U.S. Department of Agriculture: Agricultural Research Service, Lincoln, Nebraska
Date of this Version
2004
Document Type
Article
Citation
J. Anim. Sci. 2004. 82:2913–2918
Abstract
The objective of this study was to investigate a potential association of an inactive myostatin allele with early calf mortality, and evaluate its effect on growth and carcass traits in a crossbred population. Animals were obtained by mating F1 cows to F1 (Belgian Blue x British Breed) or Charolais sires. Cows were obtained from mating Hereford, Angus, and U.S. Meat Animal Research Center III ( ¼ Hereford, ¼ Angus, ¼ Pinzgauer, and ¼ Red Poll) dams to Hereford, Angus, Tuli, Boran, Brahman, or Belgian Blue sires. Belgian Blue was the source of the inactive myostatin allele. Myostatin genotypes were determined for all animals including those that died before weaning. Early calf mortality was examined in the F2 subpopulation (n = 154), derived from the F1 siresmated to F1 cows from Belgian Blue sires, to evaluate animals with zero, one, or two copies of inactive myostatin allele. An overall 1:2:1 ratio (homozygous active myostatin allele:heterozygous:homozygous inactive myostatin allele) was observed in the population; however, a comparison between calves dying before weaning and those alive at slaughter showed an unequal distribution across genotypes (P < 0.01). Calves with two copies of the inactive allele were more likely (P < 0.01) to die before weaning. Postweaning growth traits were evaluated in the surviving animals (n = 1,370), including birth, weaning, and live weight at slaughter, and postweaning ADG. Carcass composition traits analyzed were hot carcass weight, fat thickness, LM area, marbling score, USDA yield grade, estimated kidney, pelvic, and heart fat, retail product yield and weight, fat yield and weight, bone yield and weight, and percentage of carcasses classified as Choice. Charolais lack the inactive myostatin allele segregating in Belgian Blue; thus, in the population sired by Charolais (n = 645), only animals with zero or one copy of the inactive myostatin allele were evaluated. Animals carrying one copy were heavier at birth and at weaning, and their carcasses were leaner and more muscled. In the population sired by Belgian Blue × British Breed (n = 725), animals with two copies of inactive myostatin allele were heavier at birth, leaner, and had a higher proportion of muscle mass than animals with zero or one copies. Heterozygous animals were heaviest at weaning and had the highest live weight, whereas animals with zero copies had the highest fat content. The use of the inactive myostatin allele is an option to increase retail product yield, but considerations of conditions at calving are important to prevent mortality.
Comments
Copyright 2004 American Society of Animal Science. All rights reserved.