Facial eczema disease (FE) in ruminants is caused by a mycotoxm, named spondesmin, which causes liver damage. Sporidesmin toxicity is caused by its ability to generate free radicals which disrupt cellular processes and structures, resulting in cell injury and death. We analysed a number of antioxidant enzymes involved in free radical detoxication as candidate genes for FE resistance. The genes were first mapped by genetic linkage using RFLP markers. The closest-linked informative microsatellite markers were then used for linkage studies in four FE resource families which were designed to show segregation in resistance/susceptibility to the disease. The results to date indicated that CuZn-superoxide dismutase (SOD1), Mn-superoxide dismutase (SOD2), glutathione peroxidase (GPX1) and glutathione reductase (GSR) are not involved in FE resistance/susceptibility. We also ruled out a possible involvement of the serum proteins ceruloplasmin (CP) and transferrin (TF) in these families.

S. H Phua, K. G Dodds, C. A Morris, N. R Towers, A. M Crawford

Proceedings of the World Congress on Genetics Applied to Livestock Production, Volume 27: Reproduction; fish breeding; genetics and the environment; genetics in agricultural systems; disease resistance; animal welf, , 273–276, 1998
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