Pathogen-induced, NADPH oxidase-derived reactive oxygen intermediates suppress spread of cell death in Arabidopsis thaliana.

Abstract

Plant immune responses are usually accompanied by the production of extracellular superoxide at and surrounding infection sites. 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 gp91(phox) proteins related to those responsible for the respiratory oxidative burst activated in mammalian neutrophils during infection. Mutation of Arabidopsis thaliana respiratory burst oxidase (Atrboh) genes eliminated pathogen-induced ROI production but had only a modest effect on the hypersensitive response. 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 activator. 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.