Reactive oxygen intermediates modulate nitric oxide signaling in the plant hypersensitive disease-resistance response

The mechanisms involved in plant defense show several similar characteristics with the innate immune systems of vertebrates and invertebrates. In animals, nitric oxide (NO) cooperates with reactive oxygen intermediates (ROI) to kill tumor cells and is also required for macrophage killing of bacteria. Such cytotoxic events occur because unregulated levels of NO determine its diffusion-limited reaction with O-2(-) generating peroxynitrite (ONOO-), a mediator of cellular injury in many biological systems. In soybean suspension cells, unregulated NO production during the onset of a pathogen-induced hypersensitive response (HR) is not sufficient to activate the hypersensitive cell death, which is triggered only by fine tuning the NO/ROI ratio. Furthermore, that hypersensitive cell death is activated following interaction of NO with H2O2, rather than O-2(-). Increasing O-2(-) levels reduces NO-derived toxicity, and the addition of ONOO- to soybean suspensions does not affect cell viability. Consistently with the fact that ONOO- is not an essential mediator of NO/RO-induced cell death, during the HR superoxide dismutase (SOD) accelerates O-2(-) dismutation to H2O2 and therefore minimizes the loss of NO by reaction with O-2(-) and triggers hypersensitive cell death through the NO/H2O2 synergism. Consequently, the rates of production and dismutation of O-2(-) generated during the oxidative burst play a crucial role in modulating NO signaling through the cell death pathway, which proceeds through mechanisms different from those commonly observed in animals. (C) 2002 Editions scientifiques et medicales Elsevier SAS. All rights reserved.