Abstract
An Arabidopsis mutant, stm1 (for salt tolerant mutant1), has a salt-tolerant phenotype. Here, we intended to clarify the molecular basis of the phenotype. In the mutant, the salt stress-induced expression of RBOH genes encoding NADPH oxidase, the enzyme producing reactive oxygen species (ROS), was suppressed. This suppression was accompanied by a corresponding reduction in ROS accumulation. The abscisic acid (ABA)-induced expression of RBOH was also suppressed in the mutant. This coincided with impairment in the ABA-induced expression of an ABA-responsive gene, RD29A, which is regulated by ABRE-dependent ABA signaling branch. However, the expression of another ABA-responsive gene, RD22, which is induced independently of this branch, was not impaired in the mutant. These results suggest that STM1 positively regulates the salt stress-induced ROS production through the activation of the ABRE-dependent ABA signaling. We hypothesize that the stm1 mutation prevents overaccumulation of ROS, which in the wild type results in oxidative damages.
