Yellow skin is an abundant phenotype among domestic chickens and is caused by a recessive allele (W*Y) that allows deposition of yellow carotenoids in the skin. Here we show that yellow skin is caused by one or more cis-acting and tissue-specific regulatory mutation(s) that inhibit expression of BCDO2 (beta-carotene dioxygenase 2) in skin. Our data imply that carotenoids are taken up from the circulation in both genotypes but are degraded by BCDO2 in skin from animals carrying the white skin allele (W*W). Surprisingly, our results demonstrate that yellow skin does not originate from the red junglefowl (Gallus gallus), the presumed sole wild ancestor of the domestic chicken, but most likely from the closely related grey junglefowl (Gallus sonneratii). This is the first conclusive evidence for a hybrid origin of the domestic chicken, and it has important implications for our views of the domestication process.

Breed utilization, genetic improvement, and industry consolidation are predicted to have major impacts on the genetic composition of commercial chickens. Consequently, the question arises as to whether sufficient genetic diversity remains within industry stocks to address future needs. With the chicken genome sequence and more than 2.8 million single-nucleotide polymorphisms (SNPs), it is now possible to address biodiversity using a previously unattainable metric: missing alleles. To achieve this assessment, 2551 informative SNPs were genotyped on 2580 individuals, including 1440 commercial birds. The proportion of alleles lacking in commercial populations was assessed by (1) estimating the global SNP allele frequency distribution from a hypothetical ancestral population as a reference, then determining the portion of the distribution lost, and then (2) determining the relationship between allele loss and the inbreeding coefficient. The results indicate that 50% or more of the genetic diversity in ancestral breeds is absent in commercial pure lines. The missing genetic diversity resulted from the limited number of incorporated breeds. As such, hypothetically combining stocks within a company could recover only preexisting within-breed variability, but not more rare ancestral alleles. We establish that SNP weights act as sentinels of biodiversity and provide an objective assessment of the strains that are most valuable for preserving genetic diversity. This is the first experimental analysis investigating the extant genetic diversity of virtually an entire agricultural commodity. The methods presented are the first to characterize biodiversity in terms of allelic diversity and to objectively link rate of allele loss with the inbreeding coefficient.alleles ͉ biodiversity ͉ poultry

Yellow skin is an abundant phenotype among domestic chickens and is caused by a recessive allele (W*Y) that allows deposition of yellow carotenoids in the skin. Here we show that yellow skin is caused by one or more cis-acting and tissuespecific regulatory mutation(s) that inhibit expression of BCDO2 (beta-carotene dioxygenase 2) in skin. Our data imply that carotenoids are taken up from the circulation in both genotypes but are degraded by BCDO2 in skin from animals carrying the white skin allele (W*W). Surprisingly, our results demonstrate that yellow skin does not originate from the red junglefowl (Gallus gallus), the presumed sole wild ancestor of the domestic chicken, but most likely from the closely related grey junglefowl (Gallus sonneratii). This is the first conclusive evidence for a hybrid origin of the domestic chicken, and it has important implications for our views of the domestication process.

Background: One of the loci responsible for feather development in chickens is K. The K allele is partially dominant to the k+ allele and causes a retard in the emergence of flight feathers at hatch. The K locus is sex linked and located on the Z chromosome. Therefore, the locus can be utilized to produce phenotypes that identify the sexes of chicks at hatch. Previous studies on the organization of the K allele concluded the integration of endogenous retrovirus 21 (ev21) into one of two large homologous segments located on the Z chromosome of late feathering chickens. In this study, a detailed molecular analysis of the K locus and a DNA test to distinguish between homozygous and heterozygous late feathering males are presented.

An association study between SNP markers and feather condition score on the back, rump and belly of laying hens was performed. Feather condition score is a measure of feather damage, which has been shown to be closely related to feather pecking behaviour in hens housed in groups. A population of 662 hens was genotyped for 1536 SNPs of which 1022 could be used for the association study. The analysis was conducted across 9 different lines of White Leghorn and Rhode Island Red origin. Across lines linkage disequilibrium is conserved at shorter distances than within lines; therefore, SNPs significantly associated with feather condition score across lines are expected to be closer to the functional mutations. The SNPs that had a significant across-line effect but did not show significant SNP-by-line interaction were identified, to test that the association was consistent across lines. Both the direct effect of the individual's genotype on its plumage condition, and the associative effect of the genotype of the cage mates on the individual's plumage condition were analysed. The direct genetic effect can be considered as the susceptibility to be pecked at, whereas the associative genetic effect can be interpreted as the propensity to perform feather pecking. Finally, 11 significant associations between SNPs and behavioural traits were detected in the direct model, and 81 in the associative model. A role of the gene for the serotonin receptor 2C (HTR2C) on chromosome 4 was found. This supports existing evidence of a prominent involvement of the serotonergic system in the modulation of this behavioural disorder in laying hens. The genes for IL9, IL4, CCL4 and NFKB were found to be associated to plumage condition, revealing relationships between the immune system and behaviour.

The aim of the present study was to detect quantitative trait loci (QTL) for innate and adaptive immunity in laying hens. For this purpose, the associations between 1022 single nucleotide polymorphism (SNP) markers and immune traits were studied in 583 hens from nine different layer lines. Immune traits were natural antibodies for keyhole limpet haemocyanin (KLH) and lipopolysaccharide (LPS) at 20, 40 and 65 weeks, acquired antibodies to the vaccinal virus of Newcastle disease at 20 weeks, and complement activity measured on sheep and bovine red blood cells at 20, 40 and 65 weeks. We adopted a novel approach based on across-line analysis and testing of the SNP-by-line interaction. Among lines, linkage disequilibrium is conserved at shorter distances than in individual lines; therefore, SNPs significantly associated with immune traits across lines are expected to be near the functional mutations. In the analysis, the SNPs that had a significant across-line effect but did not show significant SNP-by-line interaction were identified to test whether the association was consistent in the individual lines. Ultimately, 59 significant associations between SNPs and immune traits were detected. Our results confirmed some previously identified QTL and identified new QTL potentially involved in the immune function. We found evidence for a role of IL17A (chromosome 3) in natural and acquired antibody titres and in the classical and alternative pathways of complement activation. The major histocompatibility genes on chromosome 16 showed significant association with natural and acquired antibody titres and classical complement activity. The IL12B gene on chromosome 13 was associated with natural antibody titres.

BackgroundAn association study between single nucleotide polymorphism markers (SNP) and (innate and adaptive) immune parameters but also feather condition score on the back, rump and belly of laying hens was performed. The immune parameters measured in blood samples were natural and acquired antibody titers and complement activity. Feather condition score as a measure of feather damage was determined, this parameter is closely related to feather pecking behavior in hens housed in groups.The aim of the study was to detect associations between genetic markers and immune parameters and feather condition score across nine lines of laying hens, focusing on the feather peckers as well as on the victims of feather pecking.MethodsA novel approach based on across-line analysis and testing of the SNP-by-line interaction was performed.ResultsIn total 59 significant associations between SNP and immune traits were detected. Previously identified QTL were confirmed and new associations of genes regulating immune function identified. The IL17A gene (chromosome 3) influences natural and acquired antibody titers and activation of classical and alternative complement pathways. The major histocompatibility complex on chromosome 16 showed significant association with natural and acquired antibody titers and classical complement activity. The IL12B and IRF1 genes on chromosome 13 were associated with natural antibody titers.The direct effect of the genotype of an individual on its feather condition and the associative effect of the genotype of the cage mates on the individual’s feather condition were analyzed. The direct genetic effect can be described as the susceptibility to be pecked at, and the associative genetic effect as the propensity to perform feather pecking. Eleven significant associations were detected for the direct effect, and 81 for the associative effect. The serotonin receptor 2C (HTR2C) on chromosome 4 was highlighted in both analyses.ConclusionsOur results confirmed previously identified QTL and identified new associations of genes regulating immune function. The results for feather condition score supports existing evidence of involvement of the serotonergic system in feather pecking in laying hens. Immune regulatory genes were found to be associated to feather condition score, revealing relationships between the immune system and behavior.

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