Nitric oxide inhibits blue light-induced stomatal opening by regulating the K+ influx in guard cells.
Nitric oxide inhibits blue light-induced stomatal opening by regulating the K+ influx in guard cells.
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DOI：
10.1016/j.plantsci.2011.12.007
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发表时间：
2012-03
期刊：
影响因子：
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通讯作者：
Xiang Zhao;Xin-Rong Qiao;Jing Yuan;Xiao‐fen Ma;Xiao Zhang
中科院分区：
文献类型：
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作者：
Xiang Zhao;Xin-Rong Qiao;Jing Yuan;Xiao‐fen Ma;Xiao Zhang
蓝光（BL）诱导的气孔开启和一氧化氮（NO）促进的气孔关闭是气孔调节的两个主要方面。气孔运动依赖于保护细胞中的离子流动，而BL或NO在调节离子通道活动中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诱导的气孔打开中的作用，我们将保护细胞原生质体（GCPs）置于全细胞结构中。结果表明，两次BL脉冲（100μmolm−2s−1，持续30s）可有效激活Vicia GCPs中向内整流的K+通道，激活率分别为67%和20%。红光（RL）对向内整流K+通道的影响较小。与此相一致的是，在拟南芥野生型gl1中，BL也使内向K+电流增加了54%，而在phot1-5 - phot2-1 （BL受体趋光素缺失突变体）中则没有。硝普钠（SNP， NO供体）在100μM时，抑制bcl依赖的K+内流和气孔打开，这被c-PTIO（一种特异性NO清除剂）消除。这些结果表明，NO抑制bl诱导的气孔打开可能是通过限制K+在保护细胞细胞膜上的内流来实现的。
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 (100μmolm−2s−1for 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 100μM, 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.