Genomic breeding values, SNP effects and gene identification for disease traits in cow training sets.

Holstein Friesian cow training sets were created according to disease incidences. The different datasets were used to investigate the impact of random forest (RF) and genomic BLUP (GBLUP) methodology on genomic prediction accuracies. In addition, for further verifications of some specific scenarios, single-step genomic BLUP was applied. Disease traits included the overall trait categories of (i) claw disorders, (ii) clinical mastitis and (iii) infertility from 80 741 first lactation Holstein cows kept in 58 large-scale herds. A subset of 6744 cows was genotyped (50K SNP panel). Response variables for all scenarios were de-regressed proofs (DRPs) and pre-corrected phenotypes (PCPs). Initially, all sick cows were allocated to the testing set, and healthy cows represented the training set. For the ongoing cow allocation schemes, the number of sick cows in the training set increased stepwise by moving 10% of the sick cows from the testing to the training set in each step. The size of training and testing sets was kept constant by replacing the same number of cows in the testing set with (randomly selected) healthy cows from the training set. For both the RF and GBLUP methods, prediction accuracies were larger for DRPs compared to PCPs. For PCPs as a response variable, the largest prediction accuracies were observed when the disease incidences in training sets reflected the disease incidence in the whole population. A further increase in prediction accuracies for some selected cow allocation schemes (i.e. larger prediction accuracies compared to corresponding scenarios with RF or GBLUB) was achieved via single-step GBLUP applications. Correlations between genome-wide association study SNP effects and RF importance criteria for single SNPs were in a moderate range, from 0.42 to 0.57, when considering SNPs from all chromosomes or from specific chromosome segments. RF identified significant SNPs close to potential positional candidate genes: GAS1, GPAT3 and CYP2R1 for clinical mastitis; SPINK5 and SLC26A2 for laminitis; and FGF12 for endometritis.