The oxidative burst in plant defense: Function and signal transduction

Abstract

The rapid production and accumulation of active oxygen species (AOS), the oxidative burst, has been shown to occur in a variety of plant/pathogen systems. In particular, two species, hydrogen peroxide (H 2 O 2 ) and the superoxide radical anion O 2 − have received considerable attention. H 2 O 2 and O 2 − , while acting directly as antimicrobial agents, may also serve as second messengers or catalysts in plants to activate a more diverse set of defense responses. Some of the better studied downstream responses promoted by AOS are (1) the cross‐linking of cell wall proteins, (2) the induction of defense‐related genes, (3) the stimulation of phytoalexin biosynthesis and (4) promotion of the hypersensitive response (HR). A useful model for studying the oxidative burst in plants is the neutrophil NADPH ox‐idase complex, the primary source of AOS production in mammals. Several of the subunits of the neutrophil NADPH oxidase complex have been immunologically identified in plants. Furthermore, many of the components known to be involved in the signal transduction pathway in neutrophils have also been found to play a role in the oxidative burst in plants. Just as various ligands activate the oxidase complex in neutrophils, several ligands (elicitors or pathogens) also lead to induction of the oxidative burst in plant cells. The similarities between the neutrophil and plant oxidative bursts will be elaborated in this review. Following stimulation with elicitors, different signal transduction pathways are activated in plants, depending on the source of elicitor used. While the identities and chronologies of the major intermediates in these pathways remain largely unknown, there is strong evidence at least for participation of phospholipases, H + /K + exchange, Ca 2+ influxes, protein kinases and phosphatases, and GTP binding proteins. In an effort to integrate these various signaling events into a single scheme, we have constructed a hypothetical model that proposes how different elicitors might induce the oxidative burst in the same cell by different pathways.