Submitted to: Symposium Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 5/10/2004
Publication Date: 7/19/2004
Citation: Freking, B.A., Smith, T.P., Leymaster, K.A. 2004. Meat quality and the callipyge gene, consumer acceptance and final product. In: Proceedings of the 7th World Sheep and Wool Congress 2004, July 17-24, 2004, Quebec, Canada. p. 92-102.
Interpretive Summary: Discovery of the causative polymorphism for CLPG muscle hypertrophy marks the starting point for future research efforts to determine the mechanism by which this single base change leads to such marked phenotypic alterations. New insights into basic biology of imprinting regulation in this important region of the genome for livestock and humans will certainly be an outcome of future research in this area. Functional interactions among gene products and regulatory elements or transcripts from this genetic region will need to be evaluated in greater detail. From a sheep production standpoint, implementation of this mutation in a terminal sire crossbreeding system where the paternal population is fixed for the mutated allele and the maternal population is fixed for the normal allele is now manageable with availability of a DNA diagnostic test. Evaluation of germplasm resources, both within and between breeds, that could be used in combination with the CLPG locus to shift the distribution of longissimus shear force to an acceptable level is a high priority. A genetic solution or an easily adaptable postmortem intervention strategy that solves the tenderness antagonism would have great impact on lean meat production in sheep. Detection of genomic regions favorably influencing tenderness would allow opportunities to select within specialized sire lines to capture both the benefits and mitigate the antagonisms associated with this mutation.
Technical Abstract: The callipyge (meaning beautiful buttocks) phenotype in sheep is the result of a naturally occurring mutation producing dramatic effects on muscle development and carcass composition through altered fiber type distribution (increased fast-twitch glycolytic), increased average fiber diameter, and decreased fat deposition. This hypertrophy condition was more pronounced in muscles of the hind leg and loin regions. Genetic location of the mutation (CLPG) was mapped to the distal end of sheep chromosome 18 and subsequently identified as a single nucleotide polymorphism in an imprinted domain region between the DLK1 and MEG3 genes. Imprinting status of several genes in this region was not changed by the mutation but expression levels of several transcripts have been altered. Paternally expressed transcripts are up regulated when the mutation is present on the paternal gamete and maternally expressed transcripts are up regulated when the mutation is present on the maternal gamete. Gene action exhibited at CLPG is referred to as paternal polar overdominance, due to the expression of the muscle hypertrophy phenotype only in sheep that receive a mutated allele from the sire and a normal allele from the dam. Large favorable effects of this mutation on slaughter and carcass composition traits have been identified. However, adverse effects on meat tenderness require an intervention strategy to ensure a favorable eating experience. Intervention strategies have been effective at decreasing the tenderness problem but remain difficult to implement on a commercial basis.