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Heme oxygenase-1 (HO-1) has been recently identified as an endogenous signaling system in animals. In this study, HO-1 upregulation and its role in acquired salt tolerance (salinity acclimation) were investigated in wheat plants. We discovered that pretreatment with a low concentration of NaCl (25 mmol/L) not only led to the induction of HO-1 protein and gene expression, as well as enhanced HO activity, but also to a salinity acclimatory response thereafter. The effect is specific for HO-1, since the potent HO-1 inhibitor zinc protoporphyrin IX blocks the above cytoprotective actions, and the cytotoxic responses conferred by 200 mmol/L NaCl are reversed partially when HO-1 inducer hemin is added. Heme oxygenase catalytic product, carbon monoxide (CO) aqueous solution pretreatment, mimicked the salinity acclimatory responses. Meanwhile, the CO-triggered re-establishment of reactive oxygen species (ROS) homeostasis was mainly guaranteed by the induction of total and isozymatic activities, or corresponding transcripts of superoxide dismutase, ascorbate peroxidase, and cytosolic peroxidase (POD), as well as the downregulation of NADPH oxidase expression and cell-wall POD activity. A requirement of hydrogen peroxide homeostasis for HO-1-mediated salinity acclimation was also discovered. Taken together, the above results suggest that the upregulation of HO-1 expression was responsible for the observed salinity acclimation through the regulation of ROS homeostasis.
In this study, HO-1 upregulation and its role in acquired salt tolerance (salinity acclimation) were investigated in wheat plants. We discovered that pretreatment with a low concentration of NaCl (25 mmol / L) not only led to the induction of HO-1 protein and gene expression, but also to a salinity acclimatory response thereafter. The effect is specific for HO- 1, since the potent HO-1 inhibitor zinc protoporphyrin IX blocks the above cytoprotective actions, and the cytotoxic responses conferred by 200 mmol / L NaCl are replaced by HO-1 inducer hemin is added. Heme oxygenase catalytic product, carbon monoxide (CO ), mimicked the salinity acclimatory responses. Meanwhile, the CO-triggered re-establishment of reactive oxygen species (ROS) homeostasis was mainly guaranteed by the induction of total and isozymatic activities , or corresponding transcripts of superoxide dismutase, ascorbate peroxidase, and cytosolic peroxidase (POD), as well as the downregulation of NADPH oxidase expression and cell-wall POD activity. A requirement of hydrogen peroxide homeostasis for HO-1-mediated salinity acclimation was also discovered. Taken together, the above results suggest that the upregulation of HO-1 expression was responsible for the observed salinity acclimation through the regulation of ROS homeostasis.