Search Results (1,084)

Nitrogen is an essential mineral nutrient for plant growth and development. However, the molecular response mechanisms of sugarcane under varying nitrogen regimes remain unclear. This study investigated the dynamic responses of sugarcane (GT42) leaves to nitrogen treatment using hydroponic systems. Leaf samples were collected under low nitrogen (LN, 0.2 mM NH₄NO₃) and normal nitrogen (NN, 2 mM NH₄NO₃) treatments at 1, 3, 6, 12, 24, 48, and 72 h, as well as under high nitrogen (HN, 6 mM NH₄NO₃) treatment at 3, 6, and 24 h. RNA-Seq analysis identified differentially expressed genes (DEGs) between LN/NN and HN/NN treatments at corresponding time points. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of DEGs from both LN/NN and HN/NN comparisons revealed significant enrichment in nitrogen metabolism and zeatin biosynthesis pathways. These findings aligned with our Weighted Gene Co-Expression Network Analysis (WGCNA) results from LN-treated samples. Through detailed reconstruction of the nitrogen metabolic pathway and zeatin biosynthesis co-expression networks, we established their pivotal regulatory roles in sugarcane’s adaptation to varying nitrogen availability. Our results demonstrate a dynamic, concentration-dependent regulatory network in sugarcane leaves under nitrogen treatment. These findings provide potential targets for improving nitrogen use efficiency (NUE) in sugarcane breeding programs. The study offers new insights into the molecular mechanisms underlying sugarcane’s response to nitrogen fluctuations, with implications for developing nitrogen-efficient cultivars. Full article

Soil-borne diseases represent a major constraint on the sustainable cultivation of morel mushrooms (Morchella spp.), yet the microbial ecological mechanisms driving disease occurrence and progression remain poorly understood. In this study, we conducted comparative metagenomic analyses of rhizosphere and root-adhering soils associated with healthy and diseased Morchella crops from two major production regions in China, aiming to elucidate shifts in microbial community composition, assembly processes, and functional potential. Disease conditions were linked to pronounced microbial dysbiosis, with community assembly shifting from stochastic to deterministic processes, particularly within fungal communities under host selection and pathogen pressure. Co-occurrence network analysis revealed substantial reductions in connectivity, modularity, and clustering coefficients in diseased soils, indicating the loss of ecological stability and keystone taxa. Functional annotations using CAZy, COG, and KEGG databases showed that healthy soils were enriched in genes related to carbohydrate metabolism, aerobic respiration, and ecosystem resilience, whereas diseased soils exhibited higher abundance of genes associated with stress responses, proliferation, and host defense. Furthermore, elemental cycling analysis demonstrated that healthy soils supported pathways involved in aerobic carbon degradation, nitrogen fixation, phosphate transport, and sulfur oxidation, while diseased soils favored fermentation, denitrification, phosphorus limitation responses, and reductive sulfur metabolism. Collectively, these results highlight the importance of microbial functional integrity in maintaining soil health and provide critical insights into microbiome-mediated disease dynamics, offering a foundation for developing microbiome-informed strategies for sustainable fungal crop management. Full article

Cellular organization relies on both membrane-bound organelles and membraneless biomolecular condensates formed through liquid–liquid phase separation. Recent discoveries reveal intricate coupling between lipid membrane organization and condensate assembly, reshaping our understanding of cellular compartmentalization. This review synthesizes multidisciplinary research using advanced techniques including super-resolution microscopy, fluorescence recovery after photobleaching, and in vitro reconstitution to examine lipid-condensate interactions. Lipid membranes serve as nucleation platforms that reduce critical concentrations for condensate formation by orders of magnitude through membrane anchoring and thermodynamic coupling, creating specialized microenvironments that substantially enhance enzymatic activities. Key regulatory mechanisms include phosphorylation-driven assembly and disassembly, membrane composition effects from cholesterol content and fatty acid saturation, and environmental factors such as calcium and pH. These interactions drive signal transduction through receptor clustering, membrane trafficking via organized domains, and stress responses through protective condensate formation. Dysregulation of lipid-condensate coupling, including aberrant phase transitions and membrane dysfunction, underlies metabolic disorders and neurodegenerative diseases. This coupling represents a fundamental organizing principle with significant therapeutic potential. Current challenges include developing quantitative methods for characterizing condensate dynamics in complex cellular environments and translating molecular mechanisms into clinical applications. Future progress requires interdisciplinary approaches combining advanced experimental techniques, computational modeling, and standardized protocols to advance both fundamental understanding and therapeutic innovations. Full article

Lipids are structurally diverse biomolecules that play essential roles in cellular function, energy storage, and signaling. The human lipidome, a dynamic and complex subset of the metabolome, is shaped by both endogenous factors, such as genetics, sex, age, and metabolic health, and exogenous influences like lifestyle, diet, and microbiota. Among these, diet stands out as one of the most modifiable and impactful determinants, influencing lipid composition across plasma, serum, and lipoprotein fractions. While traditional lipid profiling provides limited insight, lipidomics enables comprehensive characterization of lipid species, revealing mechanistic links between lipid metabolism and diseases such as cardiovascular disease (CVD), metabolic syndrome (MetS), and inflammatory disorders. This review explores: (1) the relationship between lipid profiles and CVD risk, (2) the internal and external modulators of the lipidome, and (3) current evidence on how specific dietary patterns, including Mediterranean, Nordic, low glycemic, and vegetarian diets, and individual nutrients such as omega-3 fatty acids (FAs), plant sterols, and mycoprotein, influence lipidomic profiles. Advances in lipidomics highlight that dietary fat quality, food matrix, and eating patterns can significantly modulate lipid species such as triacylglycerols (TAGs), ceramides (Cers), and phospholipids, with implications for cardiometabolic health. Notably, distinct responses are observed across plasma High-Density Lipoprotein (HDL) and Low-Density Lipoprotein (LDL) lipidomes, emphasizing the need for compartment-specific analyses. Understanding these diet-lipidome interactions offers promising avenues for precision nutrition and the development of lipid-based biomarkers for disease prevention and management. Full article

Arctic warming is expected to alter permafrost landscapes and shift tundra ecosystems from greenhouse gas sinks to sources. We quantified plant biomass and necromass, carbon stocks, and microbial activity across five Low-Arctic tundra sites in the Yana–Indigirka Lowland (Chokurdakh, NE Siberia) during the 2024 growing season. Above- and below-ground plant biomass was measured by harvest adjacent to 50 × 50 m permanent plots; total C and N were determined by dry combustion on an elemental analyzer. Total organic carbon (TOC) stocks were calculated by horizon from TOC (%), bulk density, and thickness. Microbial basal respiration (BR), substrate-induced respiration (SIR), microbial biomass C (MBC), and the metabolic quotient (qCO₂) were assessed in litter/organic (O), peat (T), and mineral gley horizons. Mean above-ground biomass was 15.8 ± 1.5 t ha⁻¹; total living biomass averaged 43.1 ± 1.6 t ha⁻¹. Below-ground biomass exceeded above-ground by 1.73×. Carbon in above-ground, below-ground, and necromass pools averaged 7.8, 12.2, and 12.5 t C ha⁻¹, respectively. Surface organic horizons dominated ecosystem C storage: litter–peat stocks ranged from 234 to 449 t C ha⁻¹, whereas 0–30 cm mineral layers held 18–50 t C ha⁻¹; total (surface + 0–30 cm) stocks spanned 258–511 t C ha⁻¹ among sites. Key contributors to biomass and C storage were deciduous shrubs (Salix pulchra, Betula nana), bryophytes (notably Aulacomnium palustre), and the graminoids (Eriophorum vaginatum). BR and MBC were highest in O and T horizons (BR up to 21.9 μg C g⁻¹ h⁻¹; MBC up to 70,628 μg C g⁻¹) and declined sharply in mineral soil; qCO₂ decreased from O to mineral horizons, indicating more efficient C use at depth. These in situ data show that Low-Arctic tundra C stocks are concentrated in surface organic layers while microbial communities remain responsive to warming, implying high sensitivity of carbon turnover to thaw and hydrologic change. The dataset supports model parameterization and remote sensing of shrub–tussock tundra carbon dynamics. Full article

Noccaea species (formerly Thlaspi) are Brassicaceae plants renowned for their capacity to hyperaccumulate zinc (Zn), cadmium (Cd), and nickel (Ni), which has made them model systems in studies of metal tolerance, phytoremediation, and plant adaptation to extreme environments. While their physiological and genetic responses to metal stress are relatively well characterised, the extent to which these traits influence microbiome composition and function remains largely unexplored. These species possess compact genomes shaped by ancient whole-genome duplications and rearrangements, and such genomic traits may influence microbial recruitment through changes in secondary metabolism, elemental composition, and tissue architecture. Here, we synthesise the current findings on how genome size, metal hyperaccumulation, structural adaptations, and glucosinolate diversity affect microbial communities in Noccaea roots and leaves. We review evidence from bioimaging, molecular profiling, and physiological studies, highlighting interactions with bacteria and fungi adapted to metalliferous soils. At present, the leaf microbiome of Noccaea species remains underexplored. Analyses of root microbiome, however, reveal a consistent taxonomic core dominated by Actinobacteria and Proteobacteria among bacterial communities and Ascomycetes, predominantly Dothideomycetes and Leotiomycetes among fungi. Collectively, these findings suggest that metal-adapted microbes provide several plant-beneficial functions, including metal detoxification, nutrient cycling, growth promotion, and enhanced metal extraction in association with dark septate endophytes. By contrast, the status of mycorrhizal associations in Noccaea remains debated and unresolved, although evidence points to functional colonisation by selected fungal taxa. These insights indicate that multiple plant traits interact to shape microbiome assembly and activity in Noccaea species. Understanding these dynamics offers new perspectives on plant–microbe co-adaptation, ecological resilience, and the optimisation of microbiome-assisted strategies for sustainable phytoremediation. Full article

Mitochondrial quality control (MQC) mechanisms, including proteostasis, mitophagy, mitochondrial dynamics, and biogenesis, are essential for maintaining mitochondrial function and overall cellular health. Dysregulation of these systems is a common feature of both neurodegenerative diseases and cancer, but the outcomes differ. Neurons depend strongly on healthy mitochondria and are easily damaged when MQC fails, resulting in organellar dysfunction and oxidative stress. By contrast, cancer cells often adapt by using MQC pathways to sustain survival and resist cell death. The mitochondrial unfolded protein response (mtUPR) and mitophagy are central to these processes, yet their roles are context-dependent. In neurodegeneration, activation of these pathways may help neurons survive, yet persistent stimulation can shift towards harmful effects. In cancer, these same pathways enhance metabolic flexibility, promote resistance to treatment, and support tumor progression. Although therapeutic strategies targeting MQC are being explored, their translation to the clinic is difficult, partly due to opposite effects in different diseases. The observed inverse epidemiological link between cancer and neurodegeneration may also reflect the distinct regulation of MQC pathways. A clearer understanding of these mechanisms is needed to identify new treatment strategies for disorders that are clinically distinct but share common mitochondrial defects. Full article

Lacticaseibacillus rhamnosus (Lbs. rhamnosus) is renowned for its tolerance to gastric acid and adaptability to bile and alkaline conditions, and is crucial for intestinal health and immune regulation. In this study, integrated transcriptomic and proteomic analyses were employed to elucidate the response mechanisms of Lbs. rhamnosus under osmotic stress, induced by exposure to 0.6 M sodium lactate, which elevates environmental osmotic pressure. It was shown that 792 differentially expressed genes and 138 differentially expressed proteins were detected in Lbs. rhamnosus ATCC 53103 treated with osmotic stress. The differential regulation of these genes/proteins mainly includes the inhibition of fatty acid metabolism with membrane structural remodeling (downregulation of the acetyl coenzyme A carboxylase family and fatty acid binding protein family expression), dynamic homeostasis of amino acid metabolism (restriction of the synthesis of histidine, cysteine, leucine, etc., and enhancement of the catabolism of lysine, tryptophan, etc.), and survival-oriented reconfiguration of carbohydrate metabolism (gene expression related to the glycolytic pathway increases, while gene expression related to the pentose phosphate pathway decreases). These synergistic alterations in metabolic regulation may facilitate the adaptive response of Lbs. rhamnosus ATCC 53103 to osmotic stress. Overall, our findings deepen the current understanding of the stress response mechanisms in lactic acid bacteria and offer novel insights into the survival strategies employed by Lbs. rhamnosus ATCC 53103 under hyperosmotic conditions. Full article

Indoor sports facilities face distinctive indoor air quality (IAQ) challenges due to high occupant density, elevated metabolic emissions, and diverse pollutant sources associated with physical activity. This review presents a narrative synthesis of multidisciplinary evidence concerning IAQ in sports environments. It explores major pollutant categories, including carbon dioxide (CO₂), particulate matter (PM), volatile organic compounds (VOCs), and airborne microbial agents, highlighting their sources, behavior during exercise, and associated health risks. Research shows that physical activity can increase PM concentrations by up to 300%, and CO₂ levels frequently exceed 1000 ppm in inadequately ventilated spaces. The presence of semi-volatile organics and bioaerosols further complicates pollutant dynamics, especially in humid and densely occupied areas. Measurement technologies such as optical sensors, chromatographic methods, and molecular techniques are reviewed and compared for their applicability to dynamic indoor settings. Existing IAQ standards across China, the USA, the EU, the UK, and WHO are examined, revealing a lack of activity-specific thresholds and insufficient responsiveness to real-time conditions. Mitigation strategies (e.g., including demand-controlled ventilation, use of low-emission materials, liquid chalk substitutes, and integrated HEPA-UVGI purification systems) are evaluated, many demonstrating pollutant removal efficiencies over 80%. The integration of intelligent building management systems is emphasized for enabling real-time monitoring and adaptive control. This review concludes by identifying research priorities, including the development of activity-sensitive IAQ control frameworks and long-term health impact assessments for athletes and vulnerable users. Full article

Post-exertional malaise (PEM) is a defining symptom of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), yet its molecular underpinnings remain elusive. This study investigated the temporal–longitudinal DNA methylation changes associated with PEM using a structured two-day maximum repeated effort cardiopulmonary exercise testing (CPET) protocol involving pre- and two post-exercise blood samplings from five ME/CFS patients. Cardiopulmonary measurements revealed complex heterogeneous profiles among the patients compared to typical healthy controls, and VO₂ peak indicated all patients had poor normative fitness. The switch to anaerobic metabolism occurred at a lower workload in some patients on Day Two of the test. Reduced Representation Bisulphite Sequencing followed by analysis with Differential Methylation Analysis Package-version 2 (DMAP2) identified differentially methylated fragments (DMFs) present in the DNA genomes of all five ME/CFS patients through the exercise test compared with ‘before exercise’. With further filtering for >10% methylation differences, there were early DMFs (0–24 h after first exercise test) and late DMFs between (24–48 h after the second exercise test), as well as DMFs that changed gradually (between 0 and 48 h). Of these, 98% were ME/CFS-specific, compared with the two healthy controls accompanying the longitudinal study. Principal component analysis illustrated the three distinct clusters at the 0 h, 24 h, and 48 h timepoints, but with heterogeneity among the patients within the clusters, highlighting dynamic methylation responses to exertion in individual patients. There were 24 ME/CFS-specific DMFs at gene promoter fragments that revealed distinct patterns of temporal methylation across the timepoints. Functional enrichment of ME-specific DMFs revealed pathways involved in endothelial function, morphogenesis, inflammation, and immune regulation. These findings uncovered temporally dynamic epigenetic changes in stress/immune functions in ME/CFS during PEM and suggest molecular signatures with potential for diagnosis and of mechanistic significance. Full article

Background: DNA methylation, as an epigenetic modification, is crucial in the regulatory mechanism of salt resistance in plants. Methods: To gain deeper insight into the relationship between DNA methylation and mRNA exons in halophytes and their potential roles in regulating salt tolerance, this study employed whole-genome bisulfite sequencing (WGBS) and transcriptome sequencing data to analyze the leaves of the halophyte Paspalum vaginatum, widely distributed in tropical regions. Results: The findings revealed that the methylation level of 5-methylcytosine (5mC) in the genomic elements of P. vaginatum increased with prolonged salt treatment under salt stress conditions. This observation suggested that the methylation level plays a pivotal role in the salt stress response of P. vaginatum. Notably, under salt stress, the number of variants at the mRNA exon level was significantly higher than that at the DNA level. Furthermore, comparative analysis revealed sequence variants within exonic regions of mature mRNA transcripts for several genes in salt-treated samples relative to pre-stress controls, and these changes were found to be enriched in several salt-tolerance pathways, including unsaturated fatty acid metabolism and ascorbic acid metabolism, among others. Further analysis demonstrated that the occurrence of these variants changed concomitantly with the dynamic changes in CG methylation levels in the gene body of some salt-tolerant genes. Therefore, it was speculated that mRNA exon variations probably promoted the elevation of CG 5mC methylation levels at the DNA level under salt stress conditions, further enabling the plant to adapt to the salt-stress environment. Conclusions: These findings offer preliminary insights into the relationship between DNA methylation and mRNA exon variations in P. vaginatum under salt stress, providing valuable information and avenues for further investigation into the regulatory role of mRNA in DNA methylation. Full article

Sepsis is a life-threatening syndrome caused by a dysregulated host response to infection. It follows a dynamic course in which early hyperinflammation coexists and overlaps with progressive immune suppression, a process best described as immunodynamic disruption. Key mechanisms include extensive lymphocyte death, expansion of regulatory T cells, impaired antigen presentation, and persistent activation of inhibitory checkpoints such as programmed cell death protein 1 (PD-1) and cytotoxic T lymphocyte–associated protein 4 (CTLA-4). These changes reduce immune competence and increase vulnerability to secondary infections. Clinically, reduced expression of Human Leukocyte Antigen–DR (HLA-DR) on monocytes and persistent lymphopenia have emerged as robust biomarkers for patient stratification and timing of immunomodulatory therapies. Beyond the acute phase, many survivors do not achieve full immune recovery but instead develop a Persistent Immune Remnant, defined as long-lasting immune, metabolic, and endothelial dysfunction despite apparent clinical resolution. Recognizing PIR emphasizes the need for long-term monitoring and biomarker-guided interventions to restore immune balance. To integrate these observations, we propose the SIMMP–Sepsis model (Sepsis-Associated Persistent Multiorgan Immunometabolic Syndrome), which links molecular dysfunction to clinical trajectories and provides a framework for developing precision immunotherapies. This perspective reframes sepsis not only as an acute crisis but also as a chronic immunometabolic syndrome, where survival marks the beginning of active immune restoration. Full article

The phosphoinositide 3-kinase (PI3K)/AKT signaling pathway is a crucial regulator of cellular metabolism, proliferation, and survival. It is frequently dysregulated in metabolic, cardiovascular, and neoplastic disorders. Despite the advancements in multi-omics technology, existing methods often fail to provide real-time, pathway-specific insights for precision medicine and drug repurposing. We offer Agentic RAG-Driven Multi-Omics Analysis (ARMOA), an autonomous, hypothesis-driven system that integrates retrieval-augmented generation (RAG), large language models (LLMs), and agentic AI to thoroughly analyze genomic, transcriptomic, proteomic, and metabolomic data. Through the use of graph neural networks (GNNs) to model complex interactions within the PI3K/AKT pathway, ARMOA enables the discovery of novel biomarkers, probable candidates for drug repurposing, and customized therapy responses to address the complexities of PI3K/AKT dysregulation in disease states. ARMOA dynamically gathers and synthesizes knowledge from multiple sources, including KEGG, TCGA, and DrugBank, to guarantee context-aware insights. Through adaptive reasoning, it gradually enhances predictions, achieving 91% accuracy in external testing and 92% accuracy in cross-validation. Case studies in breast cancer and type 2 diabetes demonstrate that ARMOA can identify synergistic drug combinations with high clinical relevance and predict therapeutic outcomes specific to each patient. The framework’s interpretability and scalability are greatly enhanced by its use of multi-omics data fusion and real-time hypothesis creation. ARMOA provides a cutting-edge example for precision medicine by integrating multi-omics data, clinical judgment, and AI agents. Its ability to provide valuable insights on its own makes it a powerful tool for advancing biomedical research and treatment development. Full article

Background/Objectives: Obesity and type 2 diabetes mellitus (T2DM) profoundly disrupt lipid metabolism within local microenvironments of skeletal muscle and its associated connective tissues, including adipose tissue, bone, and fascia. However, the role of local communication between skeletal muscle and its proximal connective tissues in propagating metabolic dysfunction is incompletely understood. This narrative review synthesizes current evidence on these local metabolic interactions, highlighting novel insights and existing gaps. Methods: We conducted a comprehensive literature analysis of primary research published in the last decade, sourced from PubMed, Web of Science, and ScienceDirect. Studies were selected for relevance to skeletal muscle, adipose tissue, fascia, and bone lipid metabolism in the context of obesity and T2DM, with emphasis on molecular, cellular, and paracrine mechanisms of local crosstalk. Findings were organized into thematic sections addressing physiological regulation, pathological remodeling, and inter-organ signaling pathways. Results: Our synthesis reveals that local lipid dysregulation in obesity and T2DM involves altered fatty acid transporter dynamics, mitochondrial overload, fibro-adipogenic remodeling, and compartment-specific adipose tissue dysfunction. Crosstalk via myokines, adipokines, osteokines, bioactive lipids, and exosomal miRNAs integrates metabolic responses across these tissues, amplifying insulin resistance and lipotoxic stress. Emerging evidence highlights the underappreciated roles of fascia and marrow adipocytes in regional lipid handling. Conclusions: Collectively, these insights underscore the pivotal role of inter-tissue crosstalk among skeletal muscle, adipose tissue, bone, and fascia in orchestrating lipid-induced insulin resistance, and highlight the need for integrative strategies that target this multicompartmental network to mitigate metabolic dysfunction in obesity and T2DM. Full article

Epigenetic regulation, particularly DNA methylation, plays a crucial role in plant adaptation to environmental stresses by modulating gene expression without altering the underlying DNA sequence. In response to major abiotic stresses such as salinity, drought, heat, cold, and heavy metal toxicity, plants undergo dynamic changes in DNA methylation patterns. These modifications are orchestrated by DNA methyltransferases and demethylases with variations depending on plant species, genetic background, and ontogenic phase. DNA methylation affects the expression of key genes involved in cellular, physiological, and metabolic processes essential for stress tolerance. Furthermore, it contributes to the establishment of stress memory, which can be transmitted across generations, thereby enhancing long-term plant resilience. The interaction of DNA methylation with other epigenetic mechanisms, including histone modifications, small RNAs, and chromatin remodeling, adds layers of regulatory complexity. Recent discoveries concerning N6-methyladenine have opened new avenues for understanding the epigenetic landscape in plant responses to abiotic stress. Overall, this review addresses the central role of DNA methylation in regulating plant stress responses and emphasizes its potential for application in crop improvement through epigenetic and advanced biotechnological approaches. Full article