%0 Journal Article
%T H<sub>2</sub>S在CdCl<sub>2</sub>诱导拟南芥气孔关闭中的作用及其与NO的关系<br>The Role of Hydrogen Sulfide and Its Relationship with Nitric Oxide in Cadmium Chloride-Induced Stomatal Closure in <i>Arabidopsis </i><i>t</i><i>haliana</i>
%A 马引利
%A 李先菊
%A 赵振宇
%A 梁爽爽
%A 黄丽萍
%J Botanical Research
%P 371-383
%@ 2168-5673
%D 2024
%I Hans Publishing
%R 10.12677/br.2024.134040
%X 以拟南芥(<i>Arabidopsis thaliana</i>)野生型和突变体为材料，探讨硫化氢(H<sub>2</sub>S)和一氧化氮(nitric oxide，NO)在氯化镉(CdCl<sub>2</sub>)诱导气孔运动中的作用及其相互关系。结果显示，CdCl<sub>2</sub>显著诱导拟南芥野生型气孔关闭、叶片H<sub>2</sub>S合成和L-/D-半胱氨酸脱巯基酶(L-/D-CDes)活性升高，H<sub>2</sub>S合成抑制剂显著抑制了以上效应；NO清除剂和合成抑制剂均能显著抑制CdCl<sub>2</sub>诱导的野生型保卫细胞NO合成和气孔关闭。另外，CdCl<sub>2</sub>处理不能诱导<i>Atl-cdes</i>、<i>Atd-cdes</i>、<i>Atnoa1</i>、<i>nia1-2</i>、<i>nia2-1</i>和<i>nia1-2</i><i>/</i><i>nia2-5</i>突变体气孔显著关闭。此外，NO清除剂和合成抑制剂显著抑制了CdCl<sub>2</sub>诱导的野生型H<sub>2</sub>S含量和L-/D-CDes活性的增加，而H<sub>2</sub>S合成抑制剂不能抑制野生型保卫细胞NO生成；CdCl<sub>2</sub>不能升高<i>Atnoa1</i>、<i>nia1-2</i>、<i>nia2-1</i>和<i>nia1-2</i><i>/</i><i>nia2-5</i>突变体叶片H<sub>2</sub>S水平和L-/D-CDes活性，而CdCl<sub>2</sub>能增强<i>Atl-cdes</i>和<i>Atd-cdes</i>突变体保卫细胞NO荧光水平。由此表明，NO介导的H<sub>2</sub>S生成参与CdCl<sub>2</sub>诱导的拟南芥气孔关闭，且在此过程中，L-和D-CDes负责H<sub>2</sub>S的合成，NO由NOS和NR途径产生。<br />
The roles and interrelationship of hydrogen sulfide (H<sub>2</sub>S) and nitric oxide (NO) in cadmium chloride (CdCl<sub>2</sub>)-induced stomatal movement were investigated using the <i>Arabidopsis thaliana</i> wide-type and related mutants. The results showed that CdCl<sub>2</sub> induced stomatal closure, H<sub>2</sub>S synthesis and L-/D-cysteine desulfhydrase (L-/D-CDes) activity increase of leaves in wild-type. H<sub>2</sub>S synthesis inhibitors could significantly prohibited these effects. NO scavenger and synthesis inhibitors all significantly inhibited CdCl<sub>2</sub>-caused NO production of guard cells and stomatal closure. Additionally, CdCl<sub>2</sub> couldn’t close stomata of <i>Atl-cdes</i>, <i>Atd-cdes</i>, <i>Atnoa1</i>, <i>nia1-2</i>, <i>nia2-1</i> and <i>nia1-2</i><i>/</i> <i>nia2-5</i> mutants. Furthermore, NO scavenger and synthesis inhibitors could prevent CdCl<sub>2</sub>-caused increase of H<sub>2</sub>S content and L-/D-CDes activity in wild-type, but H<sub>2</sub>S synthesis inhibitors couldn’t inhibit CdCl<sub>2</sub>-induced NO production of guard cells. CdCl<sub>2</sub> couldn’t increase H<sub>2</sub>S content and L-/D-CDes activity in <i>Atnoa1</i>, <i>nia1-2</i>, <i>nia2-1</i> and <i>nia1-2</i><i>/</i><i>nia2-5</i> mutants, but CdCl<sub>2</sub> intensified NO fluoresence levels in <i>Atl-cdes</i> and <i>Atd-cdes</i> mutants’ guard cells. From these results we concluded that NO-mediated H<sub>2</sub>S synthesis participated in CdCl<sub>2</sub>-induced stomatal closure in <i>A. </i><i>thaliana</i>, L- and D-CDes are responsible for H<sub>2</sub>S synthesis and NO was sourced from NOS and NR pathways in the physiological process.
%K 氯化镉，硫化氢，一氧化氮，信号转导，气孔关闭<br>Cadmium Chloride
%K Hydrogen Sulfide
%K Nitric Oxide
%K Signal Transduction
%K Stomatal Closure
%U http://www.hanspub.org/journal/PaperInformation.aspx?PaperID=91266