Genome-wide association study for bone strength in laying hens

Bone fracture in egg laying hens is a growing welfare and economic concern in the industry. Although environmental conditions and management (especially nutrition) can exacerbate it, the primary cause of bone weakness and the resulting fractures is believed to have a genetic basis. To test this hypothesis, we performed a genome-wide association study to identify the loci associated with bone strength in laying hens. Genotype and phenotype data were obtained from 752 laying hens belonging to the same pure line population. These hens were genotyped for 580,961 single nucleotide polymorphisms (SNPs), with 232,021 SNPs remaining after quality control. Each of the SNPs were tested for association with tibial breaking strength using the family-based score test for association (FASTA). A total of 52 SNPs across chromosomes 1, 3, 8, and 16 were significantly associated with tibial breaking strength with the genome-wide significance threshold set as a corrected P-value of 10e-5. Based on the local linkage disequilibrium around the significant SNPs, five distinct and novel QTLs were identified on chromosomes 1 (two QTLs), 3 (one QTL), 8 (one QTL) and 16 (one QTL). The strongest association was detected within the QTL region on chromosome 8, with the most significant SNP having a corrected P-value of 4e-7. A number of candidate genes were identified within the QTL regions, including the BRD2 gene which is required for normal bone physiology. Bone-related pathways involving some of the genes were also identified including chloride channel activity which regulates bone reabsorption and intermediate filament organization, which plays a role in the regulation of bone mass. Our result supports previous studies that suggest that bone strength is highly regulated by genetics. It is therefore possible to reduce bone fractures in laying hens through genetic selection, and ultimately improve hen welfare