[NO may function in the downstream of Ca2+ in ethylene induced stomatal closure in Vicia faba L].

Guo Hua Liu, Jing Liu, Li Xia Hou, Jing Tang, Xin Liu
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Abstract

Through pharmacological combined with laser scanning confocal microscope (LSCM) and spectrophotography to study the role of Ca2+ and NO in signaling during Vicia faba L. stomatal movement response to ethylene (Eth). The results showed that treatment with ethephon (0.004%, 0.04%, 0.4%) resulted in a time- and dose-dependent stomatal closure under light. NO scavenger cPTIO, nitrate reductase inhibitor NaN3, or extracellular Ca2+ chelation EGTA reduced ethylene-induced stomatal closure. Moreover, ethylene was shown to enhance nitric oxide levels and, corresponding, nitrate reductase activity. Inhibition of the nitrate reductase diminished ethylene-induced NO production in both stomatal guard cell and leaf. Finally, ethylene-induced NO levels and nitrate reductase activity decreased when Ca2+ was compromised. On the basis of biochemical and pharmacological experimental results, we can conclude that Ca2+ and NO were involved in the signal transduction pathway of ethylene induced stomatal closure. Nitrate reductase-derived NO may represents a novel downstream component of Ca2+ signaling cascade during ethylene-induced stomatal movement in Vicia faba L.

[NO可能在乙烯诱导蚕豆气孔关闭过程中Ca2+的下游发挥作用]。
通过药理学结合激光扫描共聚焦显微镜(LSCM)和光谱摄影技术,研究了Ca2+和NO在蚕豆(Vicia faba L.)气孔运动对乙烯(Eth)响应过程中的信号传导作用。结果表明:0.004%、0.04%、0.4%乙烯利处理下气孔关闭具有时间和剂量依赖性;一氧化氮清除剂cPTIO、硝酸还原酶抑制剂NaN3或细胞外Ca2+螯合EGTA可降低乙烯诱导的气孔关闭。此外,乙烯还能提高一氧化氮水平,从而提高硝酸还原酶的活性。硝酸还原酶的抑制降低了乙烯诱导的气孔保护细胞和叶片NO的产生。最后,当Ca2+受到损害时,乙烯诱导的NO水平和硝酸还原酶活性降低。根据生物化学和药理实验结果,我们可以得出Ca2+和NO参与了乙烯诱导气孔关闭的信号转导途径。硝酸还原酶衍生的NO可能代表了乙烯诱导的蚕豆气孔运动中Ca2+信号级联的一个新的下游组分。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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