Revealing genetic relationships between compounds affecting boar taint and reproduction in pigs.
ABSTRACT Boar taint is characterized by an unpleasant taste or odor in intact male pigs and is primarily attributed to increased concentrations of androstenone and skatole and to a lesser extent by increased indole. The boar taint compounds skatole and indole are produced by gut bacteria, metabolized in the liver, and stored in the fat tissue. Androstenone, on the other hand, is synthesized in the testis along with testosterone and estrogens, which are known to be important factors affecting fertility. The main goal of this study was to investigate the relationship between genetic factors involved in the primary boar taint compounds in an attempt to discover ways to reduce boar taint without decreasing fertility-related compounds. Heritabilities and genetic correlations between traits were estimated for compounds related to boar taint (androstenone, skatole, indole) and reproduction (testosterone, 17β-estradiol, and estrone sulfate). Heritabilities in the range of 0.47 to 0.67 were detected for androstenone concentrations in both fat and plasma, whereas those for skatole and indole were slightly less (0.27 to 0.41). The genetic correlations between androstenone in plasma and fat were extremely high (0.91 to 0.98) in Duroc and Landrace. In addition, genetic correlations between androstenone (both plasma and fat) and the other sex steroids (estrone sulfate, 17β-estradiol, and testosterone) were very high, in the range of 0.80 to 0.95. Furthermore, a genome-wide association study (GWA) and a combined linkage disequilibrium and linkage analysis (LDLA) were conducted on 1,533 purebred Landrace and 1,027 purebred Duroc to find genome regions involved in genetic control of the boar taint compounds androstenone, skatole, and indole, and sex hormones related to fertility traits. Up to 3,297 informative SNP markers were included for both breeds, including SNP from several boar taint candidate genes. From the GWA study, we found that altogether 27 regions were significant at a genome-wide level (P < 0.05) and an additional 7 regions were significant at a chromosomal level. From the LDLA study, 7 regions were significant on a genome-wide level and an additional 7 regions were significant at a chromosomal level. The most convincing associations were obtained in 6 regions affecting skatole and indole in fat on chromosomes 1, 2, 3, 7, 13, and 14, 1 region on chromosome 6 affecting androstenone in plasma only, and 5 regions on chromosomes 3, 4, 13, and 15 affecting androstenone, testosterone, and estrogens.
01/2011; , ISBN: 978-81-308-0469-9.
Article: New investigations around CYP11A1 and its possible involvement in an androstenone QTL characterised in Large White pigs.[show abstract] [hide abstract]
ABSTRACT: Previously, in boars with extreme androstenone levels, differential expression of the CYP11A1 gene in the testes has been characterised. CYP11A1 is located in a region where a QTL influencing boar fat androstenone levels has been detected in a Large White pig population. Clarifying the role of CYP11A1 in boar taint is important because it catalyses the initial step of androstenone synthesis and also of steroid synthesis. A genome-wide association study located CYP11A1 at approximately 1300 kb upstream from SNP H3GA0021967, defining the centre of the region containing the QTL for androstenone variation. In this study, we partially sequenced the CYP11A1 gene and identified several new single nucleotide polymorphisms (SNP) within it. Characterisation of one animal, heterozygous for CYP11A1 testicular expression but homozygous for a haplotype of a large region containing CYP11A1, revealed that variation of CYP11A1 expression is probably regulated by a mutation located downstream from the SNP H3GA0021967. We analysed CYP11A1 expression in LW families according to haplotypes of the QTL region's centre. Effects of haplotypes on CYP11A1 expression and on androstenone accumulation were not concordant. This study shows that testicular expression of CYP11A1 is not solely responsible for the QTL influencing boar fat androstenone levels. As a conclusion, we propose to refute the hypothesis that a single mutation located near the centre of the QTL region could control androstenone accumulation in fat by regulating the CYP11A1 expression.Genetics Selection Evolution 01/2011; 43:15. · 2.88 Impact Factor