Oxidative Burst-mediated Defense Responses in Plant Disease Resistance

Abstract

Plant:pathogen interactions are classified for specific plant cultivars and pathogen races as compatible (virulent pathogen, susceptible host) and incompatible (avirulent pathogen, resistant host). Incompatibility is established by the action of pairs of “corresponding single genes” (Flor 1956), a dominant plant resistance gene (R) and a dominant pathogen avirulence gene (avr) (Lamb 1994; Staskawicz et al. 1995). To fend off pathogen attack, plants have an array of defense programs that are efficiently activated in incompatible interactions leading to resistance but are not activated, or are activated after a significant delay, in equivalent compatible interactions leading to disease. Host resistance, triggered by the direct or indirect interaction of R and avr products, is often based on an active “hypersensitive response” (HR) involving the death of challenged host cells and the coordinated activation of a battery of defense responses in surrounding cells to restrict pathogen spread into healthy tissues (Keen 1990). Rapid responses include the activation of preexisting callose synthase (Köhle et al. 1985), rise in cytosolic Ca⁺⁺ (Atkinson et al. 1990), and an oxidative burst (Doke 1983a). The accumulation of hydrogen peroxide (H₂O₂) during the oxidative burst not only exerts a direct antimicrobial effect (Keppler et al. 1989; Peng and Kuc 1992; Legendre et al. 1993), but also drives the oxidative cross-linking of cell wall proteins and possibly other wall polymers (Bradley et al. 1992; Brisson et al. 1994) and the orchestration of hypersensitive cell death (Levine et al. 1994). Later defense responses requiring de novo transcription result in the biosynthesis of...