Role of Reactive Oxygen Intermediates and Cognate Redox Signaling in Disease Resistance

Biphasic accumulation of H₂O₂ during the plant oxidative burst in response to an avirulent or virulent microbial pathogen. Only phase II correlates with the establishment of disease resistance. Phase I is a non-specific response to a number of stress stimuli, including wounding.

Schematic model for engagement of the NADPH oxidase-dependent oxidative burst in plants. Pathogen recognition results in an influx of Ca²⁺, which may activate both the production of NADPH via NAD kinase and the translocation of p67^phox and p47^phox from the cytosol to the plasma membrane. Moreover, Ca²⁺ may also activate gp91^phox directly, by binding to the two EF hand motifs present in this protein, or indirectly via phosphorylation, following the Ca²⁺-mediated activation of a specific CDPK. The small GTP-binding protein, p21^rac, may also make an important contribution to the activation of the NADPH oxidase complex.