Latest ArticlesPoultry is a major nutritional source providing food for large human populations. Infectious diseases threaten the productivity of poultry flocks and diminish animal welfare. Recent advances in genome editing have significantly contributed to our understanding of various physiological aspects and have helped elucidate the interaction between the chicken host and pathogens. Several chicken lines were generated, including those with Type Ⅰ and Type Ⅲ interferon receptor knockouts, those lacking specific T cell populations, and those missing contributing factors to V(D)J recombination, such as the recombination-activating gene 1 (RAG1). In addition, researchers achieved resistance to the avian influenza virus (AIV) by targeting acidic nuclear phosphoproteins. Finally, reinstating retinoic acid-inducible gene I (RIG-I) and RING finger protein 135 (RNF135) in the chicken revealed new insights into their evolutionary role, particularly during host-pathogen interactions with AIV. This review provides an update about recent achievements in genome editing of chickens, particularly in immunology and disease resistance.
Waterfowl, primarily ducks, constitute a major commercial poultry species globally, their production efficiency is heavily influenced by dietary protein and amino acid intake. Although the National Research Council (NRC, Nutrient requirements of poultry, 1994) established fundamental recommendations for protein and amino acid requirements in ducks, tremendous improvements and changes (growth speed, rearing system, and dietary strategy) have been made in duck industry over the past decades. Consequently, these standards no longer adequately reflect the nutritional needs of modern duck production systems. This review presents updated estimates of dietary crude protein and key amino acid requirements, including methionine, lysine, threonine, tryptophan, and arginine, etc., which are essential for formulating precision diets to maximize growth performance, carcass yield in meat ducks, as well as reproductive performance in laying ducks and breeders. Furthermore, the functional roles of these amino acids as critical regulators of physiological processes are systematically examined, including lipid metabolism (methionine and threonine), intestinal barrier integrity (threonine), regulation of feed intake via nitric oxide (arginine), and the modulation of behavior and stress responses (tryptophan). The implementation of low-protein dietary strategies (crude protein levels as low as 15% for growing meat ducks, and 14.5% for laying ducks) is also discussed for maintaining performance while improving nitrogen utilization efficiency. The recent publication of updated Chinese national feeding standards for meat-type (GB/T 45103-2024) and laying ducks (GB/T 41189-2021) incorporates these modern research advances, representing a significant milestone and providing a modern framework to guide the global duck industries. In summary, this review highlights the urgent need to move beyond outdated nutritional standards and adopt modern, evidence-based amino acid requirements tailored to modern duck production. The integration of low-protein diet strategies along with a refined understanding of amino acid functions is crucial for optimizing duck production, enhancing nutrient efficiency, and reducing environmental impacts. Future research should focus on establishing the precise requirements for other essential amino acids and certain non-essential amino acids, and further elucidating how amino acids molecularly modulate gene expression, signaling pathways, and gut microbiota to develop innovative and sustainable nutritional strategies for ducks.
As global demand for milk and meat increases, young ruminants need rapid gut development and sufficient mucosal immunity immediately after birth. However, their growing intestines face oxidative and microbial challenges that can harm long-term performance. This review systematically summarizes recent advances in how host genetics, early nutrition, and emerging microbiota interact to influence intestinal development and mucosal immunity under standard rearing conditions. We explore how the host regulates the gut microbiota, the microbiota's role in maintaining gut integrity, barrier function, development, intestinal cell health, mucosal immunity, and how diet modulates gut microbiota composition in young ruminants. Microbial signals promote increased villus length and better epithelial functions. Conversely, dysbiosis delays gut closure, weakens barrier integrity, and skews immunity toward proinflammatory responses. Feeding strategies such as colostrum timing, milk replacers, and the addition of starter fiber and probiotics can alter microbial communities within days. Nonetheless, challenges remain in standardizing neonatal feeding practices, identifying microbe metabolite indicators of gut health, and integrating precision feeding technologies. By mapping the three-way interaction among host, microbiota, and diet, this review offers a blueprint for neonatal ruminant feeding that enhances both animal welfare and the productivity of future ruminant systems. This review also provides a novel mechanistic integration of host genetics, gut microbiota succession, and dietary interventions in young ruminants, filling the gap of fragmented multi-omics analyses in existing literature and offering targeted insights for optimizing gastrointestinal development and production efficiency.
The fact that feeding pigs with probiotic-fermented agricultural by-products improves pork quality has been repeatedly demonstrated and widely applied, but the underlying mechanisms remain unclear. This study explored the effects of fermented extruded brewers' spent grain (FEBSG) on meat quality in growing-finishing pigs, as well as its regulatory mechanisms.
Sixty Duroc × Landrace × Yorkshire pigs (52.25 ± 2.10 kg) were randomly assigned to five dietary treatments, in which FEBSG replaced 0, 5%, 10%, 15%, and 20% of soybean meal (SBM). The experiment spanned 10 weeks.
Compared with the control, 20% FEBSG significantly increased final body weight, average daily feed intake, and average daily gain, while decreasing feed to gain ratio (P < 0.05). Both 15% and 20% FEBSG improved carcass characteristics and meat quality, including higher carcass weight, loin eye area, and intramuscular fat content, along with lower drip loss and shear force (P < 0.05). These treatments also enhanced flavor-related amino acids and unsaturated fatty acids (P < 0.05), and improved umami and sweet taste profiles. Moreover, 20% FEBSG increased muscle fiber density and reduced fiber diameter, upregulated MyHC Ⅰ, MyHCⅡa, PGC-1α, AMPKα1, TFAM, and SDH activity, and downregulated MyHC Ⅱb and LDH activity (P < 0.05). Proteomic analysis identified 69 differentially expressed proteins, with enrichment in AMPK and PPAR signaling pathways. Metagenomic analysis revealed increased abundance of short-chain fatty acid-producing bacteria, including Clostridium, Lactobacillus, Prevotella, and Bartonella. Correlation analysis demonstrated associations between gut microbiota diversity and meat quality traits, as well as between dominant microbial genera and differentially expressed proteins, volatile fatty acids, muscle fiber characteristics, and the AMPK/PGC-1α/TFAM signaling pathway.
Partial replacement of SBM with FEBSG positively influenced growth performance and pork quality in pigs, with the underlying mechanisms may involve the activation of the AMPK/PGC-1α/TFAM signaling pathway via the gut-muscle axis, thereby enhancing mitochondrial biogenesis, muscle development, and metabolism.
The systematic exploration of novel bioactive compounds with superior functional properties is critical for driving innovations in agriculture, healthcare, and related fields, thereby becoming essential for advancing sustainable biotechnological solutions. Nonprotein amino acids (NPAAs), functional amino acids not incorporated into proteins, exhibit unique physiological activities and provide distinctive advantages in nutritional enhancement, functional product formulation, and food/feed processing. These attributes challenge the conventional perception of proteins as mere nutritional carriers, positioning NPAAs as promising bioproducts for biosynthesis and functional applications in agriculture, food, and medicine. This review summarizes the classification of the available NPAAs based on their synthetic substrates for the first time and then outlines their diverse functional roles. A comprehensive analysis of recent advances in biosynthetic pathways, engineering strategies, and production level demonstrates their primary research progress in the laboratory phase. The further sustainable biomanufacturing of NPAAs is hampered by several challenges, including poorly elucidated biosynthetic mechanisms, limited robustness and low productivity of microbial strains, and difficulties in scaling up production for industrial applications. Addressing these bottlenecks will require innovative strategies and technologies to facilitate the translation of NPAA production from bench to industry. This review offers valuable insights into the potential of NPAAs in the development of next-generation bioproducts of nutrition, immune regulation, antioxidant defense, and intestinal homeostasis maintenance, suggesting a promising direction for microbial production of high-performance bioactive molecules in agricultural synthetic biomanufacturing.
Early embryo loss is an important factor affecting the reproductive capacity of cattle. Recent studies have revealed that during the process of embryonic genome activation (EGA), epigenetic modification, such as histone lactylation remodeling, is crucial for early embryonic development. However, the effects of histone lactylation on early embryonic development in bovines and the related mechanisms remain unknown. In this study, in vitro fertilized embryos were utilized to investigate the effects of histone lactylation on EGA and early embryo development in cattle.
Histone lactylation, including pan-lysine lactylation, histone H3 lysine 9 lactylation, and histone H3 lysine 18 lactylation, occurred mainly in the nucleus and significantly decreased from the 8-cell stage to the morula stage and increased from the morula stage to the blastocyst stage. Decreased or increased levels of histone lactylation induced by GSKA or sodium lactate supplementation inhibited early bovine embryo development and blastocyst lineage differentiation. Furthermore, single-cell RNA sequencing data and 5-ethynyluridine staining revealed that a reduction in histone lactylation levels altered the expression of genes associated with DNA transcription and RNA polymerase activity, thereby impairing EGA. Importantly, β-nicotinamide mononucleotide rescued the inhibitory effects of GSKA supplementation on bovine EGA and early embryonic development.
Histone lactylation maintains early bovine embryo development by regulating EGA. Our findings provide a theoretical reference for addressing early embryo loss and thereby increasing the reproductive capacity of cattle.
Transitioning to a high-grain (HG) diet significantly alters rumen fermentation by increasing the production of short-chain fatty acids (SCFAs) and lowering rumen pH, which may contribute to subacute ruminal acidosis (SARA) and damage to the ruminal epithelium. Rapid adaptation of rumen epithelium to these metabolic shifts is essential to maintain homeostasis, but the transcriptional mechanisms underlying this adaptation remain poorly understood.
We analyzed the temporal progression of gene expression and metabolomic profile in rumen papillae collected during low-grain feeding (LG) and one week after transitioning to a HG diet (HG1), or four weeks after (HG4) in cows classified as susceptible or resistant to SARA. RNA sequencing identified 955 differentially expressed genes (DEGs) across time points, revealing a biphasic adaptation pattern. Early responses (HG1) showed moderate transcriptional changes, while HG4 was characterized by substantial transcriptional remodeling. Pathway analysis indicated three major functional categories affected during adaptation: cellular stress response, metabolic adaptation, and protein processing. Notably, sterol biosynthesis genes showed transient upregulation at HG1 followed by downregulation at HG4, coinciding with morphological changes in rumen wall thickness and n-butyrate concentration in rumen fluid. Correlation analyses comparing gene expression patterns and metabolite level changes triggered by the dietary transition revealed potential links between metabolic and transcriptional adaptation. Of particular interest, valerate levels at HG1 correlated with genes involved in tissue remodeling at HG4, implying that valerate may contribute to delayed epithelial responses. Next, transcriptional differences between SARA-susceptible and SARA-resistant animals included genes related to inflammation, cell structure, and metabolism that persisted across all time points, suggesting underlying intrinsic differences in SARA susceptibility that are present before and persist during dietary challenge. Key genes consistently differentially under-expressed in SARA-susceptible animals, CCDC196 and MYO7B, represent potential biomarkers for SARA predisposition. Finally, the SARA-resistant group showed a greater number of transcriptome-metabolome correlations, suggesting more coordinated epithelial responses to diet change compared to the SARA-susceptible group.
Our findings provide insights into the molecular mechanisms underlying rumen adaptation to HG diets and individual variation in SARA susceptibility, providing a basis for developing strategies to optimize dietary transitions in ruminant production systems.
Subclinical mastitis (SCM) is a major constraint in dairy production and is driven by complex host-pathogen interactions. Although transcriptional responses associated with SCM have been widely investigated, the epigenetic mechanisms that stably regulate these programs remain less well characterized, particularly in crossbred cattle populations. This study aimed to characterize DNA methylation-based regulatory networks by integrating whole-genome methylation and transcriptome data from milk somatic cells of Vrindavani (Bos taurus × Bos indicus) cattle. Whole-genome methylation (n = 6) and corresponding transcriptome profiling (n = 6) were performed on milk somatic cells from SCM-affected and healthy control cows.
Differential methylation analysis (q-value < 0.05) identified 62,940 differentially methylated cytosines (DMCs), 7,706 differentially methylated regions (DMRs), and 6,203 differentially methylated genes (DMGs), with a predominant bias toward hypomethylation in SCM. Integrative analysis using stringent thresholds for both methylation (≥ 10%) and expression change (|log2 fold change| ≥ 1; P of GMM < 0.001) identified 1,407 differentially methylated and expressed genes (DMEGs). Functional enrichment analysis revealed 47 KEGG pathways and 30 Gene Ontology biological process terms (FDR < 0.05), primarily associated with immune signaling and inflammatory responses. In contrast, a subset of DMEGs showed methylation-associated repression of lactation- and metabolism-related genes. Selected genes were experimentally validated by qPCR, including upregulation of the inflammatory mediator S100A8 and downregulation of CSN3 (κ-casein), a key milk protein gene.
These findings provide an integrated view of the DNA methylation and transcriptional landscape of SCM in milk somatic cells and demonstrate that epigenetic remodeling is associated with coordinated activation of immune pathways alongside repression of lactation-associated functions. The results contribute to understanding the molecular basis of subclinical mastitis and may inform future efforts toward biomarker development and epigenetically informed strategies for improving disease resilience in dairy cattle.
Rotavirus (RV) infection damages mature intestinal epithelial cells and is a leading cause of severe diarrhea in infants and young animals. However, the host cell death pathways involved in RV infection remain incompletely understood. This study used an RV-infected IPEC-J2 cell model and integrated transcriptomic, proteomic, and functional assays to investigate whether RV infection is associated with ferroptosis and NCOA4-mediated ferritinophagy.
High-throughput sequencing and data-independent acquisition (DIA)-based quantitative proteomic analysis showed enrichment of ferroptosis, autophagy, and cell death-related signaling pathways after RV infection. Functional assays showed that RV infection was associated with intracellular Fe2+ accumulation and lipid peroxidation. The ferroptosis inducer (erastin) increased VP6 expression, whereas the ferroptosis inhibitor (Fer-1) attenuated this effect. NCOA4, a ferritinophagy receptor, was upregulated after RV infection. NCOA4 knockdown reduced RV-associated Fe2+ accumulation, ROS production, ferritin degradation-related changes, and VP6 expression, whereas NCOA4 overexpression enhanced these responses. The autophagy inhibitor (3-MA) and the lysosomal blocker (CQ) attenuated RV-associated ferroptosis markers and VP6 expression, consistent with involvement of the autophagy-lysosome pathway in ferritin turnover.
These findings support a model in which RV infection promotes ferroptosis-associated changes and VP6 expression through NCOA4-mediated ferritinophagy in IPEC-J2 cells. As this study was performed in vitro and did not directly measure epithelial transport, barrier function, infectious viral yield, or diarrheal outcomes, further in vivo studies are needed to determine the contribution of this pathway to RV pathogenesis.
The importance of glucan additives has been widely recognized in farm animals. Yet the precise role of POLYCAN, a β-glucan derived from the black yeast Aureobasidium pullulans SM-2001, remains limited in companion animals. Therefore, this study aims to evaluate its effect on performance, nutrient digestibility, hematology, and the gut microbiome and serum metabolites in beagle dogs.
Eight healthy male beagle dogs (8 months old; 10.70 ± 1.79 kg body weight; 3.00 ± 0.15 body condition score) were enrolled in a 10-week study comprising two phases: Phase 1 (weeks 0-4) and Phase 2 (weeks 6-10), separated by a 2-week washout period. The dogs were divided into two groups and fed a control (CON), basal diet and CON diet supplemented with 1,000 mg/d of POLYCAN. Each of two diets were provided using a cross over design for eight weeks, with four beagles assigned to each treatment. During the washout period, all dogs were fed only the commercial basal diet.
Throughout the experimental period, POLYCAN supplementation did not affect growth performance, nutrient digestibility, or fecal pH in beagles. However, serum calcium, insulin-like growth factor-1 (IGF-1), growth hormone, and immunoglobulin G (IgG) concentrations were significantly higher (P < 0.05) in the POLYCAN-supplemented group. Alpha-diversity indices of microbial richness and evenness, as well as beta-diversity based on Bray-Curtis dissimilarity and unweighted UniFrac distances, showed no significant differences between treatment group. At the phylum level, Actinobacteria and Proteobacteria were more abundant in the POLYCAN group, followed by Fusobacteria and Bacteroidota. At family level, Lachnospiraceae, Ruminococcaceae, Coriobacteriaceae, Lactobacillaceae, Peptostreptococcaceae, and Erysipelotrichaceae exhibited higher relative abundances. Furthermore, the core gut microbiota at genus level was dominated by Micrococcus and Fusobacterium. Untargeted metabolomic analysis also revealed distinct group separation, identifying key metabolites including lumichrome, D-mannitol, and 2'-deoxycytidine. Pathway enrichment analysis indicated alterations in pyrimidine, histidine, and bile acid metabolism with higher metabolite abundance observed in the POLYCAN-treated group.
Overall, our findings validate that adding 1,000 mg/d POLYCAN to canines' diet could serve as a functional nutraceutical to enhance their immune and gut health without affecting growth and digestion.
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