Abstract
SummaryWe performed a genome-wide association study for Warner–Bratzler shear force (WBSF), a measure of meat tenderness, by genotyping 3360 animals from five breeds with 54 790 BovineSNP50 and 96 putative single-nucleotide polymorphisms (SNPs) within μ-calpain [HUGO nomenclature calpain 1, (mu/I) large subunit; CAPN1] and calpastatin (CAST). Within- and across-breed analyses estimated SNP allele substitution effects (ASEs) by genomic best linear unbiased prediction (GBLUP) and variance components by restricted maximum likelihood under an animal model incorporating a genomic relationship matrix. GBLUP estimates of ASEs from the across-breed analysis were moderately correlated (0.31–0.66) with those from the individual within-breed analyses, indicating that prediction equations for molecular estimates of breeding value developed from across-breed analyses should be effective for genomic selection within breeds. We identified 79 genomic regions associated with WBSF in at least three breeds, but only eight were detected in all five breeds, suggesting that the within-breed analyses were underpowered, that different quantitative trait loci (QTL) underlie variation between breeds or that the BovineSNP50 SNP density is insufficient to detect common QTL among breeds. In the across-breed analysis, CAPN1 was followed by CAST as the most strongly associated WBSF QTL genome-wide, and associations with both were detected in all five breeds. We show that none of the four commercialized CAST and CAPN1SNP diagnostics are causal for associations with WBSF, and we putatively fine-map the CAPN1 causal mutation to a 4581-bp region. We estimate that variation in CAST and CAPN1 explains 1.02 and 1.85% of the phenotypic variation in WBSF respectively.
Highlights
The associations between the CAST and CAPN1 loci with Warner–Bratzler shear force (WBSF) were the largest in the genome (Fig. 1), reflecting both the magnitude of effects of these genes and the increased single-nucleotide polymorphisms (SNPs) density within these regions, which improves the likelihood of finding SNP in strong Linkage disequilibrium (LD) with the causal mutations
We accomplished a much higher SNP density in the region harbouring CAPN1 than CAST, and this suggests that we had insufficient SNPs to find at least one that was in strong LD with the causal mutations within CAST in all breeds
In the case of CAPN1, the higher SNP density achieved and the use of across-breed analysis, which erodes the patterns of LD within breeds, resolved the likely location of the causal variant to a region of only 4581 bp
Summary
Force (WBSF) measurements on the longissimus dorsi muscle on chromosomes 2, 4, 5, 7, 10, 11, 15, 20, 25 and 29 (Casas et al 1998, 2000, 2001, 2003; Keele et al 1999; Rexroad et al 2001; Alexander et al 2007; Davis et al 2008; Gutierrez-Gil et al 2008; Gill et al 2009, 2010) From these reported QTL, DNA marker tests have been developed and commercialized only from calpastatin (CAST) on chromosome 7 and calpain 1, (mu/I) large subunit (CAPN1) on chromosome 29 (Page et al 2002, 2004; White et al 2005; Casas et al 2006; Van Eenennaam et al 2007). While positional candidate genes on other chromosomes have been investigated (Rexroad et al 2001; Stone et al 2005), none have resulted in commercial tests
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