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作物学报 ›› 2008, Vol. 34 ›› Issue (11): 1970-1976.doi: 10.3724/SP.J.1006.2008.01970

• 耕作栽培·生理生化 • 上一篇    下一篇

盐胁迫条件下外源Ca2+对蚕豆气孔运动及质膜K+通道的调控

赵翔;汪延良;王亚静;王西丽;张骁*   

  1. 河南省植物逆境生物学重点实验室/河南大学生命科学学院,河南开封 475004
  • 收稿日期:2008-04-18 修回日期:1900-01-01 出版日期:2008-11-13 发布日期:2008-09-06
  • 通讯作者: 张骁
  • 基金资助:

    国家自然科学基金项目(30570964)

Effects of Exogenous Ca2+ on Somatal Movement and Plasma Membrane K+ Channels of Vicia Guard Cell under Salt Stress

ZHAO Xiang,WANG Yan-Liang,WANG Ya-Jing,WANG Xi-Li,ZHANG Xiao*   

  1. Henan Key Laboratory of Plant Stress Biology, School of Life Sciences, Henan University, Kaifeng 475004, Henan, China
  • Received:2008-04-18 Revised:1900-01-01 Online:2008-11-13 Published:2008-09-06
  • Contact: ZHANG Xiao

摘要:

研究了Ca2+ 对NaCl胁迫下蚕豆气孔运动及质膜K+通道的影响。结果表明,100 mmol L-1 NaCl可明显诱导气孔开放,该现象可被10 mmol L-1 CaCl2 显著抑制。为探讨盐胁迫下Ca2+对K+和Na+跨膜运输的调控机制,我们利用膜片钳技术记录全细胞K+ 电流发现,在100 mmol L-1 NaCl胁迫下,加入10 mmol L-1 CaCl2胞外处理,显著抑制质膜K+内向及外向通道电流,这种抑制可被1 mmol L-1 La3+ (Ca2+通道抑制剂)缓解。非盐胁迫下,10 mmol L-1 CaCl2 胞外处理也能显著抑制质膜内向K+通道,但明显激活其外向通道,加入1 mmol L-1 La3+并不能被缓解。用H2O2专一的荧光探针二氯荧光素二乙酸酯(H2DCF-DA)单细胞分析保卫细胞内H2O2含量变化显示,在100 mmol L-1 NaCl盐胁迫下,10 mmol L-1 CaCl2 处理明显诱导H2O2在保卫细胞中积累;100 mmol L-1 NaCl和10 mmol L-1 CaCl2单独处理并不能诱导H2O2积累。推测Ca2+在盐胁迫下可能先诱导H2O2在胞内积累,进而激活质膜Ca2+通道,迅速提高胞内Ca2+浓度以抑制Na+通过质膜K+通道跨膜内流,同时调节Na+外流,两种效应共同作用促使气孔关闭,减少盐胁迫下水分的过度散失。上述结果将为Ca2+调控作物抗盐机制研究提供新的思路。

关键词: 盐胁迫, 钙离子, 过氧化氢, 保卫细胞, 质膜K+ 通道

Abstract:

Soil salinity is a key abiotic stress in crop production worldwide, especially in countries where irrigation is an essential aid to agriculture. Salt stress disturbs intracellular ion homeostasis of plants, which leads to membrane dysfunction, attenuation of metabolic activity, and secondary effects causing growth inhibition and ultimately death. Salt tolerance in plants is the ultimate manifestation of several physiologic processes, including ion uptake and membrane flux, ionic balance and distribution. Previous researches have shown that K+ inward rectifying channels, outward rectifying channels, high affinity K+ transporter (HKT) and low affinity cation transporter (LCT) may facilitate Na+ influx under NaCl stress. Extracellular free Ca2+ concentration ([Ca2+]ext) enhances salt tolerance and salinity stress elicits a transient increase in cytosolic free Ca2+ concentration ([Ca2+]cyt). The transient increase in [Ca2+]cyt activates the PP2B phosphatase calcineurin leading to the transcription of ENA1, which encodes the P-type ATPase that is primarily responsible for Na+ efflux across the plasma membrane or activates the SOS signal pathway which negatively controls this Na+ influx system. At the plasma membrane, high cytosolic Ca2+ levels can cause activation of anion channels and reduce the conductivity of inward K+ channels , thus reducing water loss. To better understand Ca2+ function in K+ and Na+ uptake, here, we investigated the effect of calcium on stomatal movement and K+ channels of Vicia faba under NaCl stress. The results showed that 100 mmol L-1 NaCl significantly induced stomatal opening, CaCl2 facilitated NaCl-induced stomatal opening at concentration of 0.1 mmol L-1 and significantly inhibited NaCl-induced stomatal opening at concentration of 10 mmol L-1. To gain further insights into Ca2+ function in NaCl-regulated stomatal movement, Vicia faba guard cell protoplasts were patch-clamped in a whole-cell configuration and the results showed that Ca2+ significantly inhibited inward rectifying and outward rectifying K+ current when NaCl and CaCl2 were added to the bath solution together, at concentration of 100 mmol L-1 and 10 mmol L-1 respectively, which was alleviated by LaCl3 at concentration of 1 mmol L-1. In contrast, 10 mmol L-1 CaCl2 alone significantly inhibited inward rectifying K+ current and activated outward rectifying K+ current, which was not alleviated by LaCl3. A single-cell analysis of cytosolic H2O2 using 2’,7’-dichlorofluorescin (H2DCF-DA) revealed that Ca2+ can induce the generating of H2O2 in the guard cells with 10 mmol L-1 CaCl2 under 100 mmol L-1 NaCl stress, but 10 mmol L-1 CaCl2 or 100 mmol L-1 NaCl had little effect on the accumulation of H2O2 in the guard cells, respectively. These results suggest that calcium may alleviate the damage caused by NaCl stress through inducing the production of H2O2,in turn the H2O2-activated increases in [Ca2+]cyt in guard cells decrease Na+ uptake by the regulation of plasma membrane K+ channels in guard cells leading to stomatal closure and reduction of water loss. These findings open new perspectives about Ca2+-based signaling in responsive to salt stress in plants.

Key words: Salt stress, Calcium, Hydrogen peroxide, Guard cell, Plasma membrane K+ channels

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