Ozone-induced cell death occurs via two distinct mechanisms in Arabidopsis:: the role of salicylic acid

Previous studies suggest that salicylic acid (SA) plays an important role in influencing plant resistance to ozone (O-3) TO further define the role of SA in O-3-induced responses, we compared the responses of two Arabidopsis genotypes that accumulate different amounts of SA in response to O-3 and a SA-deficient transgenic Col-0 line expressing salicylate hydroxylase (NahG). The differences observed in O-3-induced changes in SA levels, the accumulation of active oxygen species, defense gene expression, and the kinetics and severity of lesion formation indicate that SA influences O-3 tolerance via two distinct mechanisms. Detailed analyses indicated that features associated with a hypersensitive response (HR) were significantly greater in O-3-exposed Cvi-0 than in Col-0, and that NahG plants failed to exhibit these HR-like responses. Furthermore, Os-induced antioxidant defenses, including the redox state of glutathione, were greatly reduced in NahG plants compared to Col-0 and Cvi-0. This suggests that O-3-induced cell death in NahG plants is due to the loss of SA-mediated potentiation of antioxidant defenses, while Os-induced cell death in Cvi-0 is due to activation of a HR. This hypothesis is supported by the observation that inhibition of NADPH-oxidases reduced O-3-induced H2O2 levels and the O-3-induced cell death in Cvi-0, while no major changes were observed in NahG plants. We conclude that although SA is required to maintain the cellular redox state and potentiate defense responses in O-3 exposed plants, high levels of SA also potentiate activation of an oxidative burst and a cell death pathway that results in apparent O-3 sensitivity.