Nitric oxide enhances salt tolerance in maize seedlings through increasing activities of proton-pump and Na+/H+ antiport in the tonoplast
Nitric oxide enhances salt tolerance in maize seedlings through increasing activities of proton-pump and Na+/H+ antiport in the tonoplast
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DOI：
10.1007/s00425-006-0242-z
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发表时间：
2006-08-01
期刊：
影响因子：
4.3
通讯作者：
Zhang, Wenhua
中科院分区：
文献类型：
--
作者：
Zhang, Yanyan;Wang, Liling;Zhang, Wenhua
一氧化氮（NO）是动植物体内的一种内源性信号分子，参与调节生物和非生物胁迫的应答。我们以前的工作证明，100 μ M硝普钠（SNP，一种NO供体）处理玉米幼苗增加了根、叶和叶鞘中的K+积累，同时减少了Na+积累（Zhang等，J Plant Physiol Mol Biol 30：455-459，2004 b）。在这里，我们研究如何NO调节Na+，K+离子的稳态玉米。用100 μ M SNP预处理2天改善了100 mM NaCl胁迫下玉米植株的后期生长，表现为干物质积累增加，叶绿素含量增加，叶细胞膜渗漏减少。一氧化氮清除剂，亚甲蓝（MB-1），阻断SNP的作用。这些结果表明，SNP来源的NO增强了玉米对盐胁迫的耐受性。进一步分析表明，NaCl诱导玉米叶片中NO水平的瞬时增加。NO和NaCl处理均能刺激液泡膜H+-ATPase和H+-PPase活性，从而增加H+-转运和Na+/H+交换。NaCl诱导的H+-ATP酶和H+-PPase活性被MB-1减弱。1-丁醇是磷脂酶D（PLD）产生磷脂酸（PA）的抑制剂，可降低NaCl和NO诱导的H+-ATP酶激活。相反，施加PA刺激H+-ATP酶活性。这些结果表明，NO通过提高液泡膜H ~+-ATPase和H ~+-PPase的活性，为Na ~+/H ~+交换提供驱动力，从而在NaCl响应中起信号分子的作用。PLD和PA在这一过程中发挥了重要作用。
Nitric oxide (NO), an endogenous signaling molecule in animals and plants, mediates responses to abiotic and biotic stresses. Our previous work demonstrated that 100 mu M sodium nitroprusside (SNP, an NO donor) treatment of maize seedlings increased K+ accumulation in roots, leaves and sheathes, while decreasing Na+ accumulation (Zhang et al. in J Plant Physiol Mol Biol 30:455-459, 2004b). Here we investigate how NO regulates Na+, K+ ion homeostasis in maize. Pre-treatment with 100 mu M SNP for 2 days improved later growth of maize plants under 100 mM NaCl stress, as indicated by increased dry matter accumulation, increased chlorophyll content, and decreased membrane leakage from leaf cells. An NO scavenger, methylene blue (MB-1), blocked the effect of SNP. These results indicated that SNP-derived NO enhanced maize tolerance to salt stress. Further analysis showed that NaCl induced a transient increase in the NO level in maize leaves. Both NO and NaCl treatment stimulated vacuolar H+-ATPase and H+-PPase activities, resulting in increased H+-translocation and Na+/H+ exchange. NaCl-induced H+-ATPase and H+-PPase activities were diminished by MB-1. 1-Butanol, an inhibitor of phosphatidic acid (PA) production by phospholipase D (PLD), reduced NaCl- and NO-induced H+-ATPase activation. In contrast, applied PA stimulated H+-ATPase activity. These results suggest that NO acts as a signal molecule in the NaCl response by increasing the activities of vacuolar H+-ATPase and H+-PPase, which provide the driving force for Na+/H+ exchange. PLD and PA play an important role in this process.