Feed efficiency is a key economic trait that affects the cost of production in broiler farming. Reducing broiler feed costs contributes to reducing excessive feed consumption and increasing the productivity of broiler breeding. Therefore, identifying genetic regions associated with feed efficiency is crucial for broiler breeding. In this study, we performed genome-wide association (GWAS) analyses of feed conversion ratio (FCR) and residual feed intake (RFI) traits for four growth cycles (72–81, 81–89, 89–113, and 113–120 days of age) using 55K single-nucleotide microarray genotypic data of 4493 Wenchang chickens from two generations. In the single-trait GWAS, a total of 59 SNPs were identified, and 36 genes were annotated within the ±50 kb regions surrounding candidate loci (including ABCC6, CLDN10, DGKB, EXT2, FOXO1, IFT140, JAG2, among others. These candidate loci explained 1.4–7.0% of the phenotypic variance explained, and applying a filtering criterion that required a deleteriousness score greater than 8, one locus-Gallus gallus chromosome (GGA) 5:3550350 (chCADD score = 12.51524) was located within intron 3 of ANOX3. In the FCR and RFI traits in the longitudinal GWAS (LONG-GWAS) model, 80 SNPs and 191 SNPs were identified, respectively, and a total of 43 genes and 121 genes were annotated. A total of 33 candidate loci were screened by combining the locus deleteriousness scores, and 25 candidate genes were annotated within the upper and lower 50 kb ranges. Through KEGG signaling pathway analysis, it was found that the candidate genes were highly enriched mainly in autophagy, mitochondrial phagocytosis, and other pathways. In conclusion, the SNPs and potential genes identified in this study will be helpful for chicken breeding and provide fundamental data for the genetic basis of chicken feed efficiency-related traits.

Clinical investigations have highlighted disruptions in bone metabolic processes and abnormal fluctuations in serum indicator levels during the onset of leg disease (LD) in broilers. However, the presence of a genetic causal relationship for this association remains undetermined. Therefore, the aim of this study is to discern the risk factors underlying LD development using 1235 sequenced white-feathered broilers. We employed Mendelian randomization (MR) analysis to assess the associations of bone strength (BS), bone mineral density (BMD), tibial bone weight (TBW), tibial bone length (TBL), tibial bone diameter (TBD), bone ash (BA), ash calcium (Ash Ca), ash phosphorus (Ash P), serum calcium (Ca), serum phosphorus (P), serum alkaline phosphatase (ALP), and serum osteoprotegerin (OPG) with the incidence of LD. Compelling evidence underscores a causal link between the risk of developing LD and decreased BMD (odds ratio (OR) = 0.998; 95% CI: 0.983, 0.993; P < 0.001) and narrower TBD (OR = 0.985, 95% CI: 0.975, 0.994, P = 0.002). Additionally, serum OPG concentrations (OR: 0.995, 95% CI: 0.992, 0.999, P = 0.008) were associated with BMD (OR = 0.0078, 95% CI = 0.0043 to 0.0140, P < 0.001), indicating a robust genetic relationship between ALP concentrations (OR: 0.988, 95% CI: 0.984, 0.993, P < 0.001) and TBD (OR = 0.0046, 95% CI = 0.0026, 0.0083, P < 0.001). Moreover, elevated serum Ca (OR: 0.564, 95% CI: 0.487, 0.655, P < 0.001) and P (OR: 0.614, 95% CI: 0.539, 0.699, P < 0.001) levels were associated with a narrower TBD. Elevated serum levels of Ca, P, ALP, and OPG contribute to disturbances in bone metabolism, while decreased BMD and narrower TBD are associated with a greater risk of developing LD in broilers. This discovery elucidates the metabolic risk factors for LD in broilers and could provide information on LDs, such as osteoporosis, in humans.