Abstract

Simple SummaryWhen searching for genetic markers for the selection of more tender beef, it is important to maintain minimal environmental variation from pre-slaughter, right through to the ageing process, to ensure the accuracy of the obtained phenotypes. This is because beef quality traits have a large environmental component that can greatly alter the characteristics of the meat, which would not reflect a true genetic effect. We propose that variable ageing times are especially important in determining whether markers are associated with tenderization or not. Our analyses included candidate genes for the protein degrading enzyme system for calpains, because they contribute the most to tenderization. We were able to validate these markers in South African beef cattle, where they could be useful for selection. The timing of the collection of tenderness data was critical, as only a few (6/134) genetic markers sustained their association with tenderization over ageing to 20 days. A larger tenderization effect earlier in ageing, as shown here for the capn1_187 and capn1_4751 markers, would decrease the length of ageing. This would not only increase profits, but also decrease the energy needed during the storage and refrigeration of aged beef, decreasing the carbon footprint of beef production.The most important factor that determines beef tenderness is its proteolytic activity, and the balance between calpain-1 protease activity and calpastatin inhibition is especially important, while contributions can also arise from calpain-2 and, possibly, calpain-3. The meat ageing process itself affects these processes. To determine whether genotypes in the calpain–calpastatin system can enhance tenderness through a 20-day ageing period, South African purebred beef bulls (n = 166) were genotyped using the Illumina BovineHD SNP BeadChip through a gene-based association analysis targeting the cast, capn3, capn2 and capn1 genes. The Warner–Bratzler shear force (WBSF) and myofibril fragment length (MFL) of Longissimus thoracis et lumborum (LTL) steaks were evaluated between d 3 and d 20 of ageing, with protease enzyme activity in the first 20 h post-mortem. Although several of the 134 SNPs are associated with tenderness, only seven SNP in the cast, capn2 and capn1 genes sustained genetic associations, additive to the ageing-associated increases in tenderness for at least three of the four ageing periods. While most genomic associations were relatively stable over time, some genotypes within the SNP responded differently to ageing, resulting in altered genomic effects over time. The level of ageing at which genomic associations are performed is an important factor that determines whether SNPs affect tenderness phenotypes.

Highlights

  • Increased tenderness with beef ageing involves the weakening of the myofibrillar structure of muscle fibers through the degradation of myofibrillar proteins [1–3]

  • Of the total 134 single nucleotide polymorphisms (SNPs) tested in the gene-based association analyses, 62 SNPs showed some association with tenderness phenotypes in the Warner–Bratzler shear force (WBSF) or myofibril fragment length (MFL) in at least one of the ageing periods (p ≤ 0.10), while 38 SNPs associated significantly (p ≤ 0.05) with tenderness

  • More than 80% of the SNPs that could affect tenderness would likely fail to associate with tenderness from a single measurement, because they only associated with tenderness phenotypes for a short period of ageing

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Summary

Introduction

Increased tenderness with beef ageing involves the weakening of the myofibrillar structure of muscle fibers through the degradation of myofibrillar (and other) proteins [1–3]. By extending the ageing period, tougher steaks that age at a slower rate can achieve greater levels of tenderness [9] and it is important in (for example) cattle with a larger Bos indicus genetic background [10], allowing for an improved quality before going to market. This results in logistical challenges of chilled storage and tracking large amounts of beef over extended time periods, whereas the ultimate goal is to accelerate these processes as much as possible [11] and shorten the ageing period [12]. Disease resistance SNPs [24] and potential beef quality SNPs have been identified [25], association studies using detailed tenderness phenotypes in the calpain–calpastatin system have only been performed with a very limited SNP pool [26]

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