Selective genotyping and logistic regression analyses to identify favorable SNP-genotypes for clinical mastitis and production traits in Holstein dairy cattle

The objective of this study was to estimate effects of SNP-genotypes on clinical mastitis, somatic cell score (SCS) and on estimated breeding values (EBV) for production traits in Holstein dairy cattle based on selective genotyping methodology. For identification of SNPs, we focused on candidate genes for clinical mastitis. The data set was comprised of a total of 3823 Holstein cows from two Holstein contract herds located in two regions in Iran. Data included 305-d lactation records for the production traits milk yield, fat yield, protein yield, fat percentage, protein percentage, SCC, and the no. of cases of clinical mastitis per lactation. Selection of cows for selective genotyping was based on extreme values for clinical mastitis residuals (CMR) from mixed model analyses. Two extreme groups of 135 cows each were genotyped for two loci of both candidate genes for mastitis TLR4 [= TLR4(1) and TLR4(2)] and CACNA2D1 [= CACNA2D1(1) and CACNA2D1(2)] using PCR-SSCP or PCR-RFLP Associations between SNP-genotypes and traits of interest were estimated by applying logistic regression analyses, i.e. estimating the probability of the heterogeneous genotype in dependency of the EBVs and of values for CMR. The heterozygous genotype was contrasted to both homozygous genotypes allowing the estimation of effects for dominance. Allele G of TLR4(1) was associated with fewer cases for CM, and showed desired effects in production traits, e.g. higher milk yield and protein yield, and lower values for CMR. Also allele G of CACNA2D1(2) was predominant in the resistant group, and favorably associated with milk yield. Those SNPs are interesting for breeding, because they simultaneously improve both antagonistic traits. Effects of dominance ranged from 0.05 SD to 0.13 SD for the production trait (milk yield), and from 0.04 to 0.19 SD the functional trait (CMR). © 2012 Elsevier B.V.