背景:Psoropticmange,由卵螨Psoroptes引起的,正在影响比利时蓝牛的福利和生产潜力。比利时蓝牛以其高度的肌肉运动而闻名,低饲料转化率和高牛肉质量-是这种疾病的高度易感。
结果:在这项研究中,我们从商业牛肉农场的100多个不同群体中对1975年比利时蓝牛进行了表型分析,因为它们对腺体的易感性。在这些管理组中观察到了显著的个体差异,病变程度差异高达±15%。动物模型显示,对于螨的数量,病变程度和严重病变程度的估计遗传力较低(分别为0.07和0.09)和0.12。针对manage易感性的全基因组关联研究揭示了BTA6,BTA11,BTA15和BTA24上的信号。在这些地区,鉴定了候选基因GBA3、RAG2和TRAF6。
结论:尽管由于筛选的时机在对视神经腺苷酸进行表型鉴定方面存在挑战,病变的不断演变和不同的管理条件,我们成功地进行了一项关于比利时蓝牛对视黄动物的遗传易感性的研究。我们的结果清楚地表明,视神经mange处于多基因控制之下,应更彻底地研究潜在的候选基因。这是第一个为这种复杂疾病提供候选基因的研究。这些结果对比利时蓝育种已经很有价值,然而,需要进一步的研究来解开这种疾病的结构并确定因果突变。
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.