ABA-induced NO generation and stomatal closure in Arabidopsis are dependent on H2O2 synthesis
ABA-induced NO generation and stomatal closure in Arabidopsis are dependent on H2O2 synthesis
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DOI：
10.1111/j.1365-313x.2005.02615.x
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发表时间：
2006-01-01
期刊：
影响因子：
7.2
通讯作者：
Neill, SJ
中科院分区：
文献类型：
--
作者：
Bright, J;Desikan, R;Neill, SJ
一氧化氮(NO)和过氧化氢(H_2O_2)是响应各种刺激而产生的关键信号分子，参与植物多种信号转导过程。一氧化氮和过氧化氢是植物激素脱落酸(ABA)诱导气孔关闭的复杂信号网络的重要组成部分。ABA与保卫细胞中NO和H_2O_2的时空产生和作用密切相关。本研究表明，在拟南芥保卫细胞中，ABA介导的NO的产生实际上依赖于ABA诱导的过氧化氢的产生。H_2O_2诱导的气孔关闭通过NO清除剂清除NO而被抑制，ABA和H_2O_2都能刺激保卫细胞合成NO。相反，NO诱导的气孔关闭不需要H_2O_2合成，也不会诱导保卫细胞产生H_2O_2。钨酸盐抑制NO生成酶硝酸还原酶(NR)可在体外减弱亚硝酸盐以及在体内对H_2O_2和ABA的反应产生NO。遗传学数据表明，在ABA介导的H_2O_2合成过程中，NR是保卫细胞产生NO的主要来源。在NR双突变体nia1、nia2中，ABA和H_2O_2均不能诱导NO的产生或气孔关闭，但在一氧化氮合酶缺失突变体中，对H_2O_2的反应不受影响。重要的是，我们发现在NADPH氧化酶缺失的双突变体atrbohD/F中，NO的合成和气孔对ABA的关闭都严重减少，这表明ABA诱导的内源H_2O_2的产生是NO合成所必需的。综上所述，我们的生理和遗传学数据表明，ABA、内源过氧化氢和NO诱导的气孔关闭之间存在很强的相互关系。
Nitric oxide (NO) and hydrogen peroxide (H2O2) are key signalling molecules produced in response to various stimuli and involved in a diverse range of plant signal transduction processes. Nitric oxide and H2O2 have been identified as essential components of the complex signalling network inducing stomatal closure in response to the phytohormone abscisic acid (ABA). A close inter-relationship exists between ABA and the spatial and temporal production and action of both NO and H2O2 in guard cells. This study shows that, in Arabidopsis thaliana guard cells, ABA-mediated NO generation is in fact dependent on ABA-induced H2O2 production. Stomatal closure induced by H2O2 is inhibited by the removal of NO with NO scavenger, and both ABA and H2O2 stimulate guard cell NO synthesis. Conversely, NO-induced stomatal closure does not require H2O2 synthesis nor does NO treatment induce H2O2 production in guard cells. Tungstate inhibition of the NO-generating enzyme nitrate reductase (NR) attenuates NO production in response to nitrite in vitro and in response to H2O2 and ABA in vivo. Genetic data demonstrate that NR is the major source of NO in guard cells in response to ABA-mediated H2O2 synthesis. In the NR double mutant nia1, nia2 both ABA and H2O2 fail to induce NO production or stomatal closure, but in the nitric oxide synthase deficient Atnos1 mutant, responses to H2O2 are not impaired. Importantly, we show that in the NADPH oxidase deficient double mutant atrbohD/F, NO synthesis and stomatal closure to ABA are severely reduced, indicating that endogenous H2O2 production induced by ABA is required for NO synthesis. In summary, our physiological and genetic data demonstrate a strong inter-relationship between ABA, endogenous H2O2 and NO-induced stomatal closure.