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ARS Home » Plains Area » Clay Center, Nebraska » U.S. Meat Animal Research Center » Genetics and Animal Breeding » Research » Publications at this Location » Publication #306256

Title: CAPN1, CAST, and DGAT1 genetic effects on preweaning performance, carcass quality traits, and residual variance of tenderness in a beef cattle population selected for haplotype and allele equalization

item Tait Jr, Richard
item Shackelford, Steven
item Wheeler, Tommy
item King, David - Andy
item Keele, John
item Casas, Eduardo
item Smith, Timothy - Tim
item Bennett, Gary

Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/8/2014
Publication Date: 12/1/2014
Publication URL:
Citation: Tait, R.G., Jr., Shackelford, S.D., Wheeler, T.L., King, D.A., Keele, J.W., Casas, E., Smith, T.P., Bennett, G.L. 2014. CAPN1, CAST, and DGAT1 genetic effects on preweaning performance, carcass quality traits, and residual variance of tenderness in a beef cattle population selected for haplotype and allele equalization. Journal of Animal Science. 92(12):5382-5393.

Interpretive Summary: Genetic markers within mu-calpain, calpastatin, and diacylglycerol O-acyltransferase 1 genes previously associated with beef quality traits did not always have animals with two copies of the rare alleles in previous studies. Selection was performed to ensure observations with all three genotypes (2 copies of common allele, heterozygotes, and 2 copies of rare allele) could be evaluated for their effects on beef quality traits. This work confirms the importance of mu-calpain and calpastatin genetic markers for changing average beef tenderness. It also identifies the mode of inheritance for calpastatin as additive, with no interaction between calpastatin and mu-calpain on beef tenderness. Beyond changes in the average beef tenderness associated with the genetic markers, we also identified differences in variability of beef tenderness associated with the calpastatin genetic marker. This provides more information about the probability of a particular animal producing tough beef, which may not be acceptable to a consumer. The diacylglycerol O-acyltransferase 1 genetic marker significantly affected subcutaneous fat thickness, with a dominant mode of inheritance identified. Information about the effect size, mode of inheritance, and lack of interaction between genetic markers are important for developing breeding and management systems to be used by cattle producers to produce tender, high quality beef desirable to U.S. and international consumers.

Technical Abstract: Genetic marker effects and type of inheritance are estimated with poor precision when minor marker allele frequencies are low. A stable composite population (MARC III) was subjected to marker assisted selection for multiple years to equalize specific marker frequencies to 1) estimate effect size and mode of inheritance for previously reported single nucleotide polymorphisms (SNP) on targeted beef carcass quality traits (254 steers); 2) estimate pleiotropic effects of previously reported SNP on nontarget performance traits (542 or 254 steers); and 3) evaluate tenderness SNP specific residual variance for ribeye (LM) tenderness. Three haplotypes within µ-calpain (CAPN1), a SNP in calpastatin (CAST) and a dinucleotide substitution in diacylglycerol O-acyltransferase 1 (DGAT1) were successfully selected to equalize their frequencies. Traits evaluated were: body weights (at birth, weaning, yearling, and pre-harvest), dressing percent, carcass weight, fat thickness, LM area, USDA marbling score, yield grade, LM slice shear force (SSF), and visible and near infrared (VISNIR) predicted SSF. While this study lacked the power to identify a significant CAPN1 genotype effect (P = 0.12) on SSF, the direction and size of CAPN1 contrasts were consistent with previous research. Effects on SSF between divergent CAPN1 haplotypes (1.153 kg) and the additive effect of CAST (0.902 kg) were large and animals homozygous for tender alleles at both CAPN1 and CAST would have 4.11 kg lower SSF (27.5% of the mean) than animals homozygous tough for both markers. Furthermore, the interaction between CAPN1 and CAST for SSF was not significant (P = 0.40). There were significant effects for DGAT1 on adjusted fat thickness (P = 0.02) and VISNIR predicted SSF with additive and dominance modes of inheritance for both traits. Furthermore, CAST specific residual variance models fit significantly better (P < 0.001) than single residual variance models for SSF, with the tougher genotypes having progressively larger residual (and hence phenotypic) variances. Thus, risk of a tough steak from the undesired CAST genotype is increased through both an increase in mean and an increase in variation. This work is supportive of the importance of CAPN1 and CAST for mean tenderness in beef, confirms an effect of CAST on beef LM tenderness variation, and identifies an effect of DGAT1 on subcutaneous fat thickness.