Hydrogen sulfide activates calcium signaling to confer tolerance against selenium stress in Brassica rapa

Background Se (selenium) pollution is an emerging environmental concern. Excessive Se induces phytotoxicity. The endogenous H2S (hydrogen sulfide) was involved in plant adaptation to Se stress, but the signaling player of H2S remains unclear. Methods The study was conducted in a hydroponic system with different chemicals added to the treatment solution. Fluorescent tracking was performed to detect endogenous signaling molecules in plant tissues. Physiological changes were determined based on pharmaceutics and histochemical experiments. Gene expression was analyzed using qRT-PCR. The data were summarized using hierarchical cluster and Pearson correlation analysis. Results Se stress inhibited B. rapa growth (e.g. root elongation, shoot height, and seedling fresh weight and dry weight) in both dose- and time-dependent manners, with approximately 50% of root growth inhibition occurred at 20 mu M Se. Se stress induced ROS (reactive oxygen species) accumulation and oxidative injury in B. rapa. Se exposure resulted in the upregulation of LCDs (L-cysteine desulfhydrase) and DCDs (D-cysteine desulfhydrase) encoding enzymes for H2S production in B. rapa at early stage of Se exposure, followed by downregulation of these genes at late stage. This was consistent with the change of endogenous H2S in B. rapa. Enhancing endogenous H2S level with NaHS (H2S donor) stimulates endogenous Ca2+ in B. rapa upon Se exposure, accompanied the attenuation of growth inhibition, ROS accumulation, oxidative injury, and cell death. The beneficial effects of H2S on detoxifying Se were blocked by decreasing endogenous Ca2+ level with Ca2+ channel blocker or Ca2+ chelator. Finally, hierarchical cluster combined with correlation analysis revealed that Ca2+ might acted as downstream of H2S to confer Se tolerance in B. rapa. Conclusion Ca2+ was an important player of H2S in the regulation of plant physiological response upon Se stress. Such findings extend our knowledge of the mechanism for Se-induced phytotoxicity.