Genetic independence of fat depots in cattle.

Abstract

The amount and distribution of adipose tissue is important to cattle production. Fat influences the animal’s reproductive efficiency and determines its carcass value. As a cow’s reproductive efficiency is associated with a level of overall fatness, not just a particular fat depot, being able to re-partition fat to a more valuable depot while reducing fat in less valuable depots would be advantageous. Most previous research involving fat deposition in cattle focussed on subcutaneous and intramuscular fat, and usually evaluated these in relation to total fat or carcass weight rather than the relationship between individual fat depots. The hypothesis that there is a genetic basis for variation in fat distribution in cattle and a weak relationship between fat depots independent of anatomical site was tested. The principal aim of this research was to gain a better understanding of the mechanisms controlling fat deposition in cattle, including any relationship between fat depots. Marbling features (e.g. shape and orientation) and seam (intermuscular) fat area were quantified using image analysis. The seam fat area and other carcass fat measurements were used to examine the relationship between fat depots. Candidate genes for fat deposition traits were identified and sequenced in Jersey – Limousin mapping sires to find single nucleotide polymorphisms (SNPs). In all, 33 SNPs from 11 candidate genes for fat deposition were selected for association studies in the sire progeny. There was large variation in all of the measures but the variation was largely independent of other marbling factors. The seam fat area data were used to identify a quantitative trait locus on chromosome 19, and subsequently identify candidate genes for seam fat area. In general, there were low correlations between fat traits suggesting the relationship between the depots was not strong. The fixed effects of cohort, breed and myostatin variant affected general fat deposition. However, sire affected fat distribution, as no sire had progeny consistently higher or lower for all fat traits. These results suggest there is only a weak genetic link between the fat depots. The size of effect was small for most of the SNPs associated with fat deposition, although there were some candidate genes with sizeable effects, for example, tyrosine kinase, endothelial (TEK1) (channel fat, 28%) and ß, ß-carotene 15, 15'-monooxygenase (BCMO1) (subcutaneous fat, 20%). Moreover, the combined effect of all SNPs affecting a single trait explained 38% (channel fat), 26% (seam fat and subcutaneous fat) and 23% (omental fat) of the phenotypic variation. Interestingly, although some genes were associated with variation in more than one fat trait, no one gene was associated with all fat traits or overall fatness. The major conclusion from the research described herein is that there is genetic influence on fat deposition in addition to the effects of age, breed and management, the deposition of fat into the various adipose sites is controlled in an independent manner genetically and there appears to be no one gene that affects deposition in all sites. There were four principal results that support this conclusion; 1) there were low correlations between fat traits, 2) there were no sires with progeny consistently high or low for all fat traits, 3) the QTL for the various fat depots did not overlap with each other, and 4) no SNP was associated with all fat traits. These results indicate that there is large scope for selecting for and against individual fat traits without altering other fat depots.