The role of hydrogen sulfide (H₂S) and its relationship with hydrogen peroxide (H₂O₂) in brassinosteroid-induced stomatal closure in Arabidopsis thaliana (L.) Heynh. were investigated. In the present study, 2,4-epibrassinolide (EBR, a bioactive BR) induced stomatal closure in the wild type, the effects were inhibited by H₂S scavenger and synthesis inhibitors, and H₂O₂ scavengers and synthesis inhibitor. However, EBR failed to close the stomata of mutants Atl-cdes, Atd-cdes, AtrbohF and AtrbohD/F. Additionally, EBR induced increase of L-/D-cysteine desulfhydrase (L-/D-CDes) activity, H₂S production, and H₂O₂ production in the wild type, and the effects were inhibited by H₂S scavenger and synthesis inhibitors, and H₂O₂ scavengers and synthesis inhibitor respectively. Furthermore, EBR increased H₂O₂ levels in the guard cells of AtrbohD mutant, but couldn’t raise H₂O₂ levels in the guard cells of AtrbohF and AtrbohD/F mutants. Next, scavengers and synthesis inhibitor of H₂O₂ could significantly inhibit EBR-induced rise of L-/D-CDes activity and H₂S production in the wild type, but H₂S scavenger and synthesis inhibitors failed to repress EBR-induced H₂O₂ production. EBR could increase H₂O₂ levels in the guard cells of Atl-cdes and Atd-cdes mutants, but EBR failed to induce increase of L-/D-CDes activity and H₂S production in AtrbohF and AtrbohD/F mutants. Therefore, we conclude that H₂S and H₂O₂ are involved in the signal transduction pathway of EBR-induced stomatal closure. Altogether, our data suggested that EBR induces AtrbohF-dependent H₂O₂ production and subsequent AtL-CDes-/AtD-CDes-catalysed H₂S production, and finally closes stomata in A. thaliana.

硫化氢（H ₂ S）的作用及其与过氧化氢（H ₂ O ₂）的关系在油菜素类固醇诱导的拟南芥（L.）Heynh气孔关闭中。被调查了。在本研究中，2,4-表油菜素内酯（EBR，一种生物活性BR）在野生型中诱导气孔关闭，其作用被H ₂ S清除剂和合成抑制剂以及H ₂ O ₂清除剂和合成抑制剂抑制。然而，EBR未能关闭突变体Atl - cdes，Atd - cdes，AtrbohF和AtrbohD /的气孔。˚F。此外，在野生型中，EBR诱导L- / D-半胱氨酸脱氢酶（L- / D-CDes）活性，H ₂ S产生和H ₂ O ₂产生增加，并且H ₂ S清除剂和合成抑制剂，H ₂ O ₂清除剂和合成抑制剂。此外，EBR增加了AtrbohD突变体保卫细胞中的H ₂ O ₂水平，但不能提高AtrbohF和AtrbohD / F保卫细胞中的H ₂ O ₂水平。突变体。接下来，H ₂ O _2的清除剂和合成抑制剂可以显着抑制野生型EBR诱导的L- / D-CDes活性和H ₂ S产生的增加，但是H ₂ S清除剂和合成抑制剂无法抑制EBR诱导的H ₂ O ₂生产。EBR可以增加Atl - cdes和Atd - cdes突变体保卫细胞中的H ₂ O ₂水平，但EBR未能诱导AtrbohF和AtrbohD / F中L- / D-CDes活性和H ₂ S产生增加。突变体。因此，我们得出的结论是H ₂ S和H ₂ O ₂参与了EBR诱导的气孔关闭的信号转导途径。总之，我们的数据表明，EBR诱导AtrbohF依赖的H ₂ O ₂产生，以及随后的AtL-CDes- / AtD-CDes催化的H ₂ S产生，并最终关闭拟南芥气孔。