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Systemic acquired resistance is an important component of the disease resistance repertoire of plants. In this study, a novel synthetic chemical, benzo(1,2,3)thiadiazole-7-carbothioic acid S-methyl ester (BTH), was shown to induce acquired resistance in wheat. BTH protected wheat systemically against powdery mildew infection by affecting multiple steps in the life cycle of the pathogen. The onset of resistance was accompanied by the induction of a number of newly described wheat chemically induced (WCI) genes, including genes encoding a lipoxygenase and a sulfur-rich protein. With respect to both timing and effectiveness, a tight correlation existed between the onset of resistance and the induction of the WCI genes. Compared with other plant activators, such as 2,6-dichloroisonicotinic acid and salicylic acid, BTH was the most potent inducer of both resistance and gene induction. BTH is being developed commercially as a novel type of plant protection compound that works by inducing the plant's inherent disease resistance mechanisms.

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Epidermal cell monolayers prepared from partially dissected barley (Hordeum vulgare) coleoptiles were used for in vivo analysis of race-specific resistance to powdery mildew (Erysiphe graminis f. sp. hordei) specified by host genes Mla-1, Mla-12, and Mlg. Complete resistance governed by each of these genes is closely associated with hypersensitive cell death (hypersensitive response, HR) in primary leaf tissue. In contrast, Mla-12 coleoptile tissue reveals a fully compatible, Mla-1 coleoptile tissue a partially compatible, and Mlg coleoptile tissue an incompatible interaction upon challenge with pathogen races carrying corresponding avirulence functions. Quantitative recording of single plant-fungus interaction sites showed arrest of fungal development in papillae on Mlg coleoptiles. On Mla-1 and Mla-12 coleoptiles, attacked cells become predominantly penetrated by the fungus. Approximately one third of penetrated cells on Mla-1 coleoptiles subsequently undergo an HR. These sites reveal no further fungal development. Both Mlg and Mla-12 coleoptiles fail to mount an HR. The effect of cordycepin (3′-deoxyadenosine), an inhibitor of mRNA synthesis, was studied in planta on primary leaf tissue of Mla-12 and Mlg genotypes. Host cell death triggered by either gene is reduced to background levels observed in the near-isogenic compatible interaction and exhibits the same dose-dependent cordycepin sensitivity. Inhibition of Mlg-triggered, single-cell HR is not accompanied by release of fungal growth arrest, indicating cordycepin insensitivity of a papillae-associated resistance component. The data suggest that host cell death is a requisite component for expression of Mla-type but not Mlg-type resistance.

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