Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/29/2008
Publication Date: 2/5/2009
Citation: Kuehn, L.A., Nonneman, D.J., Klindt, J.M., Wise, T.H. 2009. Genetic relationships of body composition, serum leptin, and age at puberty in gilts. Journal of Animal Science. 87(2):477-483.
Interpretive Summary: Age at puberty can be used as a measure for reproductive fitness and subsequent breeding performance in swine production. However, measurement of age at puberty in gilts requires daily monitoring of gilts exposed to teaser boars. Genetic markers and correlated traits may alleviate the need to expend labor and time in measurement of age at puberty and allow selection of animals that reach puberty earlier. Body composition (backfat), body weight, and leptin levels were measured when crossbred gilts expressed their first estrus. Additionally, genetic markers within QTL regions for age at puberty and candidate genes for leptin concentration were developed and used to genotype the same set of gilts. Leptin at puberty had a strong negative genetic correlation with age at puberty and a marker in the leptin receptor was significantly associated with leptin concentrations at puberty. A marker in PAX5 on chromosome 1 was associated with decreased age at puberty. This marker, or others in this region, may be useful in a selection program for decreased age at puberty.
Technical Abstract: Leptin produced by adipocytes acts through leptin receptors in the hypothalamus to control appetite and food intake and thus communicates information about degree of fatness. It is thought that a degree of body fat is required for initiation of puberty and maintenance of reproductive function in mammals. The objective of this study was to determine whether polymorphisms in the leptin (LEP), leptin receptor (LEPR), paired box 5 (PAX5), aldo-keto reductase (AKR), and pro-opiomelnocortin (POMC) genes were associated with age, leptin concentration, backfat as an indicator of body condition, and body weight at puberty in 3 lines of gilts. The first two lines, born in 2001, were formed by crossing maternal White Cross (Yorkshire x Maternal Landrace) gilts to either Duroc (n = 210) or (lean) Landrace (n = 207) boars. The remaining line (n = 507), born in 2002, was formed by crossing progeny of the Duroc- and Landrace-sired lines. At first estrus, BW and BF were recorded and blood collected for leptin assays. Seven SNP were detected in candidate genes/regions: 1 in LEP, 3 in LEPR, 1 in PAX5, 2 in AKR, and 2 in POMC. Animals were genotyped for each of the SNP; genotypes were validated using GenoProb. The association model included fixed effects of farrowing group, covariates of genotypic probabilities (from GenoProb), and random additive polygenic effects to account for genetic similarities between animals not explained by SNP. Variance components for polygenic effects and error were estimated using MTDFREML. Leptin concentrations were logarithmically transformed for data analysis. All four traits were moderately to highly heritable (0.38 to 0.48). Age and leptin at puberty were significantly correlated at -0.63 ± 0.097, and the correlation between BW and age at puberty was 0.65 ± 0.083. Significant additive associations (a; P < 0.05) were detected at PAX5 for age at puberty (a = 3.2 d) and for BF at puberty (a = 0.61 mm). One SNP in LEPR was associated with leptin concentration (a = 0.31 log units; P < 0.05). The associations from PAX5 correspond to a QTL peak for age at puberty detected on SSC1. While not necessarily the causative mutation, this result does imply that a QTL that can decrease age at puberty without increasing BF and BW may exist in this region in commercial pigs.