Role of H2O2 dynamics in brassinosteroid-induced stomatal closure and opening in Solanum lycopersicum.

Brassinosteroids (BRs) are essential for plant growth and development; however, their roles in the regulation of stomatal opening or closure remain obscure. Here, the mechanism underlying BR-induced stomatal movements is studied. The effects of 24-epibrassinolide (EBR) on the stomatal apertures of tomato (Solanum lycopersicum) were measured by light microscopy using epidermal strips of wild type (WT), the abscisic acid (ABA)-deficient notabilis (not) mutant, and plants silenced for SlBRI1, SlRBOH1 and SlGSH1. EBR induced stomatal opening within an appropriate range of concentrations, whereas high concentrations of EBR induced stomatal closure. EBR-induced stomatal movements were closely related to dynamic changes in H(2)O(2) and redox status in guard cells. The stomata of SlRBOH1-silenced plants showed a significant loss of sensitivity to EBR. However, ABA deficiency abolished EBR-induced stomatal closure but did not affect EBR-induced stomatal opening. Silencing of SlGSH1, the critical gene involved in glutathione biosynthesis, disrupted glutathione redox homeostasis and abolished EBR-induced stomatal opening. The results suggest that transient H(2)O(2) production is essential for poising the cellular redox status of glutathione, which plays an important role in BR-induced stomatal opening. However, a prolonged increase in H(2)O(2) facilitated ABA signalling and stomatal closure.

Brassinosteroids induce plant tolerance against phenanthrene by enhancing degradation and detoxification in Solanum lycopersicum L.

Polycyclic aromatic hydrocarbons (PAHs) are toxic to both plants and animals. The enhancement of plant tolerance and detoxification capacity is important for the plant-based remediation of PAHs. Therefore, we investigated the effects of 24-epibrassinolide (EBR) on the metabolism of a three-ringed PAH (phenanthrene-PHE) and subsequent stress tolerance in tomato (Solanum lycopersicum L.) plants. Exposure to PHE (300 µM) for 21 d significantly decreased biomass and net CO(2) assimilation (P(n)) but induced photoinhibition, malondialdehyde (MDA), H(2)O(2) and antioxidant enzymes. Obvious ultrastructural alterations were observed in the PHE-treated root tip cells. Importantly, the foliar application of EBR (0.1 µM) significantly increased biomass, P(n) and antioxidant enzyme activities but decreased MDA and H(2)O(2) compared with PHE alone and saved the root cells from severe damage. The expression of detoxification genes (CYP90b3, GSH1, GST1), reduced glutathione (GSH) content and glutathione S-transferase activity in the EBR+PHE-treated plants were higher than those of PHE alone. Additionally, lower levels of PHE residues in the roots were observed as a result of EBR+PHE treatment. Taken together, our results strongly suggest an enhanced and coordinated detoxification and degradation of PHE by EBR.