Search Results (515)

This narrative review synthesizes current knowledge on MADS-Box 27 (OsMADS27), a member of the AGL17 clade in rice that has emerged as a regulatory node linking nitrate signaling, root development, and abiotic stress tolerance. Because most functional and mechanistic studies on OsMADS27 to date have been conducted in rice, this review is centered on Oryza sativa, with cross-species comparisons used for evolutionary and comparative context. Specifically, we summarize the gene and protein structure, phylogenetic position, expression profile, upstream and downstream regulation, and emerging functional significance of OsMADS27. OsMADS27 is a typical MIKC-type MADS-box protein with root-preferential expression, and its activity is strongly influenced by nitrate availability and miR444-mediated regulation. Evidence from functional genomics, transcriptomics, ChIP-based studies, and transgenic analyses suggests that OsMADS27 contributes to the regulation of root architecture, nitrate uptake, hormonal crosstalk, and stress-responsive pathways. Notably, OsMADS27 enhances salt tolerance through nitrate-dependent activation of downstream targets such as OsHKT1;1 and OsSPL7, contributing to ion homeostasis and salinity tolerance. Recent findings also suggest roles in grain size regulation and yield improvement, expanding its significance beyond root biology. This review compares OsMADS27 with AGL17-clade genes and highlights its value for crop improvement aimed at salinity tolerance and nitrogen use efficiency. However, important research gaps remain, particularly the limited field-level validation, the absence of integrated multi-omics analyses, and the lack of functional studies of OsMADS27 orthologs in non-rice crops. Overall, OsMADS27 represents promising rice-centered target for future biotechnology applications, while its translational relevance to other cereals remains to be established through orthology analysis and field-level evaluation. Full article

Plants are constantly exposed to diverse abiotic stresses, including drought, salinity, and extreme temperatures, which severely limit growth, development, and crop productivity. These stresses disrupt physiological, biochemical, and molecular processes, leading to reduced photosynthesis, altered water and ion homeostasis, and accumulation of reactive oxygen species (ROS). Plants have evolved sophisticated sensing and signaling mechanisms to perceive these stresses, with phytohormones playing central roles in mediating adaptive responses. Key hormones, including abscisic acid (ABA), salicylic acid (SA), jasmonates (JAs), gibberellins (GAs), auxin (IAA), ethylene (ET), melatonin, and strigolactones (SLs), regulate stress tolerance by controlling stomatal behavior, root architecture, antioxidant systems, osmolyte accumulation, and stress-responsive gene expression. Importantly, these hormones operate within an intricate network of crosstalk, integrating multiple signaling pathways to balance growth and stress adaptation. Interactions among ABA, GA, JA, SA, auxin, ET, SLs, and melatonin enable plants to coordinate transcriptional regulation, protein phosphorylation, and ROS signaling, optimizing survival under fluctuating environmental conditions. Understanding the molecular mechanisms underlying hormonal crosstalk and their roles in abiotic stress tolerance provides valuable insights for developing resilient crops in the face of climate change. Full article

Abiotic stresses limit crop productivity by disrupting water relations, carbon assimilation, nutrient acquisition, membrane stability, and redox homeostasis. Partial root-zone irrigation (PRI), commonly implemented as partial root-zone drying (PRD), is often viewed as a deficit-irrigation strategy to improve water-use efficiency; however, this view underestimates the biological consequences of spatial root-zone heterogeneity. This review evaluates PRI as a spatially structured, priming-like framework for crop adaptation to abiotic stress. Available evidence indicates that localized drying and wet-side water uptake can coordinate root sensing, hydraulic–chemical signaling, abscisic acid delivery, hormone crosstalk, xylem-mediated regulation, and stomatal control. Beyond gas exchange, PRI is associated with photosynthetic maintenance, osmotic adjustment, antioxidant and redox regulation, root architectural plasticity, nutrient acquisition, and metabolic reprogramming. Evidence is strongest for drought, whereas responses to low temperature, salinity, heat-associated evaporative demand, and combined stresses remain more context-dependent. Emerging work also links PRI to rhizosphere restructuring and microbiome shifts, but the causal mechanisms and field reproducibility remain unresolved. We argue that future progress requires matched PRI–deficit-irrigation comparisons, standardized switching thresholds, shared physiological and molecular readouts across crops, high-resolution root biology, and commercially realistic field validation. This framing distinguishes conserved physiological outcomes from mechanisms that may differ among crops, genotypes, and irrigation designs. Full article

Seed germination is a critical determinant of seedling establishment, stress resistance, and final yield. ABA catabolism plays a central role in releasing seed dormancy and promoting germination, and ABA8ox is the key rate-limiting enzyme in this process. In this study, we used wild-type maize B73, and ZmABA8ox1b CRISPR-Cas9 knockout mutant as materials to investigate the biological function of ZmABA8ox1b. Compared with the wild type, the zmaba8ox1b mutant significantly delayed seed germination and enhanced the sensitivity to exogenous ABA. Endogenous ABA content in mutant embryos was drastically increased, indicating that ZmABA8ox1b is essential for ABA degradation during germination. The loss of ZmABA8ox1b function led to the activation of the ABA signaling pathway and severely impaired the responsiveness to exogenous ABA. Moreover, the mutation disturbed the expression and ABA responsiveness of auxin, gibberellin, ethylene, jasmonic acid, and brassinosteroid pathways, leading to a hormonal network imbalance. In conclusion, ZmABA8ox1b positively regulates maize seed germination by coordinating ABA catabolism and multi-hormone signal crosstalk. This study preliminarily clarifies the molecular mechanism of ZmABA8ox1b in germination control and provides important gene resources and theoretical support for breeding maize varieties. Full article

Squalene is a triterpene with potent biological activities. Squalene (C₃₀H₅₀) is a linear polyunsaturated hydrocarbon composed of six isoprene units and six carbon–carbon double bonds. It serves as an essential precursor for sterols, steroid hormones, and vitamin D in humans and exhibits antioxidant, anti-tumor, and lipid-regulating properties. In plants, squalene is produced via the mevalonate (MVA) and 2-C-methyl-D-erythritol-4-phosphate (MEP) pathways. The key rate-limiting enzymes in these pathways include 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR), farnesyl diphosphate synthase (FPS), and squalene synthase (SQS). Camellia oleifera, a unique woody oil crop native to China, is valued for its high-quality edible oil and as a rich natural source of squalene. This review provides a systematic overview of recent progress in squalene biosynthesis in C. oleifera. It summarizes the structural characteristics and biosynthetic routes. It further elaborates on the multi-level regulatory network modulated by transcription factors (WRKY, bHLH, MYB, and ERF), phytohormones (jasmonic acid, abscisic acid, and gibberellin), and abiotic factors (light and drought). Notably, this review distinguishes earlier foundational studies from recent breakthroughs and integrates emerging progress on squalene’s non-canonical functions and pathway crosstalk. It further highlights novel regulatory mechanisms unique to C. oleifera (e.g., CoWRKY15, CoMYB1, and CoMYC2). By bridging molecular regulation with practical breeding and metabolic engineering, this review lays a solid theoretical foundation for cultivating high-squalene C. oleifera varieties. It represents a prominent innovation relative to previously published studies. Full article

Plants are constantly exposed to a wide range of abiotic stresses that have significant negative impacts on growth and yield. Plant acclimation to these stresses is governed by integrated classical phytohormone and plant peptide hormone signalling networks that control the ability of a plant to survive and adapt to extreme environments. Classical phytohormones, including abscisic acid, auxins, gibberellins, cytokinins, jasmonates, salicylic acid, brassinosteroids, and the recently recognised phytomelatonin, act in concert with peptide-based plant hormones, among which C-terminally encoded peptides (CEPs) play prominent roles in coordinating stress perception, signal transduction, and adaptive responses throughout the plant. These integrated networks control stomatal behaviour, photosynthesis, osmolyte and antioxidant levels, root architecture, and energy metabolism, thereby helping plants maintain homeostasis and optimise survival while sustaining minimal growth under unfavourable conditions. Under stressful conditions, these networks do not operate in isolation but form highly dynamic, context-dependent regulatory circuits in which each physiological process is simultaneously regulated by multiple hormones acting through convergent and overlapping signalling pathways. Phytomelatonin has emerged as a particularly important integrative node within these networks, functioning both as a potent direct antioxidant through sequential ROS-scavenging catabolite cascades and as a bidirectional regulator of classical phytohormone signalling under diverse abiotic stresses. New technologies in the fields of transcriptomics, proteomics, phosphoproteomics, metabolomics, and systems biology have provided new information on the dynamic relationships between classical phytohormones and plant peptide hormones, revealing candidate regulatory nodes and transcription factor networks that mediate stress adaptation at molecular, biochemical, and physiological levels. However, it is important to distinguish between correlative associations identified through omics profiling and causal regulatory relationships validated through rigorous genetic and biochemical experimentation, as most omics-derived candidates remain to be functionally established. Empirical studies demonstrate how these networks can be used to improve crops by increasing stress tolerance through modulating classical phytohormone and plant peptide hormone signalling, including through exogenous phytomelatonin application, CRISPR-mediated hormone pathway editing, and CEP pathway manipulation, to produce resilient cultivars without reducing yields. Although these advances represent significant progress, challenges remain, including the inherent complexity and redundancy of the networks, context-dependence and severity-dependence of hormonal responses, the persistence of a significant translational gap between laboratory findings and field application, and incomplete mechanistic understanding of peptide hormone roles under combined stress conditions. Addressing these challenges will require integrative multi-omics approaches, higher-order computational modelling, and rigorous field-based functional validation alongside emerging tools such as synthetic biology and precision breeding. Full article

Background/Objectives: Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease traditionally viewed through a purely dermatologic lens. However, this perspective fails to explain stress-induced flares, menstrual cycle-linked exacerbations, and severe pain and itch disproportionate to visible cutaneous inflammation. This narrative review synthesizes evidence supporting a neuroendocrine–immune model of HS pathogenesis, with emphasis on mechanisms underlying pain and itch. Methods: A comprehensive literature search was conducted using PubMed, Scopus, and Web of Science databases (January 1990–September 2025) with terms including hidradenitis suppurativa, neuroendocrine mechanisms, HPA axis, sex hormones, neuropeptides, pain (including nociceptive and neuropathic pain, burning, and dysesthesia), and pruritus (itch). Eligible studies included peer-reviewed research examining hormonal, stress-related, or neuropeptide mechanisms in HS. Data were synthesized into thematic categories: endocrine influences, HPA axis function, neuropeptide signaling, immune crosstalk, and clinical implications. Results: Sex hormones promote follicular occlusion and modulate immune responses, explaining perimenstrual flares. Prolactin amplifies inflammation during stress through immune cell activation. Insulin resistance and adipokine imbalance create pro-inflammatory conditions. Chronic stress induces HPA axis dysfunction with cortisol resistance, exacerbating inflammation. Neuropeptides released from cutaneous nerves amplify immune activation and directly mediate pain and itch. These pathways establish self-perpetuating feedback loops wherein inflammation drives stress, and neuroendocrine dysfunction amplifies immune responses. Conclusions: HS represents a systemic disorder with a strong neuroendocrine–immune component, rather than a purely dermatologic condition. This framework supports multidisciplinary management integrating hormonal therapies, targeted immunomodulation, and stress reduction. Future research should characterize neuroendocrine biomarkers and test combination therapies targeting multiple system nodes. Full article

Metamorphosis in insects is regulated by hormonal signals and metabolic pathways. In this study, we characterized a 20E-mediated miR-2788/Treh1 regulatory axis involved in the larval-to-pupal transition in the leaf beetle Galeruca daurica. Dual-luciferase assays and expression profiling suggest that miR-2788 directly targets and suppresses trehalase 1 (Treh1), a key enzyme for trehalose hydrolysis. We found that exogenous 20E treatment significantly downregulated miR-2788, leading to the derepression of Treh1 and increased expression of chitin biosynthetic genes (CHI, CHS, and GPI). Conversely, miR-2788 overexpression or Treh1 silencing via RNAi resulted in massive trehalose accumulation, reduced chitin synthesis, and lethal developmental arrest during the metamorphic transition. Furthermore, pharmacological inhibition of Treh1 with Validamycin not only recapitulated these chitin-deficiency phenotypes but was also associated with an upregulation of miR-2788. These results describe a signaling cascade where 20E modulates the conversion of carbohydrate to chitin through the miR-2788/Treh1 axis. This study advances our understanding of hormonal–miRNA–metabolic crosstalk and identifies miR-2788 as a potential target for RNAi-based biopesticide development. Full article

Cold stress (CS) represents a major environmental factor that adversely affects plant growth, development, and productivity. To cope with low-temperature conditions, plants have evolved sophisticated mechanisms for CS perception and response, mediated through complex cellular signaling networks and physiological processes. Central to these adaptive responses are phytohormones, which function either independently or through synergistic and antagonistic interactions to fine-tune CS tolerance. This review synthesizes current knowledge on the roles of major classical phytohormones and signaling metabolites in regulating CS tolerance in plants. We first outline the molecular mechanisms involved in CS sensing and signal transduction, highlighting the roles of membrane-associated sensors, calcium signaling, and downstream transcriptional networks. Then, we discuss the contributions of key classical phytohormones, including auxin, abscisic acid, ethylene, salicylic acid, cytokinin, jasmonic acid, brassinosteroids, gibberellic acid, strigolactones, and signaling metabolites, including melatonin and gamma-aminobutyric acid, to CS tolerance, highlighting their individual and interacting roles in modulating gene expression regulation, antioxidant defense and physiological adaptations. We also discuss the crosstalk between these hormones, emphasizing the dynamic and often context-dependent nature of their interactions in response to CS. Furthermore, the review highlights recent advances in CRISPR/Cas9-based genome editing strategies targeting phytohormone biosynthesis, signaling, and response pathways to improve CS tolerance in plants. By integrating hormonal signaling, molecular regulation, and modern biotechnological tools, this review provides a comprehensive framework for understanding phytohormone-mediated CS adaptation and offers perspectives for developing climate-resilient crops through genetic and agronomic approaches. Full article

In recent years, plant stress biology has moved beyond single-pathway descriptions toward an integrated framework in which stress perception, hormonal control, and gene regulation are tightly interconnected. Early events such as membrane-associated sensing, calcium influx, reactive oxygen species (ROS) generation, and kinase activation converge with phytohormonal networks to shape context-dependent responses. Within this framework, abscisic acid, salicylic acid, jasmonates, ethylene, auxin, cytokinins, gibberellins, brassinosteroids, and strigolactones function not as isolated regulators but as components of a dynamic signaling matrix that balances survival, defense, growth restraint, and recovery. These hormonal signals are ultimately translated into adaptive outcomes through extensive transcriptional and post-transcriptional reprogramming mediated by transcription factors, RNA-based regulators, chromatin remodeling, and stress memory mechanisms. This review synthesizes current understanding of how plants integrate stress perception, phytohormonal crosstalk, and transcriptional regulation to establish stress tolerance. We first examine the molecular basis of stress sensing and early signaling. We then discuss the central functions of major phytohormones and the logic of hormone–hormone interaction networks in coordinating stress adaptation. Next, we analyze transcriptional, post-transcriptional, and epigenetic mechanisms that determine response specificity, intensity, and persistence. We further highlight points of convergence between abiotic and biotic stress responses and discuss how combined stresses challenge traditional single-stress models. Finally, we consider the roles of omics, systems biology, and translational technologies in decoding and engineering stress-resilient phenotypes. By integrating these perspectives, this review presents plant stress tolerance as a multilevel systems property and outlines key priorities for future research aimed at developing climate-resilient crops. Full article

Cytokinin (CK) is a central regulator of plant development, yet its roles cannot be understood fully without considering how CK signaling was assembled during evolution and redeployed in different physiological contexts. In this review, we examine how prokaryotic two-component modules were elaborated into the land–plant CK system and how this system now integrates biosynthesis, transport, receptor selectivity, and feedback control to shape developmental and symbiotic outcomes. We argue that three recurring interpretive dimensions are especially useful for organizing current evidence: compartmentalized CK pools, context-dependent decoding of local CK availability, and the coupling of local CK responses to whole-plant nutrient status. These dimensions help organize current observations on why CK effects in arbuscular mycorrhiza (AM) are often conditional and readout-dependent, whereas evidence from legume–rhizobium symbiosis supports a more direct role for CK in cortical competence, nodule organogenesis, and autoregulation of nodulation. Rather than treating CK as a generic positive regulator of symbiosis, we propose that it functions as a spatially partitioned and nutritionally gated integrator whose outputs depend on cell type, developmental stage, transport route, and resource context. We conclude by highlighting key mechanistic gaps—particularly in transporter-resolved CK partitioning and systemic integration—and by outlining experimentally testable priorities for translating CK biology into crop improvement. Full article

Cardiac fibrosis is a central determinant of heart failure progression and arises from pathological remodeling characterized by fibroblast activation, myofibroblast differentiation, and excessive extracellular matrix deposition. In contrast, physiological remodeling permits adaptive cardiac growth without net fibrosis. Pregnancy represents an underexplored physiological model of reversible cardiac remodeling. In response to hemodynamic load, the maternal heart undergoes hypertrophic growth that resolves postpartum, constituting a natural paradigm of fibrosis-resistant cardiac adaptation. Pregnancy and lactation are accompanied by profound endocrine and immune reprogramming of maternal tissues. We propose that this hormonal milieu orchestrates coordinated crosstalk among endothelial cells, fibroblasts, and immune cell populations to suppress profibrotic pathways and preserve extracellular matrix homeostasis. Candidate regulators include estrogen, progesterone, prolactin family peptides, relaxin, oxytocin, and components of the renin–angiotensin–aldosterone system. During the postpartum and lactational period, prolactin and oxytocin may further promote reverse remodeling. These hormones likely act by modulating local cytokine and growth factor networks that otherwise drive fibroblast activation. By focusing on non-myocyte cardiac cells and extracellular matrix dynamics, this review positions pregnancy as a translational model to uncover endogenous anti-fibrotic mechanisms and identify novel therapeutic strategies for cardiac fibrosis. Full article

Light and drought antagonistically regulate stomatal movement, yet the mechanisms for integrating these conflicting signals remain unclear. In this study, the stomatal aperture and photosynthetic parameters under red light (RL), blue light (BL), and white light in different water regimes were evaluated. Transcriptome analysis was conducted during a 0–6 h period of BL exposure, with or without drought, to explore the molecular mechanisms underlying BL and drought-mediated stomatal movement. Under non-drought conditions, BL significantly enhanced stomatal conductance, transpiration rate, and stomatal aperture. After drought stress, BL-treated seedlings exhibited the greatest reductions in these indicators. Transcriptomic analysis revealed that both BL-responsive genes and drought-responsive genes were significantly enriched in overlapping pathways related to plant hormone signal transduction, and biological processes of water/fluid transport. Among these, the aquaporin gene CsPIP2;3 was identified as a core node in the crosstalk between BL and drought signals, and a potential key regulator of stomatal movement. Tissue-specific expression analysis showed its highest expression in mature leaves; GUS staining further confirmed its expression in guard cells and vascular bundles, while subcellular localization verified the plasma membrane localization of its encoded protein. The transcriptomic data provide novel insights into the mechanisms underlying stomatal movement regulated by BL and drought. Full article

Colorectal cancer (CRC) shows consistent sex-related differences in incidence, anatomic distribution, molecular subtype, immune context, and clinical outcome. However, these differences are often discussed through broad parallel themes such as hormones, genetics, or the microbiome, rather than through the biological settings in which sex meaningfully modifies tumor behavior. This review argues that sex is most informative in CRC when treated as a contextual modifier whose relevance emerges only after integrating tumor sidedness, mismatch repair status, oncogenic background, immune ecology, and age at onset. The clearest signals arise from interaction-based contexts, particularly when sex is interpreted together with tumor sidedness and dMMR/MSI-H or BRAF-linked disease states. Current evidence indicates that women are enriched for proximal or right-sided, microsatellite instability-high, mismatch repair-deficient, CpG island methylator phenotype-high, and BRAF-associated CRC, whereas men more often present with distal disease and a higher overall burden. Mechanistic studies further show that sex-related differences extend beyond hormone exposure to include KRAS–STAT4–KDM5D signaling, site-specific immune-checkpoint programs, metabolic phenotypes, epigenetic biomarker variation, and microbiota–hormone crosstalk. These effects are most evident in defined clinical niches, particularly right-sided CRC, mismatch repair-deficient disease, BRAF-mutated metastatic CRC, and early-onset CRC. A sex-aware, subtype-aware, and location-aware framework therefore offers a more clinically useful interpretation of CRC heterogeneity than descriptive male-versus-female comparisons alone. Full article

Background/Objectives: Umami peptides enhance flavor and contribute to appetite regulation (satiety) and metabolic health. By signaling to the orbitofrontal cortex, umami has been shown to improve cognitive function in Alzheimer’s disease dementia. This taste boosts the immune system and induces saliva secretion. However, the molecular mechanisms linking umami peptides to systemic physiology remain poorly understood. This study provides the first integrated analysis of neurological, immunological, and endocrinological pathways activated by umami peptides. Methods: Novel umami peptides were identified using machine-learning and deep-learning analyses from a library of marine-derived bioactive peptides. T1R1-T1R3 heterodimer is the dominant receptor for umami taste transmission in humans, expressed on taste cells, intestinal cells, and hypothalamic tanycytes. Molecular docking confirmed the binding of novel ligands to the T1R1-T1R3 receptor complex. New candidates and experimentally validated umami peptides, identified by sensomics approaches from tauco, chicken soup, pufferfish, and dry-cured ham, were analyzed using gene ontology. Results: The functional enrichment analysis revealed crosstalk among key signaling processes, including glutamatergic and opioidergic pathways. In addition to the role of µ1 opioid receptor (OPRM1), hub gene intersections highlight cholecystokinin (CCK), glucagon-like peptide 1 (GLP-1), and the anorexigenic pro-opiomelanocortin (POMC) neurons as potential regulators of the gut–brain axis in satiety signaling. Chemokine-encoding genes, melanin-concentrating hormone (MCH), oxytocin (OXT), and neurotensin (NTS) were other key target genes. Conclusions: The identified targets reveal the coordinated crosstalk between peripheral and central umami signaling that may contribute to the regulation of feeding behavior, satiety, cognition, memory, learning, and immune function. These network-based insights generate hypotheses and guide the design of nutritional and drug-like effectors for metabolic and cognitive health. Full article