Loss-of-function mutation of EIN2 in Arabidopsis exaggerates oxidative stress induced by salinity

Abstract

Accumulation of reactive oxygen species (ROS) causes oxidative stress under adverse environmental conditions, such as salinity. Ethylene decreases accumulation of ROS induced by salinity, but the mechanism is still unclear. To examine the interactions between salinity and ROS accumulation and the possible role of ethylene metabolism in regulation, we used mutant ein2-5 in Arabidopsis with loss of function in EIN2. The mutant is compared to the wild-type Col-0, completely insensitivity to ethylene at the morphological, physiological and molecular levels. The oxidative responses of the wild type and mutant to salinity were compared. Loss-of-function of EIN2 enhanced sensitivity to salinity, implying that EIN2 is required for plant response to salinity. Furthermore, salinity resulted in accumulation of large amounts of ROS in ein2-5 seedlings when compared with Col-0, suggesting that the loss-of-function of EIN2 exaggerates oxidative stress induced by salinity. Activities of the antioxidant enzymes SOD, POD and CAT decreased significantly in ein2-5 under salinity when compared with Col-0 plants. The expression profiles of the genes Fe-SOD, PODs and CAT1, which code for ROS scavenging enzymes were severely decreased in ein2-5 under salinity compared with Col-0, suggesting that EIN2 was involved in regulating expression of these genes. Taken together, our results demonstrate that loss-of-function of EIN2 increased oxidative stress induced by salinity and that EIN2 is involved in modulating ROS accumulation, at least in part, by decreasing activities of ROS-scavenging enzymes.