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Spatiotemporal patterns of oxidative burst and micronecrosis in resistance of wheat to brown rust infection
Author(s) -
Orczyk W.,
DmochowskaBoguta M.,
Czembor H. J.,
NadolskaOrczyk A.
Publication year - 2010
Publication title -
plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.928
H-Index - 85
eISSN - 1365-3059
pISSN - 0032-0862
DOI - 10.1111/j.1365-3059.2010.02257.x
Subject(s) - respiratory burst , biology , pathogen , appressorium , epidermis (zoology) , inoculation , rust (programming language) , haustorium , oxidative phosphorylation , botany , microbiology and biotechnology , horticulture , host (biology) , immunology , biochemistry , genetics , anatomy , computer science , programming language
The accumulation of H 2 O 2 (oxidative burst) and the progress of pathogen development were studied in compatible and incompatible wheat‐brown rust interactions. The accumulation of H 2 O 2 was detected in 98·7% of guard cells with appressoria 8 h post inoculation (hpi). The reaction in both susceptible and resistant plants declined 2–3 days post inoculation (dpi). The second phase of the oxidative burst was observed in the mesophyll and/or epidermis. In susceptible plants it began 4–5 dpi and was detected only in the epidermis. In resistant plants the response was observed in the mesophyll. In moderately resistant plants it was induced 1–3 dpi, and the percentage of infection units reached 80–90% 8 dpi. This corresponded with severe necrotic symptoms. In highly resistant plants, the oxidative burst was short and transient. The percentage of infection units with H 2 O 2 accumulation reached its highest level (60–70%) 2 dpi, and decreased thereafter. Four days later, the low percentage and weak DAB staining indicated very low H 2 O 2 accumulation. The localization and the time‐course changes of the oxidative burst correlated with the profiles of the micronecrotic response, haustorium mother cell formation and pathogen development termination. An early and localized induction of oxidative burst followed by its rapid quenching correlated with high resistance and almost no disease symptoms. The possible correlation of the oxidative burst and pathogen development patterns with the level and durability of resistance conferred by Lr genes are discussed.