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出 处:《植物学研究》2024年第4期371-383,共13页Botanical Research
摘 要:以拟南芥(Arabidopsis thaliana)野生型和突变体为材料,探讨硫化氢(H2S)和一氧化氮(nitric oxide,NO)在氯化镉(CdCl2)诱导气孔运动中的作用及其相互关系。结果显示,CdCl2显著诱导拟南芥野生型气孔关闭、叶片H2S合成和L-/D-半胱氨酸脱巯基酶(L-/D-CDes)活性升高,H2S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CdCl2诱导的野生型保卫细胞NO合成和气孔关闭。另外,CdCl2处理不能诱导Atl-cdes、Atd-cdes、Atnoa1、nia1-2、nia2-1和nia1-2/nia2-5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CdCl2诱导的野生型H2S含量和L-/D-CDes活性的增加,而H2S合成抑制剂不能抑制野生型保卫细胞NO生成;CdCl2不能升高Atnoa1、nia1-2、nia2-1和nia1-2/nia2-5突变体叶片H2S水平和L-/D-CDes活性,而CdCl2能增强Atl-cdes和Atd-cdes突变体保卫细胞NO荧光水平。由此表明,NO介导的H2S生成参与CdCl2诱导的拟南芥气孔关闭,且在此过程中,L-和D-CDes负责H2S的合成,NO由NOS和NR途径产生。The roles and interrelationship of hydrogen sulfide (H2S) and nitric oxide (NO) in cadmium chloride (CdCl2)-induced stomatal movement were investigated using the Arabidopsis thaliana wide-type and related mutants. The results showed that CdCl2 induced stomatal closure, H2S synthesis and L-/D-cysteine desulfhydrase (L-/D-CDes) activity increase of leaves in wild-type. H2S synthesis inhibitors could significantly prohibited these effects. NO scavenger and synthesis inhibitors all significantly inhibited CdCl2-caused NO production of guard cells and stomatal closure. Additionally, CdCl2 couldn’t close stomata of Atl-cdes, Atd-cdes, Atnoa1, nia1-2, nia2-1 and nia1-2/ nia2-5 mutants. Furthermore, NO scavenger and synthesis inhibitors could prevent CdCl2-caused increase of H2S content and L-/D-CDes activity in wild-type, but H2S synthesis inhibitors couldn’t inhibit CdCl2-induced NO production of guard cells. CdCl2 couldn’t increase H2S content and L-/D-CDes activity in Atnoa1, nia1-2, nia2-1 and nia1-2/nia2-5 mutants, but CdCl2 intensified NO fluoresence levels in Atl-cdes and Atd-cdes mutants’ guard cells. From these results we concluded that NO-mediated H2S synthesis participated in CdCl2-induced stomatal closure in A. thaliana, L- and D-CDes are responsible for H2S synthesis and NO was sourced from NOS and NR pathways in the physiological process.
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