1 AgResearch Molecular Biology Unit, Department of Biochemistry, University of Otago, PO Box 56, Dunedin, New Zealand 2 AgResearch Invermay, Private Bag 50034, Mosgiel, New Zealand 3 AgResearch Ruakura, Private Bag 3123, Hamilton, New Zealand
Facial eczema (FE) is a photosensitisation disease resulting from liver damage. The disease affects sheep, cattle, deer and goats. Injury to the liver is caused by a mycotoxin sporidesmin produced in the spores of a toxigenic saprophyte, Pithomyces chartarum, endemic in New Zealand pastures. The mechanism of sporidesmin cytotoxicity lies in its free radical production from redox cycling of the disulphide group in its epidithiopiperazinedione moiety. Taking the candidate gene approach, we have mapped and analysed the genes of five antioxidant enzymes and two serum proteins for sheep FE resistance. The genes included CuZn-superoxide dismutase (SOD1), Mn-superoxide dismutase (SOD2), glutathione peroxidase, glutathione reductase, catalase, ceruloplasmin and transferrin. The genes showed no significant linkage to disease traits when tested in FE outcross pedigrees. Two microsatellite markers (OarSHP3 and OarSHP4), which flank the catalase gene, were isolated from a catalase YAC clone. A DNA marker (KP1) was developed based on a single nucleotide polymorphisms in exon six of the catalase gene. These three catalase markers, when analysed in resistant and susceptible selection-line sheep, showed significant differences in their allele frequency distributions between the divergent genetic lines.