The relationship between the histochemical and biochemical properties of muscle and the quality of meat during selection to improving the lean tissue growth rate was studied. Pigs (n = 82) from Generations 2 and 4 were randomly sampled in a selection experiment in which the genotype x protein interaction was studied. Comparisons were made of longissimus muscle (LM) and quadriceps femoris (QF) from Generations 2 and 4, and biceps femoris (BF) in the fourth generation from pigs fed a low- or high-protein diet. A higher total growth rate, lean tissue growth rate, and lean percentage were found in pigs fed the high-protein diet than in pigs fed the low-protein diet. Pigs fed the high-protein diet had a higher glycolytic capacity in all muscles than pigs fed the low-protein diet. When the meat quality traits were compared, pigs fed the high-protein diet had a lower intramuscular fat content, higher shear force value, higher protein extractability, lower light reflectance, and somewhat higher water-holding capacity. With selection, pigs became fatter on both diets. In Generation 4, glycolytic and oxidative capacity was somewhat higher in muscle tissue than in Generation 2. Muscle metabolic profile and meat quality traits differed among muscles (LM, BF, QF) but no pronounced differences were found between generations. No marked changes were observed in Type I, IIA, or IIB fibers, either between diets or between generations. The Type IIC fibers could only be identified in Generation 4.
Quantitative trait loci (QTLs) with large effects on fatness and growth have been identified previously on pig chromosome 4 in an intercross between the European wild pig and Large White domestic pigs. Two F 2 sows, heterozygous for the actual chromosome region, were backcrossed to a Large White boar, and two backcross (BC 1 ) boars were in turn backcrossed to Large White/Landrace sows. One of the boars was heterozygous for an intact wild pig-derived QTL region, whereas the other carried a recombinant haplotype. A total of 85 BC 2 animals were produced. Phenotypical measurements included daily weight gain, ultrasonic measurements of fat depth at 70 and 90 kg and several carcass traits. QTL segregation was deduced using 15 markers previously assigned to chromosome 4. Highly significant QTL effects were observed on all fatness traits and on the length of the carcass. A small but significant effect on growth was also observed. The results confirm the presence of one or more QTLs on chromosome 4 affecting fatness and growth. There was a good agreement between the estimates of QTL effects in the F 2 and BC 2 generations. The results from the recombinant sire family allowed us to map the major QTL effect distal to the recombination breakpoint. We propose that this confirmed QTL with a major effect on fatness is designated FAT1.Keywords: abdominal visceral fat, growth, pig, quantitative trait loci, subcutaneous fat.
IntroductionGenetic dissection of complex polygenic traits is a topical subject in humans, plants and animals (Lander & Schork, 1994;Paterson, 1995;Georges & Andersson, 1996). We have previously identified quantitative trait loci (QTLs) for growth and fatness traits in an intercross between two divergent populations of pigs, the European wild pig and the Large White domestic pig (Andersson et al., 1994;Knott et al., 1998). The study was the first genome-wide screening for QTLs in outbred animals. The QTLs with the largest effect were located on chromosome 4 and explained about 12% and 18% of the phenotypical variance in the F 2 generation for growth and fatness traits respectively. The wild pig alleles at these loci were associated with reduced growth and higher fat deposition, as expected because of the intense selection for lean growth in modern domestic pigs.It is essential that the presence and location of QTLs are confirmed before attempts are made towards their cloning or exploitation in animal breeding by marker-assisted selection. There are, in fact, several reasons why one may fail to confirm the QTL in a subsequent experiment: e.g. (i) the original observation may be a type I error (see Lander & Kruglyak, 1995); (ii) the QTL effect may depend on epistasis (Frankel & Schork, 1996); (iii) a large QTL effect may be caused by several linked QTLs each with a small effect, and the linkage may break up in subsequent generations; (iv) the estimated QTL effect may be seriously inflated when the power of QTL detection is low (Georges et al., 1995); (v) segregation at the QTL in the recipient population ma...
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