Genome-wide association study for bone strength in laying hens1

Abstract

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 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. 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, 5 distinct and novel QTLs were identified on chromosomes 1 (2 QTLs), 3 (1 QTL), 8 (1 QTL) and 16 (1 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 that 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.

An eQTL in the cystathionine beta synthase gene is linked to osteoporosis in laying hens

“…Although some report QTL on chromosome 1, these do not appear to coincide with the QTL that we finemapped in this study [61,62]. Using a genome-wide association approach in one of the populations in this study, loci with a larger effect than the CBS loci have been observed, which suggests we can make progress in finding the underlying mechanism for these loci if large enough samples can be assembled [63].…”

Explanations for keel bone fractures in laying hens: are there explanations in addition to elevated egg production?

“…To summarize, there are clear genetic effects on bone quality, which can be supported by a number of direct studies in addition to between-breed studies already mentioned ( Bishop et al., 2000 ; Dunn et al., 2007 ; Podisi et al., 2012 ; Eusemann et al., 2018a ; Raymond et al., 2018 ). There are some studies that seem to corroborate the role of AFE in bone quality, but it must also be recognized that a number of studies do not show effects.…”

Multimarker and rare variants genomewide association studies for bone weight in Simmental cattle

“…PRKAR2B is the most abundant regulatory subunit in endocrine tissues. Previous endeavours have demonstrated that mutations of PRKAR2B are associated with (Kerkhof et al, 2010) and with bone strength in laying hens (Raymond, 2016). NR2F2 and RIMS2 have been scarcely investigated in livestock.…”

“…NR2F2 is a member of the nuclear receptor superfamily, which is widely expressed in the mesenchymal compartment of developing tissues and organs including the heart, blood vessels, muscles and limbs. NR2F2 was reported to induce adipogenic differentiation and suppress osteoblastic differentiation (Raymond, 2016). RIMS2, which codes for a presynaptic active zone protein that regulates synaptic vesicle exocytosis of neurotransmitters, plays an important role in controlling bone remodelling through stimulation, maturation and differentiation of osteoblasts and osteoclasts.…”