Adaptation is one of the key processes of animal domestication, environmental pressures will leave footprints in the genome. Geese are widely distributed across multiple geographical conditions with distinct adaptations. However, few reports have focused on the environmental adaptability of geese. Moreover, the key environmental drivers that trigger local adaptation and its genetic mechanisms are still unknown. To this end, 35 agro-climatic variables of 257 geese from 14 Chinese breeds were obtained, the key environmental drivers and its genetic mechanism were elucidated by combining the genome data. Five key environmental drivers, elevation, water scarcity (BIO14), two variables as proxies of food availability (Grass and Landuse), and one variable as proxy of disease resistance (Forest) were identified after dissecting 35 agro-climatic variables by using ecological niche modeling (ENM). Integrating five key environmental drivers with single-nucleotide polymorphism variations, we conduct genome-wide selection signature analyses and genome-environment analysis. This analysis identified 1984 key genes likely integral to the environmental adaptation and mainly enriched in MAPK signaling pathways and metabolic pathways. Allele frequency distribution and selective sweep analysis revealed that some genes play crucial roles in environmental adaptation, including SATB1, NTRK2 and CTIF involved in adapting to the high-altitude hypoxic environments; ARMH3 and BDH2 participated in adapting to water deficiency; COL5L1, ULK4 and PI4KA associated with disease resistance, and other genes involved in metabolic adaptations including IQSEC1, TBC1D14, GRK5, FGGY and LRP1B, etc. Notably, we noticed that feather colour differentiation in geese might be driven by human agricultural practices, with LRP1B involved in this process. Overall, our study elucidated the five key environmental drivers and their genetic mechanisms. The candidate genes related to environmental adaptability offer new insights into genetic resource development and breeding strategies of Chinese indigenous geese.

BackgroundHost antiviral defense relies on key regulatory genes that coordinate immune signaling and cellular homeostasis, yet their roles in J subgroup avian leukosis virus (ALV-J) infection remain poorly defined. Here, we identify cellular repressor of E1A-stimulated genes 1 (CREG1) as a key regulator of mitochondrial function and a critical immune-related gene involved in ALV-J infection. The objective of this study was to explore the effects and underlying mechanisms of CREG1 in the context of ALV-J infection.MethodsIn this study, transcriptomic analysis and RT-qPCR revealed that the expression of CREG1 is significantly upregulated in the spleen tissues of ALV-J infected chickens. By overexpressing and silencing CREG1 in cultured cells, and using Western blotting, transmission electron microscopy, immunofluorescence, and flow cytometry, we comprehensively validated its effects on viral replication, mitochondrial function, and apoptosis.ResultsOverexpression of CREG1 upregulates the expression of I-IFN and certain interferon-stimulated genes (ISGs), thereby suppressing viral replication. Mechanistically, overexpression of CREG1 induces mitochondrial dysfunction, characterized by a decrease in mitochondrial membrane potential (Δψm), reduced adenosine triphosphate (ATP) production and respiratory chain activity, enhanced mitophagy, and increased release of mitochondrial DNA (mtDNA), which in turn triggers the activation of innate immune responses. Mitochondrial dysfunction further leads to the cytosolic release of cytochrome c and an increase in reactive oxygen species (ROS) levels, thereby triggering a robust apoptotic response. Moreover, the regulation of mitochondrial function by CREG1 depends on its interaction with the mitochondrial chaperone protein heat shock protein 1 (HSPD1), and their co-expression synergistically amplifies the antiviral response.ConclusionsOverall, we identify CREG1 as a potent antiviral gene and underscore the pivotal roles of mitochondria-mediated innate immunity and apoptosis during ALV-J infection.

In-depth investigation of genetic variants influencing muscle yield in chickens is crucial for maximizing the efficiency of improving production performance in local chicken breeding programs. To identify variants and genes affecting muscle yield in Chinese indigenous chickens, we performed a genome-wide association study (GWAS) on growth traits using genomic variants from Xinghua chickens. Subsequently, we mapped expression quantitative trait loci (eQTLs) and splicing quantitative trait loci (sQTLs) by integrating genotypic variation and transcriptomic data from muscle tissue. We identified a co-expression module comprising 348 genes associated with protein synthesis and ribosome biogenesis. Additionally, we detected 7948 eQTL-related genes and 1526 sQTL-related genes. Among the identified e/sQTLs, approximately 60% were located within gene bodies and were enriched in regions flanking transcription start sites or splice sites. Integrated analysis revealed that the overlap between eQTLs and sQTLs, as well as between eGenes and sGenes, was less than 5%, suggesting their distinct roles in gene expression and transcript splicing. Interestingly, the overlapping eGenes and sGenes were significantly enriched in pathways related to protein synthesis and translation, highlighting the potential importance of genes and variants involved in these processes for muscle growth in yellow-feathered broilers. In conclusion, this study provides novel insights and a valuable resource for understanding the genetic regulation of gene expression and alternative splicing in muscle tissue of yellow-feathered broilers.

In recent years, chilled chicken has emerged as a new market trend. Skin feather follicle density, an important carcass appearance trait characterized by ''fine and dense'' features, is increasingly preferred by consumers. This study analyzed hair follicle density in the leg and back regions of 1,382 yellow-feathered broiler. The results showed that back feather follicle density was significantly higher than that of the leg (P < 0.01), with a significant positive correlation between the two regions. Meanwhile, feather follicle density in both the leg and back showed negative correlations with abdominal fat weight, body weight, dressed weight, full-eviscerated weight, semi-eviscerated weight. mRNA-seq analysis of leg and back skin tissues from four individuals identified differentially expressed genes (DEGs) affecting feather follicle density traits across different anatomical locations, including GTF2A1, RPSA2, COX3, and CNKSR2. Furthermore, Genome-Wide Association Study (GWAS) analysis of 505 chickens identified 223 single-nucleotide polymorphisms (SNPs) significantly associated with leg feather follicle density and 107 SNPs associated with back feather follicle density, including candidate SNPs such as C19014967G, C17514817T, G1847078C, and C34389948G, as well as candidate genes including ELF5, MAP3K1, HIF1AN, and SERPINF1. mRNA-seq analysis of skin tissues from high and low feather follicle density groups in the leg (TG vs. TD) and back (BG vs. BD) identified 541 leg-related DEGs and 1,130 back-related DEGs, respectively. Joint analysis of TG vs. TD and BG vs. BD revealed 174 commonly DEGs, including candidate genes such as NSA2, IGF2, RPL17, and NRP1. Through integrated GWAS and RNA-seq analysis, five genes significantly associated with leg feather follicle density and twelve candidate genes associated with back feather follicle density were identified. Notably, individuals with the AA genotype at the SERPINF1 SNP locus Chr19:5636537 showed extremely significantly higher feather follicle density than those with the GG genotype, and both mRNA and protein expression levels of SERPINF1 were significantly upregulated in high feather follicle density individuals.

As the first sequenced non-mammalian amniote, the chicken (Gallus gallus) has served as a major source of cost-effective and protein-enriched foods since domestication. However, how structural variations (SVs) affect 3D genome reorganization to influence domestication and production traits remains unclear in chickens. Here, fifteen de novo chromosome-level genome assemblies are newly generated, along with high-throughput chromosome conformation capture (Hi-C), ATAC and RNA sequencing data. By integrating 13 published assemblies, the first pan-3D genome resource is constructed, spanning genes, SVs, and chromatin architectures, to investigate the dynamic characteristics of the 3D genome at different levels and the roles of SVs in the conservation and reorganization of chromatin architectures. Furthermore, candidate SVs and their linked genes are identified for domestication and production traits based on 1,735 resequencing accessions. Notably, the 240-bp and 81-bp SVs in the TSHR and DIO2 genes are considered the key targets in artificial selection for seasonal reproduction, and a 266-bp deletion upstream of the KLF3 gene affects carcass performance by rewriting the chromatin loop interaction network. Finally, SVs significantly improve the predictive accuracy in genomic selection models. Collectively, this study presents a comprehensive pan-3D resource to advance functional genomic research and breeding practice for the community.

Adipose tissue accumulation represents a significant challenge to both human metabolic health and agricultural productivity. While Ras and Rab Interactor 2 (RIN2) has been characterized as a Rab5 effector protein, its precise role in adipogenesis remains poorly defined. Here, we identified RIN2 as a novel critical regulator of adipogenesis in chicken. We found that RIN2 was widely expressed across various tissues and dynamic expression patterns during adipocyte differentiation. Through comprehensive functional analyses in both ICP-1 cells and primary preadipocytes, we identified that RIN2 overexpression enhances cellular proliferation, cell cycle progression, and adipogenic differentiation, whereas RIN2 knockdown produced contrasting inhibitory effects. Transcriptomic profiling uncovered that RIN2 functions through modulation of the cholesterol metabolic pathway and promotes fatty acid metabolism. Most notably, in vivo knockdown of RIN2 specifically reduced abdominal fat deposition without compromising other carcass characteristics. In summary, our findings identify RIN2 as a key regulator of fat accumulation and highlight its potential as a genetic target for improving poultry carcass composition.

This study provides a detailed genomic and evolutionary analysis of the heat shock protein (HSP) gene family in the chicken (Gallus gallus), identifying 64 HSP genes. The HSP40 (DNAJ) subfamily was the largest, with 39 members, followed by HSP70, HSP90, and smaller subfamilies. Phylogenetic and structural analyses indicated intricate evolutionary dynamics, encompassing both ancient and recent duplication events. The Ka/Ks ratio suggests that purifying selection is the dominant force, although significant segmental duplications (e.g. DNAJC28/DNAJC30) exhibit evidence of positive selection. Analysis of the protein-protein interaction network identified HSPA8, HSPA9, and HSP90B1 as central hubs. Functional enrichment revealed significant clusters associated with chaperone-mediated protein folding, protein complex assembly, and a novel cluster related to toxin transport. Expression profiling by RT-qPCR revealed notable tissue-specificity, with HSP90 and HSP40 exhibiting the highest upregulation (fold change > 3) in leg muscle relative to liver, highlighting their involvement in musculoskeletal stress adaptation. The findings establish a foundational resource for understanding the molecular mechanisms of stress resilience in poultry, highlighting specific gene families and functional modules as potential targets for enhancing thermotolerance and productivity.

Background: This study investigated how chronic heat stress affects meat quality and post-slaughter muscle acidification in slow-growing yellow-feathered broilers, focusing on the roles of ALDOB and HSP90B1 in glycometabolism. Methods: From 100 to 120 days of age, broilers were kept either under thermoneutral conditions (25 ± 1 °C, N group) or cyclic heat stress (32 ± 1 °C for 9 h/day, H group). Meat quality traits (pH, shear force, drip loss, color) were measured at 0, 24, and 48 h of refrigeration (4 °C). Free amino acid and fatty acid profiles were analyzed. DF-1 cells were exposed to 43 °C for functional assays of ALDOB and HSP90B1. Results: Chronic heat stress reduced body weight, altered flavor precursors, and induced PSE-like characteristics (lower pH, higher shear force, increased drip loss, paler color), especially in leg muscles. ALDOB and HSP90B1 were upregulated in both tissues and cells. ALDOB overexpression promoted glucose consumption, while HSP90B1 suppressed lactic acid production. Conclusions: Chronic heat stress impairs growth and flavor precursors and exacerbates post-slaughter muscle acidification (primarily driven by ATP hydrolysis, with lactic acid as a secondary contributor). ALDOB and HSP90B1 may dually regulate glycometabolism under heat stress.

Coordinated development and homeostasis among bone, muscle, and adipose tissue are essential for the sustainable advancement of the broiler industry. Bone marrow mesenchymal stem cells (BMSCs) possess multilineage differentiation potential and provide an in vitro model for investigating regulatory mechanisms of the "bone-muscle-adipose" balance. Nevertheless, microRNA (miRNA)-mRNA regulatory network and the functions of key miRNAs during myogenic differentiation of chicken BMSCs remain unclear. We profiled mRNA and miRNA expression during this process to identify key miRNAs regulating BMSC proliferation and differentiation. mRNA sequencing (mRNA-seq) and miRNA sequencing (miRNA-seq) before and after 5-azacytidine (5-Aza) induction identified 2,233 differentially expressed genes (DEGs) and 67 differentially expressed miRNAs (DE miRNAs). DEGs were mainly enriched in cell cycle and DNA replication pathways, whereas predicted targets of DE miRNAs were predominantly enriched in calcium signaling pathway. A candidate miRNA-mRNA regulatory network was constructed using 13 skeletal muscle-related DE miRNAs and inversely expressed target mRNAs, with target genes enriched in protein processing in the endoplasmic reticulum and Wnt signaling pathways. RNAhybrid prediction and dual-luciferase reporter assays confirmed that miR-26a-5p directly targets MyoD Family Inhibitor Domain Containing (MDFIC). Functionally, miR-26a-5p overexpression suppressed proliferation markers (CCNB2, CCND2, CDK8) and myogenic markers (MYOD1, MYOG, MEF2C, MYHC, Desmin), and reduced MYOD1 protein, whereas miR-26a-5p inhibition produced opposite effects. Collectively, this study delineates the miRNA-mRNA regulatory network during myogenic differentiation of chicken BMSCs and demonstrates that miR-26a-5p negatively regulates proliferation and myogenic differentiation by targeting MDFIC. These findings identify candidate targets for understanding the post-transcriptional regulation of myogenesis in chicken BMSCs.

Ovarian follicle development in chickens is a dynamic and closely controlled biological process crucial to avian reproduction. Each stage of folliculogenesis is characterized by distinct morphological and molecular alterations, regulated by complex signaling pathways. This study employed transcriptome sequencing to investigate the molecular landscape that governs the transition from primordial (PR) to primary (PM), small white (SW), and small yellow (SY) follicles. We found stage-specific activation of critical signaling pathways involved in follicle growth and development using thorough differential gene expression and pathway enrichment analyses. Our findings showed that the PI3K/AKT/mTOR signaling pathway was highly elevated throughout the shift from PR to PM follicles, highlighting its importance in beginning cellular proliferation and protein synthesis. During development, the Wnt signaling system was regulated from the PM to the SW follicles. This included β-catenin-mediated transcriptional regulation, granulosa cell proliferation, and communication between oocytes and somatic cells. Furthermore, the transition from SW to SY follicles was characterized by a significant increase in glycerophospholipid metabolism, emphasizing the metabolic reprogramming required for rapid cellular development and membrane production. The combination of transcriptome data and route mapping provides essential insights into the molecular mechanisms underpinning folliculogenesis in chickens. The signaling pathways revealed the representative stage-specific regulatory networks required for optimal follicle development. These findings enhance our understanding of avian ovarian biology and suggest potential targets for improving reproductive efficiency in chickens.

Fatty acid (FA) is a crucial determinant of meat flavor and nutritional value. Currently, research on FA in livestock and poultry primarily focuses on the nutritional regulation of intramuscular fat (IMF) and meat flavor, leaving other adipose tissues and their functional substances less studied. The abdominal fat (AF) of chickens, as a major site of fat deposition, has edible value and flavor potential for utilization. Therefore, we summarized and discussed the recent research findings on the compositional characteristics, deposition patterns, and regulatory mechanisms of FA in both IMF and AF of chickens. We reveal that the main FA (constituting >80% of the total) in AF is identical to that in IMF. Furthermore, we established links between three primary influencing factors (diet, age, and breed) and fatty acid-derived flavor precursors (such as aldehydes), and we explored genetic factors regulating FA deposition. We found that only a few genes, notably FADS2, co-regulate FA deposition in both tissues. This review explores strategies for enriching and utilizing FA by focusing on FA composition and deposition, aiming to provide novel insights into enhancing the nutritional value and flavor profiles of poultry.

Avian leukosis virus (ALV) remains a major threat to the poultry industry due to its ability to establish persistent infection, induce immunosuppression, and promote tumorigenesis. Despite progress in eradication programs, effective control is hindered by subclinical infection, vertical transmission, and rapid viral evolution. A key limitation lies in the complexity of host–virus interactions, which are governed by multi-layered regulatory processes that cannot be fully resolved by studies focusing on single genes, pathways, or omics layers. In addition, the lack of robust and dynamic phenotypic indicators further constrains the dissection of resistance mechanisms. Recent advances in multi-omics technologies provide an opportunity to overcome these challenges by capturing coordinated changes across genomic, transcriptional, proteomic, and epigenetic levels. Integrating these data with molecular phenotypes, such as expression quantitative trait loci (eQTLs) and protein quantitative trait loci (pQTLs), enables the linking of genetic variation to functional immune responses. Furthermore, CRISPR-based functional screening offers a systematic approach for validating candidate host factors and identifying key regulators of viral replication and immune modulation. In this review, we summarize the epidemiology and molecular biology of ALV, outline current understanding of host–virus interaction networks with an emphasis on innate immune responses, and highlight how integrative multi-omics combined with functional genomics can advance the identification of critical host determinants. This framework provides a systems-level perspective for deciphering ALV–host interactions and supports the development of more effective antiviral strategies.

The duration of fertility in poultry is directly influenced by sperm store ability within specialized sperm storage tubules (SSTs) of the female uterovaginal junction (UVJ). Improving the duration of fertility reduces artificial insemination frequency, influencing animal welfare, and production costs. Here, we investigated physiological and multi-omic factors underlying sperm storage capacity in female Muscovy ducks (Cairina moschata). Phenotypes were collected from approximately 1,500 ducks for three generations, with focus on the peak and late laying stages. High and low sperm storage individuals were classified for histological evaluation and multi-omics analyses (transcriptomics, proteomics, and metabolomics).Results show sperm storage capacity significantly declines with age, associated with ciliated cell integrity in the UVJ microenvironment. Multi-omics revealed enrichment in pathways, including steroid hormone biosynthesis, glutathione metabolism, and tryptophan metabolism. Metabolites such as cholesterol and progesterone were identified as potential biomarkers. Down-regulation of LIMA1 and CYP2R1, along with altered functional pathways, suggests coordinated regulation of antioxidation balance, immune response, and steroid synthesis within the UVJ microenvironment. Our findings provide a multi-omics framework for better understanding fertility duration and offer biomarker candidates and pathways for future genetic improvement in poultry reproduction.

Hyperpigmentation of the visceral peritoneum (HVP) is a hereditary trait that significantly affects the carcass quality in bearded chickens, yet its molecular mechanisms remain unclear. This study utilized data-independent acquisition proteomics to analyze the protein expression profiles of black peritoneum (B), faded peritoneum (F), and normal peritoneum (N) in bearded chickens at 40 and 120 d of age. Combined with histopathological and functional enrichment analyses, we revealed the regulatory network underlying HVP formation. Results indicated that the melanin content was significantly elevated in HVP samples, without accompanying inflammatory responses or tumor characteristics, suggesting that its formation is driven by developmental abnormalities. A total of 9,375 high-confidence proteins were identified through proteomics, with differentially abundant proteins at 40 d of age (219 proteins) primarily enriched in ribosomal function, tyrosine metabolism, and melanin synthesis pathways. In comparison, at 120 d of age (246 proteins), they were enriched in transcription regulation and chromatin remodeling pathways. The abnormal expression of key co-expressed proteins DHRS3 and DACT1 suggests that the dysregulation of retinoic acid (RA) and the Wnt signaling pathway may promote the directed differentiation of melanocytes by regulating neural crest cells (NCCs). The reduced abundance of the chondroitin sulfate proteoglycan, VCAN, weakened the peritoneal barrier function, whereas estradiol accelerated melanin synthesis via hormonal microenvironmental regulation. Furthermore, the formation of HVP led to a reprogramming of energy metabolism, reduced fat deposition, and a downregulation of immune-related molecules, implying that pigment deposition may weaken the chicken immune response. This study systematically elucidates the molecular mechanisms of HVP and provides potential targets for molecular breeding of HVP.

This study investigates the immunological factors underlying the differential susceptibility of two chicken strains, E- and M-lines, to avian leukosis virus subgroup J (ALV-J). During the eradication of avian leukosis at a chicken breeder farm in Guangdong, we observed strain-specific differences in susceptibility to ALV-J. Moreover, E-line chickens exhibited a slower antibody response to ALV-J compared to M-line chickens. As the T cell receptor (TCR) and B cell receptor (BCR) are critical for antigen recognition, their activation triggers specific immune responses, including antibody production. Using high-throughput sequencing, we characterized the T cell receptor beta (TCRβ) and immunoglobulin heavy chain (IGH) repertoires in spleen tissues from both chicken strains. The M-line demonstrated higher clonal diversity in both TCRβ and IGH repertoires under normal conditions compared to the E-line, suggesting a broader baseline antigen recognition capacity. Following ALV-J infection, the TCRβ repertoire diversity remained unchanged, while the IGH repertoire displayed distinct clonal expansion patterns and complementarity-determining region 3 (CDR3) length distributions between the two lines, potentially affecting their ability to recognize ALV-J antigens. Our study provides the first comprehensive comparison of TCRβ and IGH repertoire dynamics in chickens with different ALV-J susceptibilities, offering new insights into the molecular and immunological mechanisms underlying resistance to ALV-J.

The chicken is a valuable model for understanding fundamental biology and vertebrate evolution and is a major global source of nutrient-dense and lean protein. Despite being the first non-mammalian amniote to have its genome sequenced, a systematic characterization of functional variation on the chicken genome remains lacking. Here, we integrated bulk RNA sequencing (RNA-seq) data from 7,015 samples, single-cell RNA-seq data from 127,598 cells and 2,869 whole-genome sequences to present a pilot atlas of regulatory variants across 28 chicken tissues. This atlas reveals millions of regulatory effects on primary expression (protein-coding genes, long non-coding RNA and exons) and post-transcriptional modifications (alternative splicing and 3'-untranslated region alternative polyadenylation). We highlighted distinct molecular mechanisms underlying these regulatory variants, their context-dependent behavior and their utility in interpreting genome-wide associations for 39 chicken complex traits. Finally, our comparative analyses of gene regulation between chickens and mammals demonstrate how this resource can facilitate cross-species gene mapping of complex traits.

Despite the implementation of purification strategies to partially limit J subgroup avian leukosis virus (ALV-J) infection, the involvement of host factors in the underlying infection mechanism remains largely undefined. Here, we identify cellular repressor of E1A-stimulated genes 1 (CREG1) as a key regulator of mitochondrial function and a critical immune-related gene involved in ALV-J infection. The objective of this study was to explore the effects and underlying mechanisms of CREG1 in the context of ALV-J infection. Overexpression of CREG1 upregulates the expression of type I interferon (I-IFN) and certain interferon-stimulated genes (ISGs), thereby suppressing viral replication. Mechanistically, overexpression of CREG1 induces mitochondrial dysfunction, characterized by a decrease in mitochondrial membrane potential (Δψm), reduced adenosine triphosphate (ATP) production and respiratory chain activity, enhanced mitophagy, and increased release of mitochondrial DNA (mtDNA), which in turn triggers the activation of innate immune responses. Mitochondrial dysfunction further leads to the cytosolic release of cytochrome c and an increase in reactive oxygen species (ROS) levels, thereby triggering a robust apoptotic response. Moreover, the regulation of mitochondrial function by CREG1 depends on its interaction with the mitochondrial chaperone protein heat shock protein 1 (HSPD1), and their co-expression synergistically amplifies the antiviral response. In this study, we identify CREG1 as a potent antiviral gene and underscore the pivotal roles of mitochondria-mediated innate immunity and apoptosis during ALV-J infection. Author summary Despite efforts to limit J subgroup avian leukosis virus (ALV-J) infection, the role of host factors in the infection process is still not fully understood. In this study, we highlight the cellular repressor of E1A-stimulated genes 1 (CREG1) as a crucial regulator of mitochondrial function and immune responses during ALV-J infection. We show that CREG1 overexpression enhances type I interferon (I-IFN) and interferon-stimulated genes (ISGs) expression, inhibiting viral replication. This is achieved through mitochondrial dysfunction, including reduced mitochondrial membrane potential, lower ATP production, and increased mitophagy and mitochondrial DNA release, which activate innate immunity. CREG1-induced mitochondrial dysfunction also triggers apoptosis by releasing cytochrome c and increasing reactive oxygen species (ROS). Furthermore, CREG1 interacts with heat shock protein 1 (HSPD1) to amplify its antiviral effects. Our findings establish CREG1 as a key antiviral gene and emphasize the importance of mitochondrial-mediated immune responses and apoptosis in ALV-J infection. ### Competing Interest Statement The authors have declared no competing interest. All the data required to support the conclusions of this paper are included within the main text and/or the Supplementary Materials. Original images of the Western blots and qPCR results are provided as supplementary content.

With the implementation of the policy of “centralized slaughtering and chilled to market” and the development of the livestock processing industry, numerous researchers have begun to focus on the selection and breeding of broilers bred for slaughter. The selection of breeds with excellent slaughtering performance and high meat production performance has become one of the most important selective breeding goals. In our previous study, we conducted transcriptome sequencing on chicken breast tissues with high and low breast muscle rates and found higher early growth response protein 1 (EGR1) expression in breast tissues with a low breast muscle ratio, thus hypothesizing that the EGR1 gene is involved in the growth and development process of chicken muscle tissues. Therefore, we analyzed the gene functions and polymorphisms of EGR1 to investigate its association with slaughter traits. We used various experimental methods, including RT-qPCR, Cell Counting Kit 8, 5-ethynyl-2’-deoxyuridine, western blot, flow cytometry, and immunofluorescence, to validate EGR1’s role in chicken primary myoblasts. The results of our functional validation experiments indicate that EGR1 is highly expressed in breast tissues with a low breast muscle content and plays a key role in regulating of muscle growth and development by promoting proliferation and inhibiting the differentiation of chicken primary myoblasts. In addition, we explored the relationship between the EGR1 gene polymorphisms and slaughter traits using mixed linear models for the first time. In a population of Jiangfeng M3 lineage partridge chickens, we identified 4 EGR1 single-nucleotide polymorphisms, 2 of which were significantly associated with slaughter traits, including live weight, slaughter weight, semi-eviscerated weight, eviscerated weight, leg weight, wing weight, and breast muscle rate. In summary, ectopic expression of EGR1 promotes the proliferation and differentiation of chicken primary myoblasts. In addition, polymorphisms in EGR1 were associated with slaughter performance, providing a potential basis for further utilization of EGR1 as a breeding marker.

Pullorum disease caused by Salmonella pullorum can negatively affect growth and egg-laying performance, resulting in significant economic losses in poultry farming. In this study, spleen tissues from SP-infected chickens (group P) and SP-uninfected chickens (group N) were analyzed for functional enrichment using whole-genome bisulfite and RNA sequencing. The function of the key gene MSX2 was verified by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay. Results indicated significant changes in the spleen methylation pattern of group P, primarily characterized by hypomethylation in the promoter, intron, and exon regions. Coanalysis identified six genes (MSX2, C21orf62, PGLYRP2, KCNQ3, SEZ6L, and SLC38A11) with significant alterations in differentially methylated regions and differentially expressed genes. MSX2 gene overexpression markedly enhanced the expression and secretion of immune factors [Interferon (IFN)-α, IFN-β, Interleukin (IL)-2, IL-3, and tumor necrosis factor-α] in chicken macrophages, suggesting that MSX2 may play a role in immune regulation in chickens. This study revealed the effects of Salmonella pullorum infection on DNA methylation and gene expression in chicken spleen tissues and screened several potential therapeutic targets, providing new insights and methods for the prevention and control of Pullorum disease.

Improving the quality of chicken meat while maintaining production efficiency is a challenging issue in poultry science. The current study was conducted to explore the effects of two feeding patterns (standard feed and omnivorous feed) on growth performance, slaughter performance, and meat quality traits of Xinghua (XH) chicken (indigenous chicken) and White Recessive Rock (WRR) chicken (commercial broiler). Feed consumption and body weight were determined weekly over 5 weeks, and meat quality traits with respect to breed and diet were evaluated. Mass spectrometry analyses facilitated the metabolomic profiling of breast muscle to reveal central metabolites associated with flavor formation. The metabolism of breast muscle was significantly altered by omnivorous feeding, which resulted in higher betaine concentrations and lower levels of creatine, acylcarnitines, and intermediates of amino acid biosynthesis. Breed-specific metabolic responses were noted: glycerophospholipid pathways were disrupted in WRR chickens, which had significantly lower levels of trimethylphosphate and triglycerides. Different flavor and texture profiles were correlated with these metabolic changes, with XH chickens exhibiting better flavor characteristics. Particularly for heritage breeds, this work offers practical advice for maximizing poultry diets while maintaining a balance between flavor enhancement and production efficiency.