Submitted to: Journal of Animal Science
Publication Type: Peer reviewed journal
Publication Acceptance Date: 6/23/2004
Publication Date: 9/1/2004
Citation: Casas, E., Bennett, G.L., Smith, T.P., Cundiff, L.V. 2004. Association of myostatin on early calf mortality, growth, and carcass composition traits in crossbred cattle. Journal of Animal Science. 82:2913-1918. Interpretive Summary: The objective of this study was to associate the form of the gene that causes double-muscling in cattle with calf mortality and see its effect on carcass traits. The inactive myostatin allele was associated with early life mortality. Animals with two copies of this allele are more susceptible to harsh conditions at birth. Producers would need to consider the conditions at calving in their management decisions before producing calves with two copies of the inactive myostatin allele. The inactive myostatin allele affects growth and carcass traits in crossbred cattle. This allele tends to produce leaner and more muscled carcasses. Production systems that produce calves with one copy of the inactive myostatin allele will benefit from heavier weaning weights and higher yield of lean, compared to calves with zero copies of the inactive myostatin allele.
Technical Abstract: The objective of this study was to investigate a potential association of an inactive myostatin allele with early calf mortality, and evaluate its impact 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 MARC 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 prior to weaning. Early calf mortality was examined in the F2 subpopulation (n = 154), derived from the F1 sires mated 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 unequally 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, and postweaning average daily gain. Carcass composition traits analyzed were hot carcass weight, fat thickness, longissimus area, marbling score, USDA yield grade, estimated kidney-pelvic-heart fat, retail product yield and weight, fat yield and weight, bone yield and weight, and percentage of carcasses classified as Choice. 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 X 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, while 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.