural features of protein-coding genes, tRNAs, and non-coding elements. Phylogenetic analyses using 13 mitochondrial protein-coding genes from 71 Scorpaeniformes and three outgroup species provided a higher-resolution phylogeny of the order, including 12 families and 31 genera. Our results support the monophyly of Tetrarogidae and Synanceiidae, placing them in an early-diverging position within the Scorpaeniformes phylogeny. This study provides insights into the phylogenetic positions of venomous fish families and lays a foundation for future research on fish venom evolution and applications.

PMID:40764620 | DOI:10.1038/s41598-025-05085-y

Nat Microbiol. 2025 Aug 5. doi: 10.1038/s41564-025-02076-7. Online ahead of print.

ABSTRACT

Microbiome engineering seeks to reshape microbial communities to improve ecosystem function. However, many efforts fail due to inadequate design principles, often resulting in a loss of key microorganisms and disruption of links between the engineered community and its intended function. In contrast, decades of research in macroecology have uncovered key principles governing the relationship between biodiversity and ecosystem function. Here we translate these ecological principles to microbiome engineering, focusing on three stages: microbiome design, colonization and maintenance. We propose new approaches that leverage underlying ecological dynamics-particularly niche dynamics-to optimize diversity and abundance to promote stability and functionality, especially in host-associated microbiomes. We also highlight key research priorities to apply macro-ecosystem insights to microbial systems. Improving microbiome engineering in this way holds promise for solving pressing challenges in medicine and agriculture, while providing understanding of ecological processes that maintain biodiversity across biological scales.

PMID:40764435 | DOI:10.1038/s41564-025-02076-7