Abstract
The growth of the wheat stem rust (Puccinia graminis f.sp. tritici, race 32) on the resistant wheat cultivar Feldkrone is restricted by cell necrosis. Those epidermal cells first invaded react hypersensitively as is shown by the appearance of autofluorescence and the formation of lignin in the invaded cells. Cell necrosis was inhibited by soy-bean agglutinin (SBA), a lectin, which reacts specifically with galactose and N-acetyl-galactosamine, by Erythrina corallodendron lectin (ECO), specific for galactose, as well as by galactose oxidase, an enzyme which acts on the non-reducing terminal D-galactosyl and N-acetyl-D-galactosaminyl residues of surface galactoconjugates. As a result of this inhibition of cell necrosis, the size of the rust colony on treated leaves in-creased, i.e. the resistance of the wheat was lowered. Since previous results had shown that SBA binds to galactolipids on the surface of wheat protoplasts, we now postulate that SBA, ECO, and galactose oxidase interfere with the interaction of host plasmalemma with the fungal haustorium wall during the initial stages of infection.
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