Evaluation of the Ovine Callipyge Locus: I. Relative Chromosomal Position and Gene Action

Authors

B. A. Freking, U.S. Meat Animal Research Center, Clay Center, NEFollow
J. W. Keele, Roman L. Hruska U.S. Meat Animal Research Center, USDA-ARS, Clay Center, NEFollow
C. W. Beattie, Roman L. Hruska U.S. Meat Animal Research Center, USDA-ARS, Clay Center, NE
S. M. Kappes, Roman L. Hruska U.S. Meat Animal Research Center, USDA-ARS, Clay Center, NE
T. P.L. Smith, U.S. Meat Animal Research CenterFollow
T. S. Sonstegard, Roman L. Hruska U.S. Meat Animal Research Center, USDA-ARS, Clay Center, NE
Merlyn K. Nielsen, University of Nebraska-LincolnFollow
Kreg A. Leymaster, University of Nebraska-LincolnFollow

Document Type

Article

Date of this Version

1998

Comments

Published in J. Anim. Sci. 1998. 76:2062–2071. Copyright © 1998 American Society of Animal Science. Used by permission.

Abstract

Genotypic and phenotypic data were collected to estimate chromosomal position of the callipyge (CLPG) gene and to test gene action. Nine Dorset rams of extreme muscling phenotype and 114 Romanov ewes composed the grandparent generation of a resource flock of 362 F₂ lambs segregating at the CLPG locus. The parent generation consisted of eight F₂ sires and 138 F₁ dams. The F₂ lambs were serially slaughtered in six groups at 3-wk intervals starting at 23 wk of age to allow comparisons at different end points. A linkage group of 25 marker loci (mean of 708 informative meioses per marker) spanning 87.2 cM was developed and improved the previous known coverage and precision of marker order and interval distance from available maps of ovine chromosome 18. Probabilities of each CLPG genotype were calculated at 1-cM intervals (0 to 107 cM). Statistical models included effects of year, sex, sire, regressions on genotypic probabilities, and genotype-specific linear and quadratic regressions on appropriate covariates. Orthogonal contrasts of CLPG genotypic effects evaluated additive, maternal dominance, and paternally derived polar overdominance models of gene action. 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 polar overdominance was maximum at position 86 cM (F = 407.4; P < .00001) with leg score as the dependent variable. These results are consistent with assignment of the 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 confined the position of CLPG to a 3.9-cM interval, facilitating positional cloning experiments.