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In planta measurements of oxidative bursts elicited by avirulent and virulent bacterial pathogens suggests that H 2 O 2 is insufficient to elicit cell death in tobacco
Author(s) -
MUR LUIS A. J.,
KENTON PAUL,
DRAPER JOHN
Publication year - 2005
Publication title -
plant, cell and environment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.646
H-Index - 200
eISSN - 1365-3040
pISSN - 0140-7791
DOI - 10.1111/j.1365-3040.2005.01301.x
Subject(s) - pseudomonas syringae , programmed cell death , biology , respiratory burst , virulence , hypersensitive response , oxidative stress , intracellular , catalase , apoplast , oxidative phosphorylation , elicitor , microbiology and biotechnology , gene , biochemistry , cell wall , apoptosis , pathogen
ABSTRACT A rapid and localized programmed cell death – the hypersensitive response (HR) – is a widely utilized plant resistance mechanism against pathogens. Studies have implicated H 2 O 2 generation as a key elicitory mechanism in the HR. The causal relationship between the kinetics of the in planta oxidative burst, the HR and certain defence gene expression was examined. H 2 O 2 generation following challenge with avirulent strains of Pseudomonas syringae pv. ( P. s. pv.) syringae occurred in two phases. The effects of ROS generation were investigated using the H 2 O 2 ‐responsive transgene AoPR10‐GUS, the dually responsive (H 2 O 2 and salicylic acid) PR1a‐GUS as well as measures of cell death. Co‐application of catalase with P. s. pv. syringae into tobacco leaf panels suppressed AoPR10‐ and PR1a‐GUS expression and cell death. Conversely, varying H 2 O 2 generation with glucose: glucose oxidase influenced both defence gene expression and cell death. AoPR10‐GUS proved to be primarily responsive to apoplastic not intracellular oxidative stress, suggesting that the apoplasm was a distinctive source of oxidative signals. A biphasic oxidative burst was also observed with virulent P. s. pv. tabaci , which, although delayed compared to that observed during HR, persisted at equivalent levels for a longer period. Taking all these data together we suggest that either (1) additional factors to the apoplastic oxidative burst are required to explain the rapid kinetics of defence signalling and cell death associated with the HR or (2) P. s. pv. tabaci successfully suppresses the effects of H 2 O 2 generation by an unknown mechanism.