Reactive carbonyl species function downstream of reactive oxygen species in chitosan-induced stomatal closure.

Abstract

An elicitor, chitosan (CHT), induces stomatal closure in plants, which is accompanied by salicylhydroxamic acid (SHAM)-sensitive peroxidases-mediated reactive oxygen species (ROS) production in guard cells. Reactive carbonyl species (RCS) function downstream of ROS in abscisic acid (ABA) and methyl jasmonate (MeJA) signalling in guard cells. However, the involvement of RCS in CHT-induced stomatal closure is still unknown. In this study, we used transgenic tobacco (Nicotiana tabacum) plants overexpressing Arabidopsis thaliana 2-alkenal reductase (AER-OE tobacco) and Arabidopsis wild-type (WT) plants to investigate whether RCS is involved in CHT-induced stomatal closure. Chitosan-induced stomatal closure was inhibited in the tobacco AER-OE plants. In the WT tobacco and Arabidopsis plants, CHT-induced stomatal closure was inhibited by RCS scavengers, carnosine and pyridoxamine. Chitosan significantly increased RCS production in the WT tobacco and Arabidopsis, but in the tobacco AER-OE plants, chitosan did not increase significantly RCS accumulation. Moreover, neither the application of RCS scavengers to both WT plants nor scavenging RCS by AER-OE affected the CHT-induced ROS accumulation. However, treatment with a peroxidase inhibitor, SHAM, significantly inhibited CHT-induced RCS accumulation in WT tobacco and Arabidopsis plants. Taken together, these results suggest that RCS acts downstream of ROS production in CHT signalling in guard cells of A. thaliana and N. tabacum.