|Smith, Timothy - Tim|
|King, David - Andy|
|Thallman, Richard - Mark|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 4/20/2009
Publication Date: 5/9/2009
Citation: Snelling, W.M., Smith, T.P., Shackelford, S.D., King, D.A., Wheeler, T.L., Kuehn, L.A., Thallman, R.M., Keele, J.W., Bennett, G.L. 2009. Whole Genome Analysis for Beef Tenderness [abstract]. Bovine Genome Consortium, Cold Spring Harbor, New York. May 9-11, 2009. Session 5 Poster Session, p. 30.
Technical Abstract: Meat tenderness is the single most important trait affecting palatability and consumer satisfaction with beef products. Current breeding values for meat tenderness traits have low accuracy because progeny phenotypes are not generally recorded. Selection for this trait could be accelerated by DNA markers associated with tenderness. Markers in the bovine mu-calpain (CAPN1) and calpistatin (CAST) genes are in commercial use, but do not completely explain genetic variation. We performed whole genome association analysis to identify loci contributing to variation in beef tenderness in a set of crossbred animals having tenderness phenotypes. Warner-Bratzler Shear Force (WBSF) of longissimus dorsi from 1,667 steers harvested between 12 and 16 months of age were analyzed. Individual SNP effects were estimated with mixed models including SNP genotype with other fixed and random polygenic animal effects. Additive polygenic and genomic variances due to sets of SNP were then estimated. Fixed effects included age of dam, contemporary group, and covariates for breed composition, heterosis and harvest age. Additive polygenic and genomic effects were considered random. Polygenic effects were correlated according to a pedigree-based relationship matrix (A). Genomic effects were correlated with genotype-based relationship matrices (As) constructed for each set. The 4,242 animals represented in both A and As included 2,918 genotyped individuals, and 1,324 animals (mostly dams) with genotypes predicted by a single-locus BLUP procedure. SNP with minor allele frequencies <.05 were excluded. Sets of SNP evaluated were the 3 SNP previously associated with WBSF, SNP associated with WBSF according to nominal P<.001 (48 SNP) and P<.01 (447). SNP with P>.10 (39,694) were separately analyzed to include SNP unlikely to affect WBSF. These latter SNP appear to account for little variation, with polygenic (h2p) and genomic heritability (h2g) estimates of .29 +/- .08 and .00 +/- .03, respectively. The CAPN1 and CAST SNP accounted for a fraction of additive variation, with h2g estimated to be .03 +/- .03 and h2p = .27 +/- .07. At P<.001, additive variance was split evenly, with h2g = .20 +/- .04 and h2p = .20 +/- .05. Additive genetic variation shifted almost wholly to the genomic components with SNP meeting P<.01; estimates were h2g = .40 +/- .03 and h2p = .04 +/- .04. Thus there is additional variation segregating in the population, in addition to that accounted for by the current markers, and selection for tenderness would benefit from specific markers for tracking this variation.