Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: April 8, 1998
Publication Date: N/A
Interpretive Summary: A resource flock of 362 F2 lambs produced from Dorset and Romanov breeds provided the carcass and genotypic data necessary to refine the map position of the callipyge gene to a 3.9 cM interval of Chromosome 18. Efforts to identify the specific gene responsible for dramatic effects on muscle development and carcass composition will be enhanced by these results. Gene action was characterized by the unique callipyge phenotype in only heterozygous animals that inherited the allele from their sire. All other genotypes had a normal phenotype. Structured mating systems can be employed to maximize the number of market progeny exhibiting the callipyge phenotype by mating homozygous carrier rams to homozygous non- carrier ewes, both of which have normal phenotypes. This gene provides an excellent example of how marker-assisted selection can be used to benefit the livestock industry, and an opportunity to better understand muscle growth and development in all species.
Genotypic and phenotypic data were collected to estimate chromosomal position of the callipyge gene (CLPG) and to test gene action, and quantify allelic effects on carcass traits. Nine Dorset rams of extreme muscling phenotype and 114 Romanov ewes comprised the grandparent generation of a resource flock of 362 F2 lambs segregating at the CLPG locus. The parent generation consisted of matings of eight F1 sires and 138 F1 dams. A linkage group of 25 marker loci (mean of 708 informative meioses per marker) spanning 87.2 cM was developed for ovine chromosome 18. Probabilities of each genotype at the CLPG locus were calculated at 1-cM intervals (0 to 107 cM). Orthogonal contrasts of genotypic probabilities produced coefficients to evaluate additive, maternal dominance, and paternally derived polar overdominance models of gene action. Statistical models included effects of year, sex, sire, and genetic contrast specific linear and quadratic regressions on appropriate covariates. The most parsimonious model did not include the additive and maternal dominance genetic contrasts. From analyses of four key traits, a consensus for position of CLPG was obtained at 86 cM relative to the most centromeric marker. An F test with 3 df representing the polar overdominance contrast was maximum at position 86 cM (F=407.4; P<.00001) when leg score was the dependent variable. These results are consistent with the assignment of CLPG locus to the telomeric region of chromosome 18 and support the polar overdominance model of gene action proposed by Cockett et al. (1996). Furthermore, recombinant individuals with definitive phenotypes were present in this population and confined the position of CLPG to a 3.9-cM interval, facilitating future positional cloning experiments.