Garcia-Mata Carlos, Lamattina Lorenzo
Instituto de Investigaciones Biológicas, Facultad de Ciencias Exactas y Naturales, Universidad Nacional de Mar del Plata, CC 1245, B7602AYJ Mar del Plata, Buenos Aires, Argentina.
Nitric Oxide. 2007 Nov-Dec;17(3-4):143-51. doi: 10.1016/j.niox.2007.08.001. Epub 2007 Aug 17.
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.
一氧化氮（NO）是脱落酸（ABA）诱导气孔关闭的重要信号成分。然而，关于NO对气孔开放抑制作用的数据尚不完整。在此，我们提供的结果表明，在蚕豆保卫细胞中，ABA介导的气孔开放抑制需要关键的Ca2+依赖性NO增加。外源NO抑制了蚕豆表皮条中光诱导的气孔开放。此外，ABA介导的气孔开放抑制被特异性NO清除剂cPTIO阻断，这支持了内源性NO参与此过程。由于Ca2+浓度升高是ABA介导的气孔开放抑制的先决条件，因此研究Ca2+、NO和ABA在抑制光诱导气孔开放过程中如何相互作用很有意思。可渗透的Ca2+特异性缓冲剂BAPTA-AM阻断了ABA和Ca2+介导的气孔开放抑制，但未阻断NO介导的抑制。NO合酶（NOS）特异性抑制剂L-NAME阻止了Ca2+介导的气孔开放抑制，表明Ca2+信号传导需要类似NOS的活性。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，除了在ABA触发的气孔关闭中发挥作用外，NO和Ca2+都是ABA抑制光诱导气孔开放信号事件的活性成分。结果还支持Ca2+通过激活类似NOS的活性诱导NO生成。
