Function of the oxidative burst in hypersensitive disease resistance

Raimund Tenhaken, Alex Levine, Louise F. Brisson, Richard A. Dixon, Chris Lamb*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

356 Scopus citations

Abstract

Microbial elicitors or attempted infection with an avirulent pathogen strain causes the rapid production of reactive oxygen intermediates. Recent findings indicate that H2O2 from this oxidative burst plays a central role in the orchestration of the hypersensitive response: (i) as the substrate driving the cross-linking of cell wall structural proteins to slow microbial ingress prior to the deployment of transcription-dependent defenses and to trap pathogens in cells destined to undergo hypersensitive cell death, (ii) as a local threshold trigger of this programmed death in challenged cells, and (iii) as a diffusible signal for the induction in adjacent cells of genes encoding cellular protectants such as glutathione S-transferase and glutathione peroxidase. These findings provide the basis for an integrated model for the orchestration of the localized hypersensitive resistance response to attack by an avirulent pathogen.

Original languageAmerican English
Pages (from-to)4158-4163
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume92
Issue number10
DOIs
StatePublished - 9 May 1995
Externally publishedYes

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