Carotenoid consumption decreases the risk of cancer, osteoporosis, or neurodegenerative diseases through interrupting the formation of free radicals. The deposition of carotenoids in chicken skin makes the skin color turn from white into yellow. The enzyme β-carotene oxygenase 2 (BCO2) plays a key role during the degradation process of carotenoids in skin. How the BCO2 affects the skin color of the chicken and whether it is the key factor that results in the phenotypic difference between yellow- and white-skin chickens are still unclear. In this research, the measurement of the concentration of carotenoids in chicken skin by HPLC showed that the carotenoid concentration in chickens with a yellow skin was significantly higher than that in white-skin chickens. Moreover, there were significant differences in BCO2 gene expression in the back skin between yellow- and white-skin chickens. Scanning the SNPs in BCO2 gene revealed a G/A mutation in exon 6 of the BCO2 gene in white and yellow skin chicken. Generally, one SNP c.890A>G was found to be associated with the chicken skin color and may be used as a genetic marker in breeding for yellow skin in Chinese indigenous chickens.

Chicken is a valuable model for understanding fundamental biology, vertebrate evolution and diseases, as well as a major source of nutrient-dense and lean-protein-enriched food globally. Although it is the first non-mammalian amniote genome to be sequenced, the chicken genome still lacks a systematic characterization of functional impacts of genetic variants. Here, through integrating 7,015 RNA-Seq and 2,869 whole-genome sequence data, the Chicken Genotype- Tissue Expression (ChickenGTEx) project presents the pilot reference of regulatory variants in 28 chicken tissue transcriptomes, including millions of regulatory effects on primary expression (including protein-coding genes, lncRNA and exon) and post-transcriptional modifications (alternative splicing and 3’ untranslated region alternative polyadenylation). We explored the tissue-sharing and context-specificity of these regulatory variants, their underlying molecular mechanisms of action, and their utility in interpreting adaptation and genome-wide associations of 108 chicken complex traits. Finally, we illustrated shared and lineage-specific features of gene regulation between chickens and mammals, and demonstrated how the ChickenGTEx resource can further assist with translating genetic findings across species. One-Sentence Summary: The ChickenGTEx provides a multi-tissue reference of regulatory variants for chicken genetics and genomics, functional genomics, precision breeding, veterinary medicine, vertebrate evolution and even human biomedicine.

Methyltransferase 3 (METTL3), which has been demonstrated to play a crucial role in a variety of biological processes, is the key enzyme for catalyzing m⁶A modification in RNA. However, the complete protein sequence of METTL3 in quail has not been annotated, and its function in skeletal muscle of quails remains unknown. In the current study, the full-length coding sequence of the quail METTL3 was obtained through the 3′ rapid amplification of cDNA ends (3’ RACE) and its homology with that of other species was predicted based on a generated phylogenetic tree. A Cell Counting Kit-8 assay and flow cytometry in a quail myoblast cell line (QM7) demonstrated that METTL3 promotes myoblast proliferation. The overexpression of METTL3 in QM7 cells significantly increased the expression levels of the myoblast differentiation markers myogenin (MYOG), myogenic differentiation 1 (MYOD1), and myocyte enhancer factor 2C (MEF2C), further demonstrating that METTL3 promotes myoblast differentiation. Additionally, transcriptome sequencing following METTL3 overexpression revealed that METTL3 controls the expression of various genes involved in RNA splicing and the regulation of gene expression, as well as pathways such as the MAPK signaling pathway. Taken together, our findings demonstrated that METTL3 plays a vital function in quail myoblast proliferation and differentiation and that the METTL3-mediated RNA m⁶A modification represents an important epigenetic regulatory mechanism in poultry skeletal muscle development.

The extensive use of antibiotics in poultry production has contributed to antimicrobial resistance, creating a need for safe and stable alternatives. This study evaluated the effects of Bacillus amyloliquefaciens F1 postbiotics (BAP) on growth performance, antioxidant status, intestinal morphology, and cecal microbiota in yellow-feathered broilers. A total of 360 one-day-old male broilers were randomly and evenly assigned to three dietary treatments for 63 days: a basal diet (control, CON), the basal diet separately supplemented with 100 g/t (BAP100) and 150 g/t (BAP150) of BAP. At 21 days, broilers in BAP-supplemented groups exhibited significantly higher body weight (approximately 7.5 % increase, P < 0.01) and average daily gain (approximately 8 % increase, P < 0.01), with a 9 % reduction in feed conversion ratio (P < 0.05) compared to the CON group. The BAP100 group maintained greater body weight at 42 days (6 % increase, P < 0.05). Serum and hepatic antioxidant enzyme activities were significantly enhanced in BAP groups, including glutathione peroxidase (GSH-Px, +24 %, P < 0.01), catalase (CAT, +28 %, P < 0.01), and total antioxidant capacity (T-AOC, +31 %, P < 0.01), while malondialdehyde (MDA) levels declined by approximately 40 % (P < 0.05). Histological examination revealed improved intestinal morphology, characterized by increased villus height and villus-to-crypt ratios in the jejunum and ileum (P < 0.05). Additionally, BAP supplementation up-regulated MUC2 mRNA expression (P < 0.05) and modulated the abundance of specific cecal bacteria at 63 days (P < 0.05), without altering overall microbial diversity. In conclusion, dietary supplementation with Bacillus amyloliquefaciensF1 postbiotics improved growth performance and intestinal health in yellow-feathered broilers, with the 100 g/t dose yielding the most pronounced early benefits.

Background: Avian Influenza virus (AIV) and Newcastle disease virus (NDV) are highly contagious immunosuppressive pathogens that cause high mortality rates and economic losses in the global poultry industry. Although vaccination to enhance the host antibody response remains the main control strategy, the genetic basis of this variation is poorly understood. In this study, we used a genome-wide association study (GWAS) to investigate the genetic architecture of the longitudinal antibody responses to AIV (subtypes H5, H7, and H9) and NDV in chickens. Results: To identify the genomic regions and candidate genes associated with the longitudinal antibody response to AIV and NDV after immunization, we conducted a GWAS using 1,359,927 SNP markers in an advanced intercross line (AIL) of the F19 resource population. We found moderate heritability for both the traits. Based on these associations, we identified the genomic regions and candidate genes for both traits. Association analysis revealed two significant SNPs located on chromosome 3, rs316474025 near NFKBIE and SLC35B2 [rs316474025], and rs312870707 near ATG5 gene, that are associated with viral antibody titers against AIV subtypes H5 and H7, respectively. Additionally, one variant on chromosome 27, rs318005864 near DDK12 and RPL19 genes, was strongly linked to the antibody response associated with NDV at mid-phase (40 days post-immunization). Furthermore, another variant, rs737164663, near FRMD5 and GLCE genes, was strongly linked to the antibody titer associated with both AIV subtype H9 and NDV in the late phase (60 days post-immunization). Genes located in these regions may be responsible for the immune response in chickens. Before implementation in breeding programs, the efficacy and long-term persistence of selecting these antibody response traits should be validated in larger independent cohorts. Conclusions: We confirmed the presence of genetic variability and identified SNPs significantly associated with antibody titer traits in F19 chickens. These findings highlight genomic regions contributing to variation in antibody responses and provide valuable information for improving antibody-related traits through selective breeding programs.

Chicken is a valuable model for understanding fundamental biology and vertebrate evolution, as well as a major source of nutrient-dense and lean-protein-enriched food globally. Although it is the first non-mammalian amniote genome to be sequenced, the chicken genome still lacks a systematic characterization of functional variation. Here, through integrating bulk RNA-Seq of 7,015 samples, single-cell RNA-Seq of 127,598 cells and 2,869 whole-genome sequences, we presented an atlas of regulatory variants across 28 chicken tissues and 43 cell types, including millions of regulatory effects on primary expression (protein-coding genes, lncRNA and exon) and post-transcriptional modifications (alternative splicing and 3’ untranslated region alternative polyadenylation). We highlighted distinct molecular mechanisms underlying these regulatory variants and their context dependence and utility in interpreting genome-wide associations of 108 chicken complex traits. Finally, we illustrated lineage-specific features of gene regulation between chickens and mammals, and demonstrated how this resource can assist with cross-species gene mapping of complex traits.