Nitric oxide blocks blue light-induced K+ influx by elevating the cytosolic Ca2+ concentration in Vicia faba L. guard cells.
Nitric oxide blocks blue light-induced K+ influx by elevating the cytosolic Ca2+ concentration in Vicia faba L. guard cells.
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DOI：
10.1111/jipb.12038
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发表时间：
2013-06
影响因子：
11.4
通讯作者：
Xiang Zhao;Yuanyuan Li;Hui-Li Xiao;Chang Xu;Xiao Zhang
中科院分区：
文献类型：
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作者：
Xiang Zhao;Yuanyuan Li;Hui-Li Xiao;Chang Xu;Xiao Zhang
Ca（2+）在一氧化氮（NO）促进气孔关闭中起着关键作用。然而，Ca（2+）在NO抑制蓝光（BL）诱导的气孔开放中的作用仍不清楚。在此，我们分析了Ca（2+）在蚕豆BL和NO信号转导系统中的作用。守卫细胞细胞外Ca（2+）对BL诱导的气孔开放具有剂量依赖性调节作用，5 μM Ca（2+）可显著抑制BL诱导的K（+）内流。NO供体硝普钠（SNP）对BL诱导的K（+）内流和气孔开放反应的影响不大，但在细胞外Ca（2+）缺乏的情况下，SNP对K（+）内流和气孔开放反应有抑制作用。有趣的是，虽然SNP和BL都能激活质膜Ca（2+）通道，引起胞浆Ca（2+）浓度升高，但SNP和BL处理后Ca（2+）通道活性和胞浆Ca（2+）浓度的变化不同。100 μM的SNP明显激活质膜Ca（2+）通道，使胞浆Ca（2+）浓度升高102.4%。相反，BL脉冲（100 μmol/m2/s，持续30 s）轻微激活Ca（2+）通道，仅导致Ca（2+）升高20.8%。细胞内Ca（2+）浓度在0.5 μM或以下时促进K（+）内流，而在5 μM或以上时显著抑制K（+）内流。总之，我们的研究结果表明，Ca（2+）在保卫细胞BL和NO信号之间的串扰中起着双重和独特的作用，在较低浓度下作为激活剂介导BL诱导的K（+）内流，在较高浓度下作为抑制剂介导NO阻断的K（+）内流。
Ca(2+) plays a pivotal role in nitric oxide (NO)-promoted stomatal closure. However, the function of Ca(2+) in NO inhibition of blue light (BL)-induced stomatal opening remains largely unknown. Here, we analyzed the role of Ca(2+) in the crosstalk between BL and NO signaling in Vicia faba L. guard cells. Extracellular Ca(2+) modulated the BL-induced stomatal opening in a dose-dependent manner, and an application of 5 μM Ca(2+) in the pipette solution significantly inhibited BL-activated K(+) influx. Sodium nitroprusside (SNP), a NO donor, showed little effect on BL-induced K(+) influx and stomatal opening response in the absence of extracellular Ca(2+), but K(+) influx and stomatal opening were inhibited by SNP when Ca(2+) was added to the bath solution. Interestingly, although both SNP and BL could activate the plasma membrane Ca(2+) channels and induce the rise of cytosolic Ca(2+), the change in levels of Ca(2+) channel activity and cytosolic Ca(2+) concentration were different between SNP and BL treatments. SNP at 100 μM obviously activated the plasma membrane Ca(2+) channels and induced cytosolic Ca(2+) rise by 102.4%. In contrast, a BL pulse (100 μmol/m(2) per s for 30 s) slightly activated the Ca(2+) channels and resulted in a Ca(2+) rise of only 20.8%. Consistently, cytosolic Ca(2+) promoted K(+) influx at 0.5 μM or below, and significantly inhibited K(+) influx at 5 μM or above. Taken together, our findings indicate that Ca(2+) plays dual and distinctive roles in the crosstalk between BL and NO signaling in guard cells, mediating both the BL-induced K(+) influx as an activator at a lower concentration and the NO-blocked K(+) influx as an inhibitor at a higher concentration.