一氧化氮通过调节保卫细胞中的 K+内流抑制蓝光诱导的气孔开放。
Nitric oxide inhibits blue light-induced stomatal opening by regulating the K+ influx in guard cells.
机构信息
State Key Laboratory of Cotton Biology, Key laboratory of Plant Stress Biology, College of Life Sciences, Henan University, Kaifeng 475004, People's Republic of China.
出版信息
Plant Sci. 2012 Mar;184:29-35. doi: 10.1016/j.plantsci.2011.12.007. Epub 2011 Dec 16.
Blue light (BL)-induced stomatal opening and nitric oxide (NO)-promoted stomatal closure comprise two main aspects of stomatal regulation. Stomatal movement depends on ion fluxion in guard cells, whereas the physiological roles of BL or NO in regulating ion channel activities remain largely unknown. For gaining further insights into NO function in mediating BL-induced stomatal opening, guard cell protoplasts (GCPs) were patch-clamped in a whole-cell configuration. The results showed that twice BL pulses (100 μmol m⁻² s⁻¹ for 30s) effectively activated inward rectifying K⁺ channels by 67% and 20% in Vicia GCPs, respectively. In contrast, Red light (RL) showed little effect on inward rectifying K⁺ channels. In accord with this, BL also increased inward K⁺ currents by 54% in Arabidopsis thaliana wild type gl1, but not in phot1-5 phot2-1 (BL receptor phototropin deletion mutant). Sodium nitroprusside (SNP, a NO donor), at 100 μM, inhibited BL-dependent K⁺ influx and stomatal opening, which were abolished by c-PTIO (a specific NO scavenger). These results indicated that NO inhibits BL-induced stomatal opening maybe through restricting the K⁺ influx across plasma membrane in guard cells.
蓝光（BL）诱导的气孔开放和一氧化氮（NO）促进的气孔关闭构成了气孔调节的两个主要方面。气孔运动取决于保卫细胞中的离子流，而 BL 或 NO 在调节离子通道活性方面的生理作用在很大程度上仍然未知。为了进一步了解 NO 在介导 BL 诱导的气孔开放中的作用，采用全细胞模式对保卫细胞原生质体（GCPs）进行了膜片钳钳制。结果表明，两次 BL 脉冲（100 μmol m ⁻² s ⁻¹ ，持续 30s）分别有效地激活了 Vicia GCPs 中的内向整流 K ⁺ 通道 67%和 20%。相比之下，红光（RL）对内向整流 K ⁺ 通道几乎没有影响。与此一致，BL 还使拟南芥野生型 gl1 中的内向 K ⁺ 电流增加了 54%，但在 phot1-5 phot2-1（BL 受体光受体突变体）中则没有。硝普钠（SNP，一种 NO 供体）在 100 μM 时抑制 BL 依赖的 K ⁺ 内流和气孔开放，而 c-PTIO（一种特定的 NO 清除剂）则消除了这种抑制作用。这些结果表明，NO 通过限制保卫细胞质膜上的 K ⁺ 内流来抑制 BL 诱导的气孔开放。
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