A candidate gene analysis to identify QTL and causal variants for meat tenderness in Nelore cattle

The objective of this study was to detect QTLs and search for causal mutations in candidate genes for meat tenderness trait in Nelore cattle using haplotypes of varying size and overlapping sliding windows. Two significant haplotypes, located in ASAP1 and CAPN1 genes, were associated (P <= 0.10) to meat tenderness trait among 52 candidate genes in 1616 animals, after Bonferroni correction. Twenty-one new SNPs (17 in CAPN1 and 4 in ASAP1), identified by sequencing, were analyzed along with all SNPs from the BovineHD assay located in these genes. Six regions explained the highest genetic variances for meat tenderness, from which one is in CAPN1 and the other five are in ASAP1. CAPN1 encodes u-calpain, which degrades myofibrillar proteins post-mortem. Fitting all the SNPs of CAPN1 simultaneously in the model explained 0.025% of the total additive genetic variance. The region that explained the greatest amount of additive genetic variance in CAPN1 is explaining 0.002%, located within introns 15 through 20. ASAP1 encodes a signal transduction protein that enhances the potential of fibroblasts to differentiate into adipocytes. The proportion of additive genetic variance explained by the SNPs present in ASAP1 was 0,22%, seven times more than CAPN1. This suggests that a strategy to improve meat tenderness in Nelore cattle may be to increase the amount of adipocytes within the muscle which would likely also impact the flavor and palatability of the meat. There may be as many as 5 putative distinct QTL regions present in ASAP1 for meat tenderness in this population. The first QTL is in the intron 1, the second QTL is situated from intron 2 through intron 3, the third is in intron 3, the fourth is located in intron 5 and the last QTL spans the region from intron 16 to 25 of ASAP1. These QTLs are explaining 0.0014%, 0.0016%, 0.0014%, 0.0022% and 0.002% of the total additive genetic variance in meat tenderness in this population, respectively. However, we did not find evidence for single variants having causal effects on meat tenderness and suspect that they may be effects on regulatory function or the translational efficiency of transcripts of these genes.