Genetic and genomic analysis of Belgian Blue's susceptibility for psoroptic mange

Abstract

Background: Psoroptic mange, caused by Psoroptes ovis mites, is affecting Belgian Blue cattle's welfare and production potential. The Belgian Blue cattle-known for its high degree of muscling, low feed conversion ratio and high beef quality-is highly susceptible for this disease.

Results: In this study, we phenotyped 1975 Belgian Blue cattle from more than 100 different groups on commercial beef farms for their psoroptic mange susceptibility. Substantial individual differences were observed within these management groups, with lesion extent differences up to ± 15%. Animal models showed that estimated heritabilities were low for lesion extent and severe lesion extent (0.07 and 0.09, respectively) and 0.12 for the number of mites. A genome wide association study for mange susceptibility revealed signals on BTA6, BTA11, BTA15 and BTA24. In these regions, candidate genes GBA3, RAG2, and TRAF6 were identified.

Conclusions: Despite the challenges in phenotyping for psoroptic mange due to the timing of screening, the continuous evolution of lesions and different management conditions, we successfully conducted a study on the genetic susceptibility to psoroptic mange in Belgian Blue cattle. Our results clearly indicate that psoroptic mange is under polygenic control and the underlying candidate genes should be studied more thoroughly. This is the first study providing candidate genes for this complex disease. These results are already valuable for Belgian Blue breeding, however, further research is needed to unravel the architecture of this disease and to identify causal mutations.

Fig. 1

Histograms of lesion extent (LE) and severe lesion extent (SLE). LE and SLE are expressed as % of body surface of the animal and show a right-skewed distribution of psoroptic lesion extent

Fig. 2

Manhattan plots of four haplotype-based GWAS for mange susceptibility in Belgian Blue. Top left shows the case–control approach on the medium density dataset (29,010 SNPs), top right shows the quantitative (lesion extent, LE) approach on medium density, bottom left the case–control approach on the high density dataset (633,512SNPs) and bottom right the quantitative analysis on high density

Fig. 3

Frequency of inferred ancestral haplotypes within cases and controls for the top SNPs. (top) shows top SNP of the signal on BTA6, (middle) the top SNP of the signal on BTA15 in the medium density analysis, and (bottom) the top SNP on BTA6 in the high density analysis. Large differences between cases and controls could indicate an associated haplotype to psoroptic mange sensitivity at the top SNP position of the signal