Combined effect of microbially derived cecal SCFA and host genetics on feed efficiency in broiler chickens.

BACKGROUND: Improving feed efficiency is the most important goal for modern animal production. The regulatory mechanisms of controlling feed efficiency traits are extremely complex and include the functions related to host genetics and gut microbiota. Short-chain fatty acids (SCFAs), as significant metabolites of microbiota, could be used to refine the combined effect of host genetics and gut microbiota. However, the association of SCFAs with the gut microbiota and host genetics for regulating feed efficiency is far from understood. RESULTS: In this study, 464 broilers were housed for RFI measuring and examining the host genome sequence. And 300 broilers were examined for cecal microbial data and SCFA concentration. Genome-wide association studies (GWAS) showed that four out of seven SCFAs had significant associations with genome variants. One locus (chr4: 29414391-29417189), located near or inside the genes MAML3, SETD7, and MGST2, was significantly associated with propionate and had a modest effect on feed efficiency traits and the microbiota. The genetic effect of the top SNP explained 8.43% variance of propionate. Individuals with genotype AA had significantly different propionate concentrations (0.074 vs. 0.131 µg/mg), feed efficiency (FCR: 1.658 vs. 1.685), and relative abundance of 14 taxa compared to those with the GG genotype. Christensenellaceae and Christensenellaceae_R-7_group were associated with feed efficiency, propionate concentration, the top SNP genotypes, and lipid metabolism. Individuals with a higher cecal abundance of these taxa showed better feed efficiency and lower concentrations of caecal SCFAs. CONCLUSION: Our study provides strong evidence of the pathway that host genome variants affect the cecal SCFA by influencing caecal microbiota and then regulating feed efficiency. The cecal taxa Christensenellaceae and Christensenellaceae_R-7_group were identified as representative taxa contributing to the combined effect of host genetics and SCFAs on chicken feed efficiency. These findings provided strong evidence of the combined effect of host genetics and gut microbial SCFAs in regulating feed efficiency traits. Video Abstract.

Several models combined with ultrasound techniques to predict breast muscle weight in broilers.

The weight of breast muscle (WBM) is a highly monitored indicator in broiler breeding that can be obtained after slaughtering. Currently, due to the lack of accurate in vivo phenotypes for both genomic and phenotypic selection, genetic gains in WBM fall short of initial expectations. In this study, 1,006 market-age (42 d) broilers from 3 generations over 2 yr were randomly selected, and the breast width (BW), fossil bone length (FBL), breast muscle thickness (BMT), and live weight (LW) were measured exactly in vivo. Eight models, including multiple linear regression (MLR), ridge regression (RR), least absolute shrinkage and selection operator (LASSO), and elastic net (EN), were fitted to explore the best regression relationships between breast muscle weight and these indicators. Support vector machine (SVM) methods with both linear kernels and radial kernels were used to fit the models, while 2 decision tree-based machine learning algorithms, random forest (RF), and extreme gradient boosting (XGBoost), were used to establish the prediction model. The predictive effects of different combinations of independent variables were compared, leading to the conclusion that the EN model achieves the best predictive power when all 4 live features are used as inputs and is slightly better than the other models (R2 = 0.7696). This method could be applied in practical production and breeding work, leading to substantial cost savings and enhancements in the breeding process.

SPOP promotes ubiquitination and degradation of MyD88 to suppress the innate immune response.

As a canonical adaptor for the Toll-like receptor (TLR) family, myeloid differentiation primary response protein 88 (MyD88) has crucial roles in host defense against infection by microbial pathogens, and its dysregulation might induce autoimmune diseases. Here, we demonstrate that the chicken Cullin 3-based ubiquitin ligase adaptor Speckle-type BTB-POZ protein (chSPOP) recognizes the intermediate domain of chicken MyD88 (chMyD88) and degrades it through the proteasome pathway. Knockdown or genetic ablation of chSPOP leads to aberrant elevation of chMyD88 protein. Through this interaction, chSPOP negatively regulates NF-κB pathway activity and thus the production of IL-1ß upon LPS challenge in chicken macrophages. Furthermore, Spop-deficient mice are more susceptible to infection with Salmonella typhimurium. Collectively, these findings demonstrate MyD88 as a bona fide substrate of SPOP and uncover a mechanism by which SPOP regulates MyD88 abundance and disease susceptibility.