Release 56
(Apr 24, 2025)

Reference # 22497262 Details:

Authors:Gutiérrez-Gil B, Wiener P, Williams J L, Haley C S (Contact: pam.wiener@roslin.ed.ac.uk)
Affiliation:Departamento de Producción Animal, Facultad de Veterinaria, Universidad de León, León, 24071, Spain.
Title:Investigation of the genetic architecture of a bone carcass weight QTL on BTA6.
Journal:Animal Genetics, 2012, (6): 654-61 DOI: 10.1111/j.1365-2052.2012.02322.x
Abstract:

A previous analysis of an F(2) /Backcross Charolais × Holstein cross population identified the presence of a highly significant QTL on chromosome 6 (BTA6) affecting the proportion of bone in the carcass. Two closely linked QTL affected birth weight (BW) and body length at birth (BBL). In this report, the marker density around the QTL on BTA6 was increased, adding four additional microsatellite markers across the chromosome and 46 SNPs within the target QTL confidence interval. Of the SNPs, 26 were in positional candidate genes and the remaining 20 provided an even distribution of markers in the target QTL region. As a bone-related trait, the sum of the bone weight for all the left fore- and hindquarter joints of the carcass was analysed. We also studied the BW and BBL. Analyses of the data substantially reduced the QTL confidence interval. No strong evidence was found that the QTL for the three traits studied are different, and we conclude that the results are consistent with a single pleiotropic QTL influencing the three traits, with the largest effects on the proportion of bone in the carcass. The analyses also suggest that none of the SNPs tested is the sole causative variant of the QTL effects. Specifically, the SNP in the NCAPG gene previously reported as a causal mutation for foetal growth and carcass traits in other cattle populations was excluded as the causal mutation for the QTL reported here. Polymorphisms located in other previously identified candidate genes including SPP1, ABCG2, IBSP, MEPE and PPARGC1A were also excluded. The results suggest that SNP51_BTA-119876 is the polymorphism in strongest linkage disequilibrium with the causal mutation(s). Further research is required to identify the causal variant(s) associated with this bone-related QTL.

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