Genetics of muscle and meat quality in chicken

Skeletal muscles in broilers are generally characterised by pathological muscle damage, indicated by greater plasma creatine kinase (CK) activity, higher incidence of haemorrhages, lighter and less coloured breast muscles, compared with layers and traditional breeds of chicken. Muscle damage is further exacerbated by exposure to stressful conditions such as high ambient temperatures which results in a further decrease in the quality of broiler meat and leads to the production of pale, soft and exudative (PSE) meat. This growing incidence of poor quality poultry meat is causing substantial losses to the meat industry. However, in contrast to pork the genetics of poor muscle and meat quality in chicken is unknown. The present project was conducted to identify the underlying genetics of this low quality meat by using heat-stress as a tool to amplify muscle damage and expression of the relevant genes. Whole-genome expression studies in broiler and layer breast muscles were conducted before and after heat-stress and some phenotypic data were also recorded. From the gene expression studies, 2213 differentially expressed genes (P<0.05) were found. About 700 of these genes had no gene ontology (GO) terms associated with them for biological process or function. The significant gene set was analysed in BioLayout Express and interesting clusters of the genes, based on their positive correlation with each other, were selected for further investigation. Genes were grouped together in 6 different categories or clusters, on the basis of their expression pattern. The genes in the selected clusters were analysed in Ingenuity Pathway Analysis (IPA) software, for each category separately, and relevant biological pathways and networks for those genes were studied. Similarly, the genes filtered out by BioLayout Express at a Pearson threshold of 0.80 were also analysed in IPA separately and interesting pathways and networks were selected. From the pathways and networks analyses of these genes, it was discovered that genes involved in inflammatory, cell death, oxidative stress and tissue damage related functions were up-regulated in control broilers compared with control and similar to heat-stressed layers. After exposure to heat-stress the expression levels of these genes were further increased in broilers. These results led us to develop the hypothesis that breast muscles in broilers are under stress-related damage even under the normal rearing conditions. This hypothesis was tested by rearing the broilers birds at normal/conventional and comparatively low ambient temperature and its effects on breast muscle quality and meat quality were studied. Significant improvement of breast muscle redness was observed. Additionally substantial numerical improvements for other meat and muscle quality traits like breast muscle lightness and histopathology were observed. From the key positions of interesting significant pathways and networks, candidate genes were selected for further investigation. In total, 25 candidate genes were selected for SNP genotyping: 19 genes were selected from the interesting pathways and networks and 6 genes were selected on the basis of their GO terms. For each gene 4-5 SNPs were selected, where possible, that were present in exons and promoter regions of the candidate genes. The selected SNPs were genotyped for muscle and meat quality traits in 34 breeds of chicken and significant causative SNPs for each trait including plasma CK activity, pHi and pHu for breast muscles, colour (L*, a*, and b*) traits for breast and thigh muscles were found. These SNPs were responsible for explaining a moderate to high (15-55%) percentage of phenotypic variance for these traits. To our knowledge this is the first study in which gene-expression in chicken breast muscle was conducted in response to heat-stress and additionally, for the first time, a set of novel SNPs for all of these traits were identified. Some of the significant causative SNPs were lying in the protein coding sequences and some were present in the promoter regions of the candidate genes.