Abstract

Background : As an effort to reduce the incidence of boar taint, surgical castration is routinely performed on young male piglets. However, the practice of castration raises animal welfare concerns and is undesirable from a production point of view since the elimination of sex hormones reduces feed efficiency and growth. Androstenone is one of the major chemical compounds responsible for boar taint which is characterized by an unpleasant taste and smell from the meat. Primary objectives of this study were to discover new single nucleotide polymorphisms (SNPs) within androstenone associated QTL region reported earlier on SSC13 and then utilize a batch of these SNPs for testing the association between three proposed positional candidate genes- solute carrier family 22 (organic anion transporter), member 13 (SLC22A13) and solute carrier family 22 (organic anion transporter), member 14 (SLC22A14) and activin receptor type-2B precursor (ACVR2B) and fat androstenone levels in a population of 922 Norwegian Duroc pigs. Results : In this paper, we discovered several thousands of putative new single nucleotide polymorphisms (SNPs) within this QTL region using ~4.92 billion 100bp paired-end illumina whole genome re-sequencing reads of 23 Norwegian Duroc sires. A subset of these SNPs (n=83) in addition to 27 SNPs from the Porcine illumina SNP60 BeadChip were utilized for genotyping on 922 Norwegian Duroc offspring with androstenone records. Overall 66 new and 15 illumina genotyped SNPs were further used for testing associations with the levels of androstenone in fat tissue. The association study revealed that a total of 5 new SNPs and one illumina SNP of sodium channel, voltage-gated (SCN) genes was significantly affecting the levels of fat androstenone (p<0.05). Further analysis determined a significant (p<0.05) haplotype block of 23-SNP . Conclusions : Genotyped SNPs in three proposed candidate genes were not explaining any phenotypic variance for androstenone levels but 5 new SNPs and one illumina SNP within another cluster of SCN genes (SCN5A, SCN10A and SCN11A) were, however, significantly affecting levels of fat androstenone.

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