Abscisic acid (ABA) inhibits light-induced stomatal opening through calcium- and nitric oxide-mediated signaling pathways
Abscisic acid (ABA) inhibits light-induced stomatal opening through calcium- and nitric oxide-mediated signaling pathways
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DOI：
10.1016/j.niox.2007.08.001
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发表时间：
2007-11-01
影响因子：
3.9
通讯作者：
Lamattina, Lorenzo
中科院分区：
文献类型：
--
作者：
Garcia-Mata, Carlos;Lamattina, Lorenzo
一氧化氮（NO）是aba诱导气孔关闭的重要信号成分。然而，关于NO对气孔开放的抑制作用，目前的研究资料并不完整。在这里，我们提出的结果支持，在蚕豆保护细胞中，有一个关键的Ca2+依赖的NO增加需要aba介导的气孔打开抑制。外源NO对蚕豆表皮条光致气孔打开有抑制作用。此外，aba介导的气孔打开抑制被特异性NO清除剂cPTIO阻断，支持内源性NO参与这一过程。由于Ca2+浓度的升高是ABA介导的气孔打开抑制的先决条件，因此建立Ca2+， NO和ABA如何在光诱导的气孔打开抑制中相互作用是很有趣的。渗透性Ca2+特异性缓冲剂BAPTA-AM可阻断ABA-和Ca2+-，但不能阻断no介导的气孔打开抑制。NO合成酶（NOS）特异性抑制剂L-NAME阻止Ca2+介导的气孔打开抑制，表明Ca2+信号通路需要NOS样活性。此外，使用NO特异性荧光探针DAF-2DA的实验表明，Ca2+诱导内源性NO增加。这些结果表明，NO和Ca2+除了在ABA触发的气孔关闭中起作用外，还是ABA抑制光诱导气孔打开信号事件的活性组分。结果还支持Ca2+通过激活nos样活性诱导NO的产生。(c) 2007爱思唯尔公司版权所有。
Nitric oxide (NO) is an important signaling component of ABA-induced stomatal closure. However, only fragmentary data are available about NO effect on the inhibition of stomatal opening. Here, we present results supporting that, in Vicia faba guard cells, there is a critical Ca2+-dependent NO increase required for the ABA-mediated inhibition of stomatal opening. Light-induced stomatal opening was inhibited by exogenous NO in V. faba epidermal strips. Furthermore, ABA-mediated inhibition of stomatal opening was blocked by the specific NO scavenger cPTIO, supporting the involvement of endogenous NO in this process. Since the raise in Ca2+ concentration is a pre-requisite in ABA-mediated inhibition of stomatal opening, it was interesting to establish how does Ca2+, NO and ABA interact in the inhibition of light-induced stomatal opening. The permeable Ca2+ specific buffer BAPTA-AM blocked both ABA- and Ca2+- but not NO-mediated inhibition of stomatal opening. The NO synthase (NOS) specific inhibitor L-NAME prevented Ca2+-mediated inhibition of stomatal opening, indicating that a NOS-like activity was required for Ca2+ signaling. Furthermore, experiments using the NO specific fluorescent probe DAF-2DA indicated that Ca2+ induces an increase of endogenous NO. These results indicate that, in addition to the roles in ABA-triggered stomatal closure, both NO and Ca2+ are active components of signaling events acting in ABA inhibition of light-induced stomatal opening. Results also support that Ca2+ induces the NO production through the activation of a NOS-like activity. (c) 2007 Elsevier Inc. All rights reserved.