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

Abstract

Summary: 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, O 3‐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 O 3‐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 H 2 O 2 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.