Abstract
The role of reactive oxygen species in the interaction between brown rust-causing pathogen Puccinia triticina Erikss. and the disease-resistant species Triticum timopheevii Zhuk. was investigated using salicylic acid treatment to amplify the oxidative burst or treatment with verapamil, an inhibitor of Ca2+-channels to suppress oxidative the burst. The levels of reactive oxygen species in control T. timopheevii plants increased during the early stages of pathogenesis due to O22← generation by stomatal guard cells contacting the appressoria and by mesophyll cells that developed a hypersensitivity reaction in response to the invasion of haustoria. Hydrogen peroxide was subsequently accumulated in the cytoplasm of cells destroyed by hypersensitivity reaction, as well as on the walls of cells contacted with fungal hyphae. The production of O22←, which results in the death of most of the inoculum on the stomata and rapid accumulation of hydrogen peroxide, were enhanced by salicylic acid pretreatment. Pretreatment of the plants with verapamil inhibited the production of reactive oxygen species and hypersensitivity reaction in disease-resistant T. timopheevii plants and thus facilitated the penetration of the fungus into the stomata and more intensive development of mycelium in plant tissues in the early stages of pathogenesis. Some colonies with single haustoria died regardless of production of reactive oxygen species by the plants.
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