Analysis of cytosolic isocitrate dehydrogenase and glutathione reductase 1 in photoperiod‐influenced responses to ozone using Arabidopsis knockout mutants

Oxidative stress caused by ozone (O3) affects plant development, but the roles of specific redox‐homeostatic enzymes in O3 responses are still unclear. While growth day length may affect oxidative stress outcomes, the potential influence of day length context on equal‐time exposures to O3 is not known. In Arabidopsis Col‐0, day length affected the outcome of O3 exposure. In short‐days (SD), few lesions were elicited by treatments that caused extensive lesions in long days (LD). Lesion formation was not associated with significant perturbation of glutathione, ascorbate, NADP(H) or NAD(H). To investigate roles of two genes potentially underpinning this redox stability, O3 responses of mutants for cytosolic NADP‐isocitrate dehydrogenase (icdh) and glutathione reductase 1 (gr1) were analysed. Loss of ICDH function did not affect O3‐induced lesions, but slightly increased glutathione oxidation, induction of other cytosolic NADPH‐producing enzymes and pathogenesis‐related gene 1 (PR1). In gr1, O3‐triggered lesions, salicylic acid accumulation, and induction of PR1 were all decreased relative to Col‐0 despite enhanced accumulation of glutathione. Thus, even at identical irradiance and equal‐time exposures, day length strongly influences phenotypes triggered by oxidants of atmospheric origin, while in addition to its antioxidant function, the GR‐glutathione system seems to play novel signalling roles during O3 exposure. The present report reveals a significant influence for growth day length conditions in determining the phenotypic outcome of Arabidopsis exposed to O3. Loss of cytosolic NADP‐isocitrate dehydrogenase function (knockout icdh mutant) did not markedly affect the response to O3, likely reflecting redundancy with other cytosolic NADPH‐producing enzymes. Unlike icdh, a knockout mutant for glutathione reductase 1 (GR1) strongly affected the response by decreasing O3‐triggered lesions, salicylic acid accumulation and induction of PR1. Thus, the GR1‐glutathione system seems to play novel signalling roles during ozone exposure.