Nature Genetics
37, 1130 - 1134 (2005)
Published online: 18 September 2005; | doi:10.1038/ng1639
Pathogen-induced, NADPH oxidase−derived reactive oxygen intermediates suppress spread of cell death in Arabidopsis thalianaMiguel Angel Torres1, Jonathan D G Jones2
& Jeffery L Dangl1, 31
Department of Biology, University of North Carolina, CB# 3280, Coker Hall, Room 108, Chapel Hill, North Carolina, 27599-3280, USA. 2
Sainsbury Laboratory, John Innes Center, Colney, Norwich, NR4 7UH, UK. 3
Curriculum in Genetics, Department of Microbiology and Immunology and Carolina Center for Genome Sciences, University of North Carolina, CB# 3280, Coker Hall, Room 108, Chapel Hill, North Carolina, 27599-3280, USA.
Correspondence should be addressed to Jeffery L Dangl dangl@email.unc.edu Plant immune responses are usually accompanied by the production of extracellular superoxide at and surrounding infection sites1,
2,
3. Extracellular reactive oxygen intermediates (ROIs) in plants were proposed to drive programmed cell death correlated with disease resistance (the hypersensitive response). ROIs derived from this oxidative burst are generated by plasma membrane NADPH oxidases, anchored by gp91phox proteins related to those responsible for the respiratory oxidative burst activated in mammalian neutrophils during infection4,
5. Mutation of Arabidopsis thaliana respiratory burst oxidase (Atrboh) genes eliminated pathogen-induced ROI production but had only a modest effect on the hypersensitive response4. We show that Atrboh function can be activated by exogenous ROIs. Unexpectedly, the subsequent oxidative burst can suppress cell death in cells surrounding sites of NADPH oxidase activation. This cell death requires salicylic acid, a plant immune system activator6. Thus, ROIs generated by Atrboh proteins can antagonize salicylic acid−dependent pro-death signals. These results have implications for understanding how salicylic acid activates defense signaling in cells spatially removed from infection sites without causing cell death.
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