U.S. Department of Agriculture: Agricultural Research Service, Lincoln, Nebraska
Date of this Version
2016
Document Type
Article
Citation
From: 2016 Beef Improvement Federation Annual Meeting & Symposium, June 14 - 17, 2016, Hilton Garden Inn, Manhattan, Kansas.
Abstract
Historic surveys of retail beef have identified beef tenderness as a critical issue to consumer acceptability of beef and suggested continued investigation of pre-harvest and postharvest interventions to improve beef tenderness (Morgan et al., 1991). Koohmaraie (1996) identified the protease μ-calpain (CAPN1) and its inhibitor calpastatin (CAST) as major factors affecting post-mortem tenderization in meat. Genetic markers in CAPN1 (Page et al., 2002; White et al., 2005) and CAST (Casas et al., 2006; Morris et al., 2006) are commercially available to beef producers. However, early studies evaluating these markers had low frequency of rare homozygote animals and occasionally ignored those animals from analysis (White et al., 2005; Morris et al., 2006) – removing the opportunity to evaluate mode of inheritance (additive or dominance) for a genetic marker. Therefore, selection was used in 2 populations (Angus and U.S. Meat Animal Research Center III – ¼ Angus, ¼ Hereford, ¼ Red Poll, and ¼ Pinzgauer composite) to equalize the allele frequency of CAPN1 haplotypes and CAST genotypes to enhance estimates for slice shear force (SSF) of: 1) effect size, 2) mode of inheritance, and 3) interaction between CAPN1 and CAST (Tait et al., 2014a; Tait et al., 2014b). Furthermore, these studies evaluated the potential for genotype specific residual variances and found these models to fit significantly better than single residual variance models for CAST genotypes.
Comments
Copyright 2016 The Authors.