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质膜中的 NADPH 氧化酶参与由脱氢抗坏血酸诱导的气孔关闭。

NADPH oxidase in plasma membrane is involved in stomatal closure induced by dehydroascorbate.

机构信息

National Key Laboratory of Tobacco Planting, Physiology and Biochemistry, 450002 Zhengzhou, China.

出版信息

Plant Physiol Biochem. 2012 Feb;51:26-30. doi: 10.1016/j.plaphy.2011.09.014. Epub 2011 Oct 1.

DOI:10.1016/j.plaphy.2011.09.014
PMID:22153236
Abstract

Stoma is surrounded by two guard cells, and regulates the contents of water and CO(2) in plant, its opening and closing was affected by various factors. Recently, dehydroascorbate was found to induce stomata closure and H(2)O(2) generation. However, the mechanism of H(2)O(2) production is not clear. DPI and imidazole inhibit the flavoprotein and the b(-type) cytochrome components of the NADPH oxidase complex. Application of DPI or imidazole with DHA together impaired stomatal closure and elevation of H(2)DCF-DA fluorescent intensity induced by DHA in guard cells. CoCl(2) and PD98059, as the blocker of calcium channel and the inhibitor of MAPKKK, both impaired stomatal closure induced by DHA. The results suggested that DHA-induced H(2)O(2) generation via activation of NADPH oxidase, and thus resulting in stomatal closure. Moreover, Ca(2+) channel and MAPK cascades were involved in stomatal closure induced by DHA.

摘要

气孔由两个保卫细胞包围,调节植物体内的水分和 CO(2)含量,其开闭受多种因素影响。最近发现脱氢抗坏血酸能诱导气孔关闭和 H(2)O(2)的产生。然而,H(2)O(2)产生的机制尚不清楚。DPI 和咪唑抑制 NADPH 氧化酶复合物的黄素蛋白和 b(-型)细胞色素成分。用 DPI 或咪唑与 DHA 一起处理,会损害 DHA 诱导的保卫细胞中气孔关闭和 H(2)DCF-DA 荧光强度的升高。CoCl(2)和 PD98059 作为钙通道阻断剂和 MAPKKK 抑制剂,均损害 DHA 诱导的气孔关闭。结果表明,DHA 通过激活 NADPH 氧化酶诱导 H(2)O(2)的产生,从而导致气孔关闭。此外,DHA 诱导的气孔关闭涉及 Ca(2+)通道和 MAPK 级联。

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