S. I. Duchemin1,2, M. Visker1, J. van Arendonk1, and H. Bovenhuis1
1Animal Breeding and Genomics Centre, Wageningen University, PO Box 338, 6700 AH Wageningen, the Netherlands, 2Swedish University of Agricultural Sciences, Department of Animal Breeding and Genetics, Uppsala, Sweden; firstname.lastname@example.org
It is well established that milk-fat composition in dairy cattle shows genetic variation and is influenced by genes, such as DGAT1 located on BTA14 and SCD1 on BTA26. In addition, a genomic region on BTA17 has been found to be associated with milk fatty acids (FA), however, no candidate gene or causal variant has been identified so far. Based on the 50k SNP array, we previously identified 10 significantly associated SNPs distributed over 3.7 Mbp on BTA17. The aim of this study was to fine-map this region using the 777k SNP array. FA were determined based on winter and summer milk samples of 2,001 cows on 398 herds. Phenotypes were available on 14 FA (saturated C4:0 through C18:0, and unsaturated C10:1 through C18:1-cis9, trans11 (CLA)). 50k SNP genotypes were available on 1,813 daughters and 55 sires. 777k SNP genotypes were available on the same 55 sires. Daughters were imputed from 50k to 777k SNP genotypes using Beagle. Imputation was based on 777k genotypes of an independent set of 1,330 animals, in addition to the 777k genotypes available for the sires. After imputation the number of SNPs on BTA17 increased from 1,570 to 22,240. Single SNP analysis was done with an animal model in ASReml. Our results indicated significant association of C6:0, C8:0, C10:0 and C12:0 with 29 SNPs distributed over 2.8 Mbp. From these 29 SNPs, one was the most significantly associated with all four traits. The minor allele frequency of this SNP was 0.44 and its association with C6:0, C8:0, C10:0, and C12:0 was in the same direction, both in winter as well as in summer milk samples. However, the effects in summer were up to twice as large as in winter milk samples. Adjusting for DGAT1 K232A and SCD1 A293V polymorphisms does not change the effects which suggests that this gene on BTA17 acts independently of the previously identified genes affecting FA composition.