欢迎访问《环境科学学报》编辑部网站！

快速检索			高级检索

研究报告

Involvement of nitric oxide synthase in stomatal movement regulation in the response of Vicia faba L. to sulfur dioxide stress

基金项目：国家自然科学基金项目(No.30870454, 30470318, 31371868);高等学校博士学科点专项科研基金(No. 20070108007, 20121401110007)

摘要：以蚕豆为材料,研究一氧化氮合酶(NOS)途径在SO₂诱发气孔运动中的作用.研究发现:浓度7.5~200 μmol·L^-1的SO₂衍生物处理后,蚕豆叶面气孔开度减小,气孔开度与SO₂衍生物浓度呈负相关;SO₂衍生物处理组叶组织中NOS活性增强;加入NO清除剂c-PTIO或NOS抑制剂L-NAME可抑制SO₂衍生物诱发的气孔关闭;SO₂衍生物处理组保卫细胞内NO和Ca²⁺水平升高,用c-PTIO降低胞内NO水平后Ca²⁺水平随之下降.结果表明,SO₂衍生物胁迫可诱发保卫细胞内NO合成增加,NO通过调节胞内Ca²⁺水平升高,激活下游信号转导途径,调节气孔运动;NOS途径介导的NO合成参与了SO₂胁迫下蚕豆气孔运动的调节.

Abstract：The potential role of nitric oxide synthase (NOS) in stomatal movement regulation in the response of plants to sulfur dioxide (SO₂) was investigated in Vicia faba L. The results showed that SO₂ hydrates significantly decreased stomatal aperture in the concentration range of 7.5 to 200 μmol·L^-1. SO₂ hydrates induced stomatal closure in a concentration-dependent manner. SO₂ hydrates-evoked stomatal closure was correlated with increasing activities of NOS in the whole leaves from four-week-old V. faba plants. Both NO scavenger c-PTIO and NOS inhibitor L-NAME can block SO₂ hydrates-evoked stomatal closure. Moreover, exposure to SO₂ hydrates enhanced the intracellular levels of NO and Ca²⁺ in guard cell. Application of exogenous NO scavenger c-PTIO blocked the increases of intracellular NO and Ca²⁺ levels in SO₂-treated guard cells. These results indicated that SO₂ hydrates-triggered NO production mediated stomatal movement regulation via Ca²⁺ signaling, and that nitric oxide synthase-dependent NO production played a crucial role in SO₂ hydrates-evoked stomatal movement in V. faba.