Involvement of salicylic acid signal transduction in aluminum-responsive oxidative burst in Arabidopsis thaliana cell suspension culture.

To date, a number of studies have documented the toxic impacts of Al ions in plant cells. One of the key factors required for Al cytotoxicity is the generation of reactive oxygen species (ROS). Here we observed that Al treatments of suspension-cultured Arabidopsis thaliana cells resulted in biphasic superoxide generation monitored with chemiluminescence. Among six respiratory burst oxidase homologs (Atrbohs) coding for plant NADPH oxidase, AtrbohD was shown to be the only gene responsive to Al. As the expression of AtrbohD was rapid and long-lasting (1 min to 24 h). Al-induced superoxide generation, AtrbohD expression and cell death were all inhibited by NADPH oxidase inhibitor and superoxide dismutase. Interestingly, Al-induced AtrbohD expression and cell death were inhibited in the mutant and transgenic cell lines lacking salicylic acid biosyhthesis and accumulation (sid2 and NahG). Involvements of salicylic acid signaling in Al-induced AtrbohD expression and cell death development were also confirmed by the use of npr1 mutant cells and NPR1-overexpressing cells. Taken together, there would be a loop of SA signaling and SA-dependent expression of AtrbohD gene leading to prolonged ROS production and cell death development in the Al-exposed Arabidopsis cells.