Search Results (133)

The improvement of sucrose yield in sugarcane is impeded by the crop’s complex polyploid genome and slow progress in breeding. To clarify how arginine (Arg) regulates sugar metabolism and identify key genes associated with sucrose transport and accumulation in sugarcane, a screening experiment was performed by spraying L-arginine hydrochloride on the leaves and leaf sheaths of three sugarcane varieties (YZ05-51, YZ08-1609, and YT93-159), which differ in growth vigor, leaf morphology and other phenotypic traits. YZ05-51 exhibited the most prominent sugar-increasing effect, and subsequent optimization experiments on its leaf sheaths revealed that 20 g/mu L-arginine hydrochloride at pH 7.0 was optimal, significantly enhancing stem sucrose content. Transcriptomic analysis revealed the upregulation of genes related to sucrose synthesis and transport, with candidate genes enriched in pathways such as starch-sucrose metabolism, glycolysis/gluconeogenesis, and ATP-binding cassette (ABC) transporters. Metabolomic analysis detected 32 sugar metabolites across three categories, of which 24 were differentially abundant (e.g., glucose, galactose, fructose, and mannose). Integrated multi-omics analysis identified key regulatory genes, including SBEs and TPS1 (sucrose synthesis and carbon flux regulation), RBSK, α-amylases, GH28 (starch breakdown, glycolysis, and sugar mobilization), ABC transporters, GTs, and TIM10/TIM12 (sucrose transporter). Collectively, these analyses demonstrate enhanced activity of genes and metabolites involved in sucrose synthesis/transport in leaf sheaths, accompanied by reduced synthesis of other monosaccharides and oligosaccharides. Vigorously metabolizing leaf sheaths is more conducive to sucrose transport. This study provides valuable insights into the molecular mechanisms underlying Arg-mediated sucrose accumulation specifically in the sugarcane YZ05-51 sugarcane, highlighting its critical regulatory roles. Full article

Background: Acetaminophen (APAP) overdose remains a major cause of acute liver injury. Although N-acetylcysteine (NAC) is the clinically established antidote for APAP toxicity, its efficacy is greatest when administered early, and additional therapeutic strategies are still needed for patients with delayed presentation or progressive injury. Because APAP hepatotoxicity involves coupled disturbances in redox control, mitochondrial performance, and cellular metabolism, metabolic enzymes that sustain NADPH availability may critically influence disease severity. Malic enzyme 1 (ME1), a cytosolic NADPH-generating enzyme, has not been functionally defined in this context. Methods: To determine the contribution of ME1 to APAP-induced liver injury (AILI), we used hepatocyte-specific ME1 knockout mice, hepatic overexpression and reconstitution approaches, primary mouse hepatocytes, and an enzymatically inactive ME1 mutant. Liver injury and associated changes in oxidative stress, mitochondrial function, energy metabolism, autophagic flux, and endoplasmic reticulum (ER) stress were evaluated using biochemical, histological, molecular, and ultrastructural analyses, together with pharmacological interventions. Results: Genetic loss of ME1 did not substantially alter early APAP metabolic activation-related indices, including APAP-protein adduct formation, but markedly increased hepatocellular metabolic vulnerability after APAP challenge. This phenotype was characterized by enhanced lipid peroxidation, impaired mitochondrial polarization, reduced ATP availability, defective autophagic flux, and amplified ER stress, leading to more severe liver damage. In contrast, ME1 overexpression or reconstitution promoted a more adaptive metabolic response and limited tissue injury. These effects depended largely on ME1 catalytic activity, as protection was markedly weakened with the mutant enzyme. Pharmacological analyses further supported the involvement of AMPK/mTOR-associated autophagy regulation and ER stress adaptation in the downstream actions of ME1. Malic acid also partially attenuated APAP-induced hepatotoxicity in vivo and in vitro. Conclusions: ME1 functions as an endogenous metabolic factor that influences the outcome of APAP-induced liver injury. Its catalytic activity supports hepatocyte survival primarily by preserving reductive capacity, bioenergetic balance, and adaptive stress responses, rather than by altering APAP metabolic activation. Full article

While Peribacillus simplex has been reported to alleviate abiotic stress-induced damage in diverse plant species, its precise functional mechanism in mediating salt tolerance in asparagus remains unclear. The present study sought to uncover the molecular regulatory mechanisms through which strain P10 enhances the salt adaptability of asparagus seedlings. We investigated physiological responses, as well as transcriptomic and metabolomic alterations, in P10-inoculated asparagus seedlings grown under saline conditions. The results demonstrated that P10 inoculation alleviated salt-induced physiological damage by enhancing antioxidant enzyme activities and promoting the accumulation of osmotic regulatory substances. Comparative transcriptomic and metabolomic analyses identified 1659 differentially expressed genes (DEGs) and 128 differentially accumulated metabolites (DAMs) between P10-inoculated and non-inoculated seedlings under salt stress. These DEGs were primarily associated with multiple biological pathways, including phenylpropanoid biosynthesis, nitrogen metabolism, and flavonoid biosynthesis pathways (flavone, flavonol, and total flavonoid synthesis). Metabolomic profiling indicated that organic acids constituted the most abundant class of DAMs, followed by amino acids and their derivatives, and flavonoids. Integrated transcriptomic and metabolomic analyses suggested that P10 optimized the amino acid metabolic network under salt stress by upregulating genes involved in nitrogen assimilation, glutathione biosynthesis, and polyamine biosynthesis, thereby promoting amino acid accumulation and enhancing glutathione and polyamine levels. In addition, P10 markedly stimulated flavone and flavonol biosynthesis while maintaining elevated anthocyanin levels. Overall, P10 mitigated salt stress injury in asparagus by regulating amino acid metabolism to improve osmotic balance and growth stability, while simultaneously redirecting phenylpropanoid flux toward flavone and flavonol biosynthetic pathways to fine-tune stress responses. Full article

Squalene, a high-value triterpenoid precursor widely used in pharmaceuticals and vaccine adjuvants, is primarily sourced from shark liver oil—an unsustainable practice that has driven interest in developing plant-based production alternatives. The first committed reaction in triterpenoid biosynthesis is catalyzed by squalene synthase (SQS), yet no SQS gene has been characterized in Amaranthus tricolor, a species recognized for its high squalene content. Here, we cloned and functionally characterized AtrSQS, a novel squalene synthase gene isolated from A. tricolor for the first time. Sequence analysis revealed that AtrSQS contains conserved domains and six characteristic motifs shared among plant SQSs, with high homology to orthologs from dicotyledonous species. To investigate its functional role in squalene biosynthesis, AtrSQS was overexpressed in Nicotiana tabacum under the CaMV 35S promoter. Transgenic lines exhibited significantly increased AtrSQS expression and accumulated squalene up to 6.81 μg/g dry weight, a 4.76-fold increase over wild-type plants. Additionally, the content of downstream product 2,3-oxidosqualene was also significantly elevated in the transgenic lines. Integrated transcriptomic and metabolomic analyses revealed that AtrSQS overexpression upregulated key mevalonate pathway genes (AACT, HMGS, MVD) and FPPS. Meanwhile, it suppressed competitive carotenoid biosynthesis and the production of an SQS-specific inhibitor, indicating a successful redirection of metabolic flux toward squalene production. These findings demonstrate that AtrSQS is crucial for squalene biosynthesis and provide both a valuable genetic resource and mechanistic insights for engineering plant-based squalene production systems. Full article

Chromochloris zofingiensis, a photosynthetic microalga, has attracted considerable attention due to its ability to simultaneously accumulate lipids and astaxanthin. However, the induction of lipid and secondary metabolite biosynthesis by abiotic stress is typically accompanied by growth inhibition, resulting in a trade-off between metabolite accumulation and biomass production. In recent years, phytohormones have emerged as an effective strategy for regulating microalgal metabolism, owing to their high specificity and low effective dosage. In this study, 5-aminolevulinic acid (5-ALA) was applied under nitrogen-deficient conditions, and its effects on growth, photosynthesis, lipid metabolism, and carotenoid biosynthesis were systematically evaluated through integrated physiological, biochemical, and transcriptomic analyses. The results showed that 5-ALA had no significant effect on biomass accumulation or photosynthetic performance. However, at 2 μM, 5-ALA exhibited the strongest promotive effect on lipid and astaxanthin accumulation, with total fatty acids (TFA) and triacylglycerol (TAG) contents increasing by 13.3% and 25.7%, respectively, and total carotenoids and astaxanthin contents increasing by 15.6% and 17.2%, respectively. Under semi-continuous cultivation, TAG and astaxanthin productivities were enhanced by 13.9% and 22.9%, reaching 164 mg L⁻¹ d⁻¹ and 2.15 mg L⁻¹ d⁻¹, respectively. Transcriptomic analysis revealed that 5-ALA induced only limited transcriptional changes but enhanced glycolysis, central carbon metabolism, and nitrogen recycling, thereby increasing the supply of carbon precursors and energy. Notably, no significant transcriptional changes were observed in the carotenoid biosynthesis pathway, indicating that the enhanced accumulation of total carotenoids and astaxanthin was likely driven by increased metabolic flux. In terms of lipid metabolism, the upregulation of pathways involved in the conversion of membrane lipids into TAG, together with the downregulation of TAG degradation pathways and enhanced carbon flux, collectively promoted TAG accumulation. Overall, this study demonstrates that supplementation with 2 μM 5-ALA provides a practical and cost-effective strategy for the efficient co-production of lipids and astaxanthin in C. zofingiensis. Full article

Enhancing egg production in geese without antibiotics remains a challenge in poultry science. This study compared the effects of Lactobacillus (LAB) and Bacillus (BAC) probiotics on laying performance, gut microbiota, and serum metabolism in Zhedong White geese. Birds were fed a control diet or diets supplemented with LAB or BAC. Egg production and quality were monitored throughout the trial. Serum metabolomics and fecal 16S rRNA sequencing were integrated with KEGG enrichment and correlation analyses to uncover functional mechanisms. Both probiotics improved laying performance and egg quality. Total egg production of the LAB group was 8.5% higher than that of the BAC group (p < 0.05). The LAB group’s advantage in egg production was consistent with its stronger activation of the steroid hormone biosynthesis pathway (elevated serum corticosterone and tetrahydrocorticosterone indicated an overall enhancement of steroidogenic flux). Simultaneously, the LAB group exhibited a more efficient conversion of L-phenylalanine to catecholamine precursors, which drove activation of the neuroendocrine reproductive axis. The BAC group showed more significant changes in nitrogen and energy metabolism pathways and a more pronounced expansion of energy-harvesting Firmicutes. These findings reveal two strain-specific regulatory pathways: LAB functions through the “aromatic amino acid–neuroendocrine–steroid hormone axis,” while BAC relies on the “gut microbiota–energy metabolism” pathway, with direct implications for the precise application of probiotics under antibiotic-free farming conditions. Full article

Algae rarely occur as solitary phototrophs in nature or engineering; instead, they are embedded in complex bacterial consortia that control their physiology, productivity and ecological performance. The phycosphere, a microscale niche rich in algal exudates, promotes extensive metabolic exchange and chemical signaling, defining these associations. Bacteria capitalize on the dissolved organic carbon released by algae, providing growth supporting molecules such as vitamins, trace metals, and siderophores, as well as regenerated inorganic nutrients. Bidirectional beneficial interactions range from obligate mutualism to facultative commensalism and antagonism, depending on environmental context and community membership. Bacterial partners can stimulate algal growth, morphogenesis, and stress tolerance, as well as modulating defense and programmed cell death during the decline and bloom succession of algae resulting from algicidal taxa. Metabolic cooperation, QS signaling, extracellular enzyme activity, and chemically induced gene expression produce the exometabolome in the phycosphere, which in turn reprograms gene expression in all partners. Recent advances in multi-omics toolboxes, single-cell isotopic analyses, and microfluidics have greatly enhanced our understanding of the functional and spatiotemporal orientation of algal microbiomes. Ecologically, algal–bacterial interactions manage the phytoplankton community structure, control HABs, and modulate carbon and nutrient fluxes in both marine and freshwater realms. Biotechnologically, engineered algal–bacterial consortia are a promising tool for enhancing biomass production, stabilizing large-scale cultivation, improving wastewater treatment, and upgrading biofuels and fine chemicals. Despite these notable research advances, the context- and species-dependent complexity of multispecies interactions remains a major obstacle to their practical modeling and scalable implementation. Integrative research frameworks that combine molecular, ecological, and bioengineering approaches are urgently needed to unlock the full potential of sustainable applications in the future. Full article

Fruit flesh thickness is one of the key factors affecting the yield and quality of bitter melon, and its regulatory mechanisms remain unclear. One thick-flesh germplasm (KF) and one thin-flesh germplasm (NF) with significantly different flesh thicknesses were screened from 70 bitter melon germplasms. Through phenotypic surveys, combined metabolomic and transcriptomic analyses, and exogenous sugar treatments, the regulatory mechanisms on flesh thickness were preliminary investigated. The results showed that flesh thickness of the two germplasms remained stable during different years and seasons. Metabolomic and transcriptomic analyses revealed that fructose and mannose metabolism pathway significantly enriched in both omics datasets. The expression of key enzyme encoding genes from this pathway exhibited various expression patterns. In KF, most genes showed significantly higher expression levels than NF, with synergistic expression predominating among genes. Soluble sugar content was positively correlated with gene expression, while HXK, SDH, and TPI activities were negatively correlated with most genes, and FBP activity was positively correlated with most genes. Genes affect carbon source metabolic flux distribution by promoting sugar synthesis and inhibiting sugar respiration consumption. Exogenous sugar treatment exhibited germplasm-specific and concentration-dependent influence of gene expression, with KF primarily showing negative feedback and NF predominantly activating expression. Fruit flesh thickness was significantly positively correlated with the synergistic high expression of sugar metabolism genes and soluble sugar accumulation. This study provides a theoretical basis for molecular improvement of bitter melon fruit flesh thickness. Full article

Environmental pH plays a critical role in microbial fermentation processes. Weizmannia coagulans attracts particular attention for exceptional acid tolerance and lactic acid productivity. Yet acidic stress impacts on its cell division regulation remain unclear. Here, a critical pH value (pH 4.20) for growth inhibition of the Gram-positive bacterium Weizmannia coagulans strain BC99 was first established. Transcriptomic analysis of metabolic pathways was then performed. The multi-layered regulatory network underlying acid stress-induced cell division was elucidated. Integrated transcriptomic and physiological analyses reveal that acid stress triggers multigene expression reprogramming. This drives core metabolic network reorganization, coordinately regulating division processes. RNA-seq analysis demonstrated acid stress triggered differential expression of division genes (FtsZ/Q downregulation), ATP synthase suppression, and peptidoglycan transport reduction, while enhancing membrane rigidification (Cfa) and magnesium homeostasis (CorA). The PhoPR dual-component system emerged as a central regulator, inhibiting septal assembly via RipA hydrolase and RpsU ribosomal suppression while rerouting carbon flux to glycolysis, elucidating bacterial acid adaptation mechanisms. Collectively, these adaptive changes prioritize cell survival over active proliferation under acidic conditions. This study provides molecular insights into how W. coagulans preserves viability under acid stress, offering a theoretical basis for optimizing its performance in probiotic applications. Full article

Background/Objectives: Metabolic reprogramming is a hallmark of cancer, enabling tumor cells to sustain proliferation, survive under metabolic stress, and develop therapeutic resistance. While oncogenic signaling pathways regulating cancer metabolism have been extensively studied, increasing evidence indicates that non-coding RNAs (ncRNAs) play essential roles in coordinating metabolic adaptation. This review aims to synthesize current knowledge on long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) as important but relatively less characterized regulators of cancer metabolic adaptation and discuss their potential as biomarkers and therapeutic targets. Methods: We analyzed their roles across multiple types of cancer, prioritizing studies that integrate ncRNA profiling with metabolomics and mechanistic investigations, with particular attention to their diagnostic, prognostic, and predictive value. Results: LncRNAs and circRNAs regulate major metabolic pathways, including glycolysis, mitochondrial function, glutaminolysis, lipid metabolism, and redox balance. They act through transcriptional and epigenetic mechanisms, protein scaffolding, peptide encoding, and miRNA sponging, frequently converging on key regulators such as HIF-1α, c-Myc, p53, AMPK, and mTOR. However, many reported associations remain largely correlative, with limited integration of quantitative metabolic flux analyses and insufficient validation in physiologically relevant models. Conclusions: Although lncRNAs and circRNAs constitute an important context-dependent regulatory layer linking oncogenic signaling to metabolic reprogramming, future studies should combine ncRNA perturbation with stable isotope tracing, fluxomics, spatial metabolomics, long-read sequencing, and single-cell approaches to define causal and spatially resolved metabolic functions. Such integrative strategies may improve biomarker development and support ncRNA-informed, metabolism-oriented therapeutic interventions. Full article

Soybean seed quality is defined by an inverse relationship between oil and protein content. Understanding the spatiotemporal regulation of this trade-off is crucial for breeding. This study aims to dissect the transcriptomic networks governing carbon and nitrogen partitioning during seed development. Here, transcriptomic and co-expression network analyses were performed on cotyledon and seedcoat tissues of high-protein (HP) and low-protein (LP) soybean cultivars across three seed developmental stages. We identified 4910 HP/LP-specific differentially expressed genes (DEGs), with striking transcriptional alterations in the early developmental stage. Notably, some important DEGs were enriched in carbon/lipid metabolism, protein folding, and hormone/circadian signaling pathways, among which key gene families (e.g., OLEs, SWEETs, HSPs), core regulators (e.g., LACS, L1L, ABF1), and QTL-localized candidate genes (e.g., FA9) were characterized. Mechanistically, C/VIF1-mediated post-translational inhibition of CWINV1 may restrict carbon flux to oil synthesis in HP seeds; upstream circadian/hormone signaling and L1L-sHSPs jointly promote protein deposition, uncoupling the oil–protein trade-off and enabling HP trait formation. In contrast, LP cultivars upregulated SWEETs, OLEs, and LTPs to facilitate high carbon flux into lipid biosynthesis and storage. These findings provide valuable genetic targets for precision breeding programs aimed at optimizing resource allocation. Full article

This study compared the bioenergetic profiles of immature and in vitro–matured bovine cumulus–oocyte complexes (COCs) using Seahorse extracellular flux technology, with the aim of establishing standardized conditions for real-time metabolic assessment during in vitro maturation (IVM). Groups of five COCs were analysed prior to maturation and after 22 h of IVM using the Seahorse XFp Analyzer to measure oxygen consumption rate (OCR, pmoL/min) and extracellular acidification rate (ECAR, mpH/min), providing dynamic readouts of oxidative phosphorylation and glycolysis that extend beyond conventional endpoint assays. To optimize assay performance, three media were first evaluated: TCM199, DMEM/F12, and HEPES-buffered synthetic oviductal fluid (HSOF). HSOF yielded the most reliable readings for immature COCs, whereas TCM199 provided superior conditions for mature COCs. Adhesion strategies were then tested by comparing uncoated wells with wells coated with fibronectin, concanavalin A, or Matrigel^®. Sequential injections of oligomycin and rotenone plus antimycin A enabled partitioning of mitochondrial and glycolytic contributions to ATP production. COC maturation was associated with a clear metabolic shift from glycolysis toward oxidative metabolism. Immature COCs displayed a predominantly glycolytic phenotype, while mature COCs showed increased active mitochondrial ATP production. Adhesion conditions markedly affected the detected metabolic profile: concanavalin A and fibronectin supported effective attachment and were associated with robust energy metabolism, whereas Matrigel^® and poor adhesion were linked to quiescent profiles with low OCR and ECAR signals. Together, these data define practical assay parameters for extracellular flux analysis of COCs and highlight the increasing reliance on mitochondrial function as a hallmark of oocyte maturation, supporting improved metabolic phenotyping for IVM optimization. Full article

Mollisols represent foundational agricultural soils in which high organic carbon (C) and active microbiomes sustain fertility and mediate global C cycling. However, decades of intensive cultivation have depleted soil organic C (SOC) and degraded soil structure and function. Enhancing C sequestration in agricultural Mollisols through the incorporation of organic residue, such as crop residues, organic waste, and spent mushroom substrates has become an urgent scientific and management priority. This review integrates advances from the past decade, combining stable isotope probing, multi-omics analyses, and ultrahigh-resolution molecular characterization to elucidate how microorganisms mediate C sequestration during organic residue return and decomposition. We propose a four-dimensional conceptual framework, “substrate–microenvironment–metabolic pathway–residue stabilization,” that links microbial metabolism with long-term C persistence in Mollisols. We further highlight that organic residue inputs promote CO₂ sequestration via fermentation–autotrophy coupling, nitrifying autotrophy, and microbial mixotrophy. Major C sequestration pathways operate synergistically across redox microenvironments, forming stratified metabolic networks that sustain continuous C cycling. The chemical composition and decomposition kinetics of organic residue governs substrate and energy fluxes for microbial C sequestration, while soil redox status, and nutrient coupling (Carbon–Nitrogen–Phosphorus–Sulfur) collectively direct C flow toward stabilization. Microbial necromass and extracellular polymers achieve long-term C storage through mineral adsorption and microaggregate formation. Finally, we summarize recent methodological advances for tracing microbial CO₂ sequestration in agricultural Mollisols and identify key research needs on residue formation, C use efficiency, and aggregate-mineral protection mechanisms. This synthesis establishes a mechanistic foundation for biologically regulated C management and offers guidance for sustainable cropland restoration. Full article

Although the role of proline (Pro) as an important osmolyte has been extensively studied, there are few comprehensive studies on their metabolism under salinity conditions. We investigated Pro metabolism in two habanero pepper varieties with contrasting salinity responses: Mayan Chan (tolerant) and Mayan Ba’alche (sensitive). First, a phylogenetic analysis of enzymes participating in their biosynthesis, P5CS and P5CR, and in its degradation, PDH, was performed. Additionally, the levels of their transcripts, the enzymatic activity, and Pro content were determined in plants subjected to 150 mM NaCl by short (0, 24, 48 and 72 h) and long (seven days) periods. Potassium flux in roots exposed to NaCl, in the absence or presence of Pro, was also measured. Phylogenetic analysis showed that the sequences were grouped according to their taxonomic family and not by salt tolerance of the species. Molecular and biochemical analyses showed significant differences between organs and varieties; the tolerant variety showed highest levels of transcripts, biosynthesis enzymes activities and accumulation of Pro. The results suggested that Pro metabolism in habanero pepper is a complex process, that is regulated at different levels and differentially between organs and varieties. Exogenous Pro only reduced potassium efflux in the sensitive variety exposed to NaCl, suggesting that a precise threshold of this amino acid is required to perform this function. Full article

Colorectal cancer (CRC) progression and therapy resistance are driven in part by metabolic reprogramming and the persistence of cancer stem-like cells (CSCs). The seven in absentia homolog 2 (SIAH2)/with-no-lysine kinase 1 (WNK1) signaling axis has emerged as a potential regulator of these processes, yet its functional role in CRC metabolism and tumor–stroma crosstalk remains incompletely understood. Integrated analyses of The Cancer Genome Atlas–Colon Adenocarcinoma (TCGA-COAD) and Gene Expression Omnibus (GEO, GSE17538) datasets revealed significant upregulation of SIAH2 and WNK1 in CRC tissues, with strong positive correlations to glycolysis- and hypoxia-associated genes, including PFKP, LDHA, BPGM, ADH1A, ADH1B, and HIF-1α. Single-cell and clinical profiling further demonstrated preferential enrichment of SIAH2 in undifferentiated, stem-like tumor cell populations. Functional studies across multiple CRC cell lines showed that SIAH2 silencing suppressed proliferation, clonogenic growth, tumor sphere formation, and cell-cycle progression, whereas SIAH2 overexpression exerted opposite effects. Seahorse extracellular flux analyses established that SIAH2 promotes glycolytic capacity and metabolic flexibility. At the protein level, SIAH2 regulated glycolytic enzymes and WNK1/hypoxia-inducible factor-1α (HIF-1α) signaling, effects that were amplified by cancer-associated fibroblast (CAF)-derived conditioned medium. CAF exposure enhanced SIAH2 expression, CSC spheroid growth, and resistance to fluorouracil, leucovorin, and oxaliplatin (FOLFOX) chemotherapy, whereas SIAH2 depletion effectively abrogated these effects. Collectively, these findings identify the SIAH2/WNK1 axis as a central metabolic regulator linking glycolysis, CSC maintenance, and microenvironment-driven therapy resistance in CRC, highlighting its potential as a therapeutic target. Full article