College of Life Sciences, Shanxi Normal University, Linfen 041004, People's Republic of China; and Corresponding author. Email:
College of Life Sciences, Shanxi Normal University, Linfen 041004, People's Republic of China.
Funct Plant Biol. 2021 Jan;48(2):195-205. doi: 10.1071/FP20205.
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.
研究了硫化氢（H2S）及其与过氧化氢（H2O2）在油菜素内酯诱导拟南芥气孔关闭中的关系。在本研究中，2,4-表油菜素内酯（EBR，一种生物活性 BR）诱导野生型气孔关闭，该效应被 H2S 清除剂和合成抑制剂以及 H2O2 清除剂和合成抑制剂抑制。然而，EBR 未能关闭 Atl-cdes、Atd-cdes、AtrbohF 和 AtrbohD/F 突变体的气孔。此外，EBR 诱导野生型中 L-/D-半胱氨酸脱硫酶（L-/D-CDes）活性、H2S 产生和 H2O2 产生增加，该效应分别被 H2S 清除剂和合成抑制剂以及 H2O2 清除剂和合成抑制剂抑制。此外，EBR 增加了 AtrbohD 突变体保卫细胞中的 H2O2 水平，但不能提高 AtrbohF 和 AtrbohD/F 突变体保卫细胞中的 H2O2 水平。接下来，H2O2 的清除剂和合成抑制剂可显著抑制 EBR 诱导的野生型 L-/D-CDes 活性和 H2S 产生增加，但 H2S 清除剂和合成抑制剂不能抑制 EBR 诱导的 H2O2 产生。EBR 可以增加 Atl-cdes 和 Atd-cdes 突变体保卫细胞中的 H2O2 水平，但 EBR 不能诱导 AtrbohF 和 AtrbohD/F 突变体中 L-/D-CDes 活性和 H2S 产生的增加。因此，我们得出结论，H2S 和 H2O2 参与了 EBR 诱导的气孔关闭的信号转导途径。总的来说，我们的数据表明，EBR 诱导 AtrbohF 依赖性 H2O2 产生，随后是 AtL-CDes-/AtD-CDes 催化的 H2S 产生，最终导致拟南芥气孔关闭。
