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Summary: Aggression in group‐housed pigs is a welfare concern and can negatively affect production. Skin lesions are reliable indicators of aggression and are moderately heritable, suggesting that selective breeding may reduce aggression. To further understand the genetic control of behavioral traits, such as the aggressive response to regrouping, associated single nucleotide polymorphisms (SNPs) can be identified within the genome, and the region in which these SNPs are located can be related to known genes. To investigate SNPs associated with aggression, 1093 purebred Yorkshire pigs were strategically remixed into new groups of familiar and unfamiliar animals at three life stages and lesion counts were recorded. Genomic best linear unbiased prediction (GBLUP) models were fitted for each trait. The genetic additive effect was obtained from a genetic relationship matrix constructed from the 50 924 SNPs. SNP effects and their variances were estimated from the GBLUP objects. SNPs that were associated with a significant portion of the trait variance were identified for lesions to the anterior (three SNPs, FDR <5%) and central (one SNP, FDR <5%) portions of the body in grow‐finish pigs. These SNPs were located on chromosome 11, suggesting that chromosome 11 contains a region explaining variation in lesion counts that should be further explored to identify genes underlying biological control of aggression. [ABSTRACT FROM AUTHOR]

The identification of genomic regions that affect additive genetic variation and contain genes involved in controlling growth and fat deposition has enormous impact in the farm animal industry (e.g., carcass merit and meat quality). Therefore, a genomewide association study was implemented in an F2 pig population using a 60,000 SNP marker panel for traits related to growth and fat deposition. Estimated genomic EBV were linearly transformed to calculate SNP effects and to identify genomic positions possibly associated with the genetic variability of each trait. Genomic segments were then defined considering the markers included in a region 1 Mb up- and downstream from the SNP with the smallest P-value and a false discovery rate < 0.05 for each trait. The significance for each 2-Mb segment was tested using the Bonferroni correction. Significant SNP were detected on SSC2, SSC3, SSC5, and SSC6, but 2-Mb segment significant effects were observed on SSC3 for weight at birth (wt_birth) and on SSC6 for 10th-rib backfat and last-rib backfat measured by ultrasound at different ages. Furthermore, a 6-Mb segment on SSC6 was also considered because the 2-Mb segments for 10 different fat deposition traits were overlapped. Although the segment effects for each trait remain significant, the proportion of additive variance explained by this larger segment was slightly smaller in some traits. In general, the results confirm the presence of genetic variability for wt_birth on SSC3 (18.0-20.2 Mb) and for fat deposition traits on SSC6 (133.8-136.0 Mb). Within these regions, fibrosin (FBRS) and myosin light chain, phosphorylatable, fast skeletal muscle (MYLPF) genes could be considered as candidates for the wt_birth signal on SSC3, and the SERPINE1 mRNAbinding protein 1 gene (SERBP1) may be a candidate for the fat deposition trait signals on SSC6. [ABSTRACT FROM AUTHOR]

The leptin receptor (LEPR) is a type I cytokine receptor that binds the leptin protein known to regulate food intake and energy metabolism, and is a functional candidate gene for regulating economically important phenotypic traits in pigs. The objective of our research is to determine the effect of a single nucleotide polymorphism (SNP) in exon 14 of the LEPR gene on adipose tissue LEPR transcript abundance and carcass composition phenotypes in the Michigan State University Pig Resource Population. This population is a F2 cross between Duroc and Pietrain breeds. A total of 51 female pigs were selected based on LEPR exon 14 SNP genotypes (n=17 per CC, CT, and TT genotype). Total RNA was isolated from subcutaneous fat tissue samples and analyzed using real-time RT-PCR to obtain LEPR expression levels, with SDHA and ACTB as controls. A conditional analysis was performed using Genomic Best Linear Unbiased Prediction with the LEPR exon 14 genotypes as fixed effects, and LEPR gene expression and carcass composition phenotypes as response variables. A significant dominance effect was identified with the TT genotype showing significantly lower expression than the CC and CT genotypes (p=1.20e-02 and 4.05e-02, respectively). The presence of a C allele was associated with significantly higher LEPR expression than the T allele (p=8.61e-03). The heritability of LEPR gene expression was found to be moderate at 0.29. However, the proportion of variance explained by the LEPR SNP was 12% of the total gene expression variance. Conditional analysis for carcass composition phenotypes identified significant dominance effects for eight phenotypic traits including marbling, carcass loin muscle area, ham and loin weight and four backfat thickness measures (p≤0.05). The T allele was significantly associated with decreased backfat thickness and increased carcass loin muscle area, and ham and loin weight. A genome-wide association analysis identified two quantitative trait loci (QTL) for tenth-rib and last-lumbar backfat phenotypes on SSC6. The heritability of these traits were moderate at 0.43. The conditional analysis for these two backfat phenotypes completely removed the significance of the QTLs on SSC6, accounting for up to 8% of the phenotypic variance. This study highlights the LEPR exon 14 SNP as a candidate marker regulating variation in LEPR transcript abundance, and backfat and muscle phenotypes, with the C allele associated with increased LEPR gene expression and backfat thickness, and decreased muscle mass. [ABSTRACT FROM AUTHOR]