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PubMed2004

Census of orthologous genes and self-organizing maps of biologically relevant transcriptional patterns in chickens (Gallus gallus).

The launch of large-scale chicken expressed sequence tags (EST) projects has placed the chicken in the lead for the number of EST sequences in agriculturally important animals. More than 451,000 chicken ESTs derived from over 158 libraries have been deposited in the NCBI dbEST database as of December 2003. But how many genes these ESTs represent and how they are expressed in different chicken tissues/organs remain undetermined. In the present research, we developed a human gene-based strategy for census of chicken orthologous genes and identification of their expression patterns. Among 34,157 human coding genes used in the study, BLAST analysis revealed that 11,066 genes provisionally matched 248,628 chicken ESTs. Based on the average EST abundance of the orthologous genes, the current public repository of chicken ESTs could represent approximately 20,000 provisional genes. Analysis of gene expression in 14 single tissues/organs showed that approximately 15% of genes were expressed exclusively in single tissue/organ whereas the remaining approximately 85% of genes were co-expressed in two or more tissues/organs. A majority (91.15%) of genes expressed in chicken embryos were also expressed at post-hatch stages, indicating that most genes activated in chicken embryos could serve housekeeping functions. Self-organizing maps (SOM) analysis organized 8807 provisional genes in selected chicken tissues into 98 clusters with each cluster being indicative of common regulatory factors and pathways. A total of 969 provisional orthologous genes were identified as preferentially expressed genes (PEGs) in various chicken tissues/organs (LOD>3.0). No doubt, the present study on gene expression patterns will provide insight into dynamics of metabolic pathways and tissue/organ programming and reprogramming in chickens.

Algorithms↗

PubMed2026

Genome-wide interactions with cadmium exposure in dysglycemia: Populational effects and molecular insights.

Dysglycemia is a complex metabolic disorder governed by the interplay between environmental exposures and genetic factors, yet the precise molecular mechanisms driving these gene-environment (G×E) interactions remains poorly understood. Here, we characterized the population-level landscape and molecular causality underlying the interactions between cadmium (Cd), a widespread environmental toxicant, and genetic susceptibility loci in dysglycemia. By conducting a Genome-wide Environmental Interaction (GWEI) study within a sub-cohort of the China National Human Biomonitoring (CNHBM) cohort (N = 1298), we identified 29 genetic risk loci that significantly interact with Cd burden to exacerbate elevated fasting plasma glucose levels. Functional enrichment integrated with metabolomic profiling unmasked a profound multi-omics convergence, positioning epigenetic modifications (e.g. H3K27me3) and zinc-finger transcription factors (e.g. OVOL2, KLFs) as central regulatory hubs that disrupt metabolic homeostasis. To establish causality, we demonstrated that the rs11743277 A>T variant at the lead G×E locus functions as a Cd-responsive enhancer element, facilitating recruitment of TEAD3 and upregulating TICAM2 expression in CRISPR/Cas9-edited HepG2 cells, especially upon Cd exposure. This initiates a TICAM2-mediated inflammatory response, with elevated pro-inflammatory cytokines (IFN-β, TNF-α, IL-6) impairing downstream insulin signaling and glucose utilization. Collectively, these findings establish a robust paradigm for G×E interactions in complex metabolic disorders, revealing how environmental stressors reprogram genetic susceptibilities through molecular checkpoints and paving the way for tailored, precision-prevention strategies in environmental health.

CRISPR/Cas9 editing↗

PubMed2002

Artificial mammalian gene regulation networks-novel approaches for gene therapy and bioengineering.

Recently developed strategies for targeted molecular interventions in mammalian cells have created novel opportunities in biotechnological and biomedical research with huge economic and therapeutic impact: the design of mammalian cells with desired phenotypes for biopharmaceutical manufacturing, tissue engineering and gene therapy. These advances have been enabled by constructing artificial gene regulation systems with control modalities similar to those evolved in key regulatory networks of mammalian cells. This review highlights recurring cellular regulation strategies and artificial gene regulation technology currently in use for rational reprogramming of cellular key events including metabolism, growth, differentiation and cell death to achieve sophisticated bioprocess and therapeutic goals.

Animals↗

PubMed2026

Tryptophan-driven metabolomic shift in Acidobacteriaceae reveals phytohormones and antifungal metabolites.

UNLABELLED: Acidobacteriota is one of the most abundant phyla in soils and has recently attracted attention for its potential role in promoting phytosanitary benefits. The metabolomic capabilities of this phylum remain poorly characterized, with few experimentally confirmed metabolites described. To address these gaps, we combined untargeted metabolomic profiling with comparative genomic analyses to explore the functional potential of newly isolated Acidobacteriaceae strains. Genome mining across the Acidobacteriota phylum revealed the presence and taxon-specific enrichment of genes associated with plant-related traits, including phytohormone biosynthesis. In parallel, metabolomic analyses of OSMAC-derived extracts uncovered pronounced condition-dependent metabolic variation. Tryptophan supplementation was associated with marked metabolomic reprogramming, including changes in indole-derived metabolites, such as indole-3-acetic acid. Subsequent analyses linked these metabolic shifts to the suppression of phytopathogenic fungi and enabled the identification of malassezindoles and pityriacitrins as active compounds, confirmed by structure elucidation using NMR spectroscopy. Overall, these findings shed light on the previously unexplored metabolic potential of the Acidobacteriota phylum, emphasizing its ecological importance for phytosanitary applications. IMPORTANCE: Despite their ubiquity and genomic diversity, the functional metabolism of members of the Acidobacteriota has largely remained uncharacterized. This study links genomic predictions to experimentally verified metabolomic outputs of Acidobacteriaceae, demonstrating tryptophan-responsive metabolic shifts translating to phytohormones and metabolites suppressing fungal growth. Our work underscores the emerging role of Acidobacteriota as important contributors to soil ecosystem functioning and plant-microbe interactions.

Acidobacteriota↗

PubMed2006

Energetics of the failing heart: new insights using genetic modification in the mouse.

Genetic modification in the mouse heart has provided new and important insights into many aspects of ATP synthesis, supply and utilization and how this changes in the failing heart. Here, three topics based on recent literature will be reviewed: direct manipulation of precursor pool for creatine; the path linking creatine, purine nucleotides and metabolic remodeling; and long-term reprogramming of ATP synthesis pathways. These examples illustrate the value of deleting, over-expressing and mutating specific proteins in our quest for understanding the energetics of the failing heart.

5'-Nucleotidase↗

PubMedDate not supplied

Modulation of glycolysis in neuroepithelial tumors.

Among the features of the reprogrammed neoplastic phenotype there is the metabolic property to display an increased glycolytic capacity and the ability to convert glucose to lactic acid in the presence of oxygen. Human gliomas in vivo and in vitro are capable to metabolize glucose in a way strictly related to the pathological degree of malignancy. The drug Lonidamine [1-(2,4-dichlorobenzyl)-1H-indazol-3 carboxylic acid)] (LND) is able to selectively block hexokinase (HK) activity and, consequently, lactate production only in highly glycolytic (highly malignant) gliomas, stimulating, on the contrary, that of low grade gliomas; this basically depends on the different HK patterns between low and high grade gliomas. LND is under clinical trial in order to evaluate its effectiveness in glioma therapy.

Antineoplastic Agents↗

PubMed1995

Genetic engineering of hybridoma glutamine metabolism.

The murine hybridoma PQXB1/2 cannot be adapted to grow in culture media containing < 0.5 mM glutamine. Transformants selected following electroporation of PQXB1/2 cells with vectors containing a Chinese hamster glutamine synthetase (GS) cDNA under the control of the SV40 early promoter also failed to grow in the absence of glutamine in the culture medium. PQXB1/2 cells have, however, been transformed to glutamine independence following electroporation with a vector containing this glutamine synthetase cDNA under the control of the human cytomegalovirus immediate early promoter. In these cells, sufficient active glutamine synthetase was expressed from one vector per cell to enable growth in glutamine-free media. The specific activity of glutamine synthetase in two transformed cell lines producing parental levels of antibody was increased by 128 and 152%, respectively (0.57 and 0.63 mumol min-1 per 10(6) cells in transformants compared with parental levels of 0.25 mumol min-1 per 10(6) cells). This reprogramming of glutamine synthetase expression and glutamine metabolism is important for developing strategies to deal with ammonia toxicity and the production of cell lines with improved metabolic processes.

Animals↗

PubMed2004

Transcriptional reprogramming in murine liver defines the physiologic consequences of biliary obstruction.

BACKGROUND/AIMS: While the metabolic and histological responses to cholestasis are recognized, the consequences of impaired biliary flow on liver gene expression are largely undefined. We hypothesized that biliary obstruction results in transcriptional reprogramming that dictates the physiologic response. METHODS: We determined global gene expression in murine livers 1-21 days following bile duct ligation. Total hepatic cRNA from experimental and sham mice was hybridized to Affymetrix gene chips. Gene expression data was analyzed by GeneSpring software and validated by Northern analysis. RESULTS: We found 92 genes over-expressed > or =2-fold at one or more time points following bile duct ligation. Functional classification of these genes revealed the activation of three main biological processes in a sequential and time-restricted fashion. At day 1, genes involved in sterol metabolism were uniquely over-expressed, including HMG-CoA reductase, the rate-limiting enzyme of cholesterol biosynthesis. This was followed by an increased expression of growth-promoting genes at day 7, the time point coinciding with peak cholangiocyte proliferation. In later phases (days 14-21), the liver over-expressed genes encoding structural proteins and proteases. CONCLUSIONS: Transcriptional reprogramming in the liver following biliary obstruction favors the activation of genes regulating metabolism, cell proliferation, and matrix remodeling in a time-restricted and sequential fashion.

Animals↗

PubMed2004

Ultra-high-frequency acoustic stimulation and tinnitus control: a positron emission tomography study.

Ultra-high-frequency (UHF) external acoustic stimulation with the UltraQuiet device (UQ) has been reported to provide significant relief of severe disabling-type tinnitus. The nuclear medicine imaging technique of positron emission tomography (PET) was selected as a monitoring system to compare objectively metabolic alterations in brain function before and after UHF/UQ and to correlate the PET data with the subjective behavioral response of patients reporting tinnitus relief. PET of brain was completed on 6 patients randomly selected from a cohort of 15 patients included in a protocol to establish long-term tinnitus relief with UHF/UQ. Twelve specific regions of interest (ROI) were selected for PET of brain examination on the basis of results obtained with single-photon emission computed tomography (SPECT) of brain examinations recommended for patients with severe disabling-type tinnitus and demonstrating significant perfusion asymmetries in the right and left brain ROI of the primary auditory cortex; frontal, temporal, parietal, and medial temporal lobes; and cerebellum. PET of brain results included ratios of post- and pre-UHF/UQ stimulation that demonstrated no random response in the selected PET of brain ROI and ratios of post- and pre-UHF/UQ stimulation that demonstrated three categories of response in the selected PET brain ROI for all six patients: hypermetabolism in three patients; hypometabolism in two; and a mixed response in one. Correlation was established for each patient among PET and electrophysiological responses of alteration in minimal masking levels, the residual UHF neuronal response as reflected in the UHF audiogram, and the subjective reported behavioral responses of patients (obtained from outcome questionnaires for tinnitus relief, which focused on tinnitus intensity, annoyance, severity index, and a subjective scale of value of the UHF/UQ device for tinnitus relief. The subjective behavioral response for tinnitus relief with UHF/UQ was found to reflect a dual effect: acoustic stimulation of the residual neuronal function in the UHF range (10-14 kHz) and audiometric thresholds of 40-50 dB sound pressure level (SPL), and the metabolic activity at brain cortex for neuronal reprogramming. The PET of brain categories of response suggested that the UHF/UQ "masking" is predominantly reflective of neuronal reprogramming at the brain cortex. Nuclear medicine PET of brain imaging has provided an objective monitoring system for attempting to establish the efficacy of UHF/UQ for tinnitus relief. No complication of the tinnitus was reported secondary to the PET of brain examination. This limited PET of brain study supports the clinical recommendation of the efficacy of UHF/UQ external acoustic stimulation for a selected population of patients with tinnitus of the severe disabling type.

Acoustic Stimulation↗

PubMed2025

Epitranscriptomic reprogramming in response to low CO2 stress and m6A engineering to enhance biomass production in Nannochloropsis oceanica.

N6-adenine methylation (m6A) as an epitranscriptomic mark is the most abundant modification in eukaryotic RNA and plays a dynamically regulated role. However, m6A dynamics, deposition and engineering in microalgae remain largely unknown. Here, in Nannochloropsis oceanica, the dynamic alterations and reprogramming in m6A RNA modifications after the shift from high to low CO2 conditions were first investigated using methylated RNA immunoprecipitation sequencing. The m6A peaks in N. oceanica were mainly enriched in 3'UTR. A positive association between m6A abundance and mRNA transcription of CO2-responsive genes was observed; moreover, N. oceanica cells adopted versatile strategies in a dynamic reprogramming of m6A in response to low CO2 stress. Secondly, knockout of two putative m6A methylases including NoMTA (NO04G02990) and NoMTB (NO07G02450) by genome editing induced methylation reprogramming, which was associated with expression changes of low-CO2 responsive genes such as carbon/nitrogen metabolism, and photorespiration genes that underlie reductions in growth and biomass. Lastly, m6A modification reprogramming was first engineered to increase low-CO2 stress tolerance and biomass productivity by the CRISPR/dCas13 system combined with MTA and NoMTB under low CO2 in N. oceanica. Therefore, these strides would pave the way for microalgal epigenetics and future industrial applications.

Microalgae↗

PubMed2026

Next-generation macrophage engineering in cancer therapy: From TAM reprogramming to CAR-macrophages.

Macrophages are central regulators of the tumor microenvironment (TME), shaping immune suppression, angiogenesis, metabolism, and therapeutic resistance in solid cancers. While early strategies sought to deplete tumor-associated macrophages (TAMs) or block monocyte recruitment, limited efficacy and compensatory mechanisms revealed the need for functional reprogramming rather than elimination. Recent advances in viral vectors, CRISPR-Cas genome editing, and RNA-based delivery platforms have enabled precise genetic modification of macrophages, giving rise to chimeric antigen receptor macrophages (CAR-Ms) and related engineered products. Beyond antigen targeting, effective macrophage engineering requires stabilization of pro-inflammatory identity, resistance to tumor-induced repolarization, metabolic reinforcement, and integration of checkpoint modulation pathways. This review synthesizes current strategies across DNA, mRNA, and siRNA-based platforms, highlighting convergent design principles that connect TAM reprogramming with CAR-M development. We discuss reshaping phagocytosis checkpoints, metabolic and transcriptional stabilization, cytokine augmentation, and synthetic receptor architecture, emphasizing combinatorial and context-aware engineering, while proposing new candidate gene targets. Engineered macrophages are thus evolving from simple effector cells into programmable immune coordinators capable of converting immunologically "cold" tumors into inflamed, therapy-responsive niches.

CAR-M↗

PubMed2001

Altered expression of the carboxylesterases ES-4 and ES-10 by peroxisome proliferator chemicals.

The nonspecific carboxylesterases (EC.3.1.1.1) are a large group of enzymes that play important roles in the metabolism of foreign xenobiotics and endogenous lipids, including activators of the peroxisome proliferator-activated receptor alpha, a nuclear receptor that is the central mediator of peroxisome proliferator (PP) effects in the rodent liver. A number of reports have demonstrated that PP exposure leads to alterations in levels of carboxylesterases in the liver. In this study, we determined by Western blot analysis whether exposure to diverse PP results in alteration of expression of two highly expressed microsomal carboxylesterases. Chronic exposure to the PP WY-14,643 (WY) and gemfibrozil (GEM), but not di-n-butyl phthalate (DBP), led to decreases in ES-4 in male rat livers. ES-4 was increased in female rat livers treated with GEM. WY exposure led to decreases in ES-10 in male and female rat livers. ES-10 was increased in female rats treated with DBP. Compared with other end points that are altered within days after PP exposure, the downregulation of ES-4 and ES-10 by WY was considerably slower, occurring between 1 and 5 weeks of exposure. Decreased expression of ES-4 was observed at doses of WY or GEM as low as 10 or 8000 ppm, respectively, whereas decreased expression of ES-10 was more resistant to changes by any PP occurring only with WY at doses as low as 50 ppm. After chronic exposure to WY or diethylhexyl phthalate in wild-type mice, kidney, but not liver, expression of ES-4 and ES-10 was downregulated. These decreases in kidney ES expression were not observed in PPARalpha-null mice lacking a functional PPARalpha gene, demonstrating the importance of this transcription factor in these changes. These studies demonstrate that ES protein expression is under complex control by PP that is sex- and compound-dependent. These results lend support to the hypothesis that PP exposure leads to a reprogramming of expression of enzymes important in the metabolism of PPARalpha activators.

Animals↗

PubMed2026

Mechanisms linking the gut microbiota to colorectal cancer development and progression.

Colorectal cancer remains a leading cause of global cancer mortality, with a concerning rise in early-onset cases driven by complex interactions between environmental exposures, lifestyle factors, and host genetics. Mounting evidence indicates that gut microbiota dysbiosis critically modulates this oncogenic process, acting as an active participant rather than a passive bystander. This review systematically synthesizes the dichotomous roles of the intestinal microbiome in colorectal tumorigenesis through the conceptual framework of the driver-passenger model. We discuss how early initiating driver bacteria, such as Polyketide synthase-positive Escherichia coli and enterotoxigenic Bacteroides fragilis, compromise mucosal barriers, induce chronic mucosal inflammation, and inflict direct genomic instability. As the local tumor microenvironment undergoes profound metabolic remodeling, opportunistic passenger pathogens, notably Fusobacterium nucleatum, become enriched, further promoting cellular proliferation and facilitating tumor immune evasion. Conversely, protective commensals, exemplified by Clostridium butyricum and Streptococcus thermophilus, exert robust tumor-suppressive effects through multifaceted mechanisms. These beneficial microbes actively antagonize malignant progression by redirecting tumor metabolic fluxes toward oxidative stress, orchestrating deep epigenetic reprogramming, and degrading core oncoproteins to reverse chemoresistance. Transitioning from fundamental mechanisms to clinical application, we evaluate a comprehensive spectrum of microbiota-targeted interventions, encompassing non-invasive diagnostic biomarkers, fecal microbiota transplantation, engineered bacteria, phage therapy, and postbiotics. Finally, we critically address the formidable translational challenges associated with microbial heterogeneity, long-term safety, and regulatory standardization, aiming to provide a balanced perspective on integrating microbiome-based strategies into next-generation precision oncology for colorectal cancer.

Humans↗

PubMed2004

Six1 and Eya1 expression can reprogram adult muscle from the slow-twitch phenotype into the fast-twitch phenotype.

Muscle fibers show great differences in their contractile and metabolic properties. This diversity enables skeletal muscles to fulfill and adapt to different tasks. In this report, we show that the Six/Eya pathway is implicated in the establishment and maintenance of the fast-twitch skeletal muscle phenotype. We demonstrate that the MEF3/Six DNA binding element present in the aldolase A pM promoter mediates the high level of activation of this promoter in fast-twitch glycolytic (but not in slow-twitch) muscle fibers. We also show that among the Six and Eya gene products expressed in mouse skeletal muscle, Six1 and Eya1 proteins accumulate preferentially in the nuclei of fast-twitch muscles. The forced expression of Six1 and Eya1 together in the slow-twitch soleus muscle induced a fiber-type transition characterized by the replacement of myosin heavy chain I and IIA isoforms by the faster IIB and/or IIX isoforms, the activation of fast-twitch fiber-specific genes, and a switch toward glycolytic metabolism. Collectively, these data identify Six1 and Eya1 as the first transcriptional complex that is able to reprogram adult slow-twitch oxidative fibers toward a fast-twitch glycolytic phenotype.

Animals↗

PubMed2026

Retinoid dynamics in immune cells during age-related diseases.

Retinoids comprise vitamin A and its structurally related natural and synthetic derivatives. Retinoid dynamics involves multiple retinoid forms, carrier proteins, and enzymes that orchestrate the absorption, transport, storage and biotransformation of dietary vitamin A. Beyond their canonical metabolic functions, metabolites and proteins involved in retinoid metabolism also play distinct roles in signal transduction and transcriptome reprogramming, broadening the mechanisms that influence immune cell fate decisions. Age‑related changes in retinoid bioavailability and signaling intensity alter immune cell polarization and function, thereby contributing to the pathogenesis of chronic inflammation in neurodegenerative diseases, cardiovascular diseases, osteoarthritis, and other age-related diseases. In this review, we focus on age-related alterations in the retinoid metabolic pathway and their impact on inflammation and the progression of age-related diseases. This review highlights the pivotal role of retinoid metabolism in anti-ageing interventions and considers future directions and challenges in this field.

Humans↗

PubMed2004

Genomics of preconditioning.

Brief episodes of ischemia can protect against subsequent damaging ischemic events; however, the molecular mechanisms responsible for protection are poorly understood. Identifying genes involved in this process could provide insight into cell survival and treatment of stroke. We developed a murine model of ischemic preconditioning and subsequent stroke and used gene expression profiling to identify genes that may be involved in neuroprotective pathways. Middle cerebral artery occlusions were performed in mice for 15 minutes. (preconditioning), 60 minutes (stroke), or 15 minutes, followed 72 hours later with 60 minutes (preconditioning plus stroke) of middle cerebral artery occlusions. RNA from a region of cortex that is protected by ischemic preconditioning was hybridized to oligonucleotide microarrays. Follow-up experiments used patch clamp to examine cell conductance in cultured neurons exposed to oxygen-glucose deprivation. Stroke, ischemic preconditioning, and ischemic preconditioning plus stroke all induced gene changes that overlapped little among conditions. Stroke induced robust upregulation of gene expression whereas preconditioning followed by stroke resulted in a marked downregulation. Genes upregulated by stroke suggested activation of stress/inflammatory pathways and increased metabolism and ion channel function. Preconditioning tended to decrease genes involved in these pathways. Follow-up experiments show that preconditioning decreased voltage-gated potassium currents in vitro and increased bleeding time. Preconditioning reprograms the response to ischemic injury via transcriptional changes that may suppress metabolic pathways and immune responses, reduce ion channel activity, and decrease blood coagulation. These changes resemble evolutionarily conserved responses to decreased blood flow and oxygen availability that occur during hibernation.

Animals↗

PubMed2006

Transcriptional and metabolic profiles of stress-induced, embryogenic tobacco microspores.

Higher plant microspores, when subjected to various stress treatments in vitro, are able to reprogram their regular gametophytic development towards the sporophytic pathway to form haploid embryos and plants. Suppression subtractive hybridization (SSH) and metabolic profiling were used to characterize this developmental switch. Following differential reverse Northern hybridizations 90 distinct up-regulated sequences were identified in stressed, embryogenic microspores (accessible at www.univie.ac.at/ntsm). Sequence analyses allowed the classification of these genes into functional clusters such as metabolism, chromosome remodeling, signaling, transcription and translation, while the putative functions of half of the sequences remained unknown. A comparison of metabolic profiles of non-stressed and stressed microspores using gas chromatography/mass spectrometry (GC/MS) identified 70 compounds, partly displaying significant changes in metabolite levels, e.g., highly elevated levels of isocitrate and isomaltose in stressed microspores compared to non-stressed microspores. The formation of embryogenic microspores is discussed on the basis of the identified transcriptional and metabolic profiles.

Blotting, Northern↗

PubMed2026

Single-cell transcriptional profiling identifies the swimming crab Portunus trituberculatus in response to bacterial infection.

Crustaceans rely entirely on innate immunity, yet the cellular composition, functional specialization, and pathogen-induced remodeling of their immune system remain poorly resolved. Here, we generated a high-resolution single-cell transcriptomic atlas of hemocytes from the swimming crab Portunus trituberculatus following Vibrio parahaemolyticus infection using 10× Genomics scRNA-seq. Seven putatively distinct hemocyte clusters were identified, including granulocytes, semigranular hemocytes, prohemocytes, unresolved hemocytes, hyalinocyte-like hemocytes, biosynthetically active secretory hemocytes, and regulatory hemocytes. Although the overall cellular composition remained relatively stable after infection, hemocytes exhibited pronounced cluster-specific transcriptional reprogramming involving Toll/NF-κB signaling, antimicrobial peptide synthesis and metabolic rewiring. By integrating single-cell and bulk transcriptomes, we identified multiple anti-lipopolysaccharide factors (ALFs) as key secretory effectors and experimentally validated their antibacterial activities. FITC-based bacterial engulfment assays and RNA-seq of sorted phagocytes demonstrated that phagocytic capability was shared across multiple hemocyte clusters. Notably, the immunoglobulin superfamily receptor DSCAM displayed extensive alternative splicing and strong infection-induced activation in unresolved hemocytes. Immune-training experiments showed that prior bacterial exposure was associated with altered DSCAM expression and reduced early cumulative mortality upon secondary challenge, suggesting a memory-like immune phenotype. These findings provide a foundational framework for understanding crustacean immunity and advancing disease-resistant breeding in aquaculture.

Antimicrobial peptides↗