Modulation of reactive oxygen species by salicylic acid in arabidopsis seed germination under high salinity
Modulation of reactive oxygen species by salicylic acid in arabidopsis seed germination under high salinity
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DOI：
10.4161/psb.5.12.13159
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发表时间：
2010-01-01
影响因子：
2.9
通讯作者：
Park, Chung-Mo
中科院分区：
文献类型：
--
作者：
Lee, Sangmin;Park, Chung-Mo
水杨酸（SA）对许多植物种子萌发的潜在作用已被探索。然而，它仍然是有争议的SA如何调节种子萌发，主要是因为结果已经有些变量，这取决于植物基因型和实验条件。我们发现SA促进拟南芥种子在高盐条件下萌发。SA生物合成缺陷的突变体B12的种子萌发对高盐敏感，但在生理浓度的SA存在下抑制作用降低。包括高盐在内的非生物胁迫对植物产生氧化胁迫。H_2O_2含量在突变体中较高。然而，外源SA的施用降低了内源活性氧（ROS）水平，表明SA参与了非生物胁迫条件下植物对ROS介导的损伤的响应。赤霉素（GA），一种与种子萌发密切相关的植物激素，也可以逆转高盐对种子萌发和幼苗建立的抑制作用。在高盐条件下，GA通过诱导SID2基因来促进SA的生物合成。值得注意的是，SA还诱导编码GA生物合成酶的基因。这些观察结果表明，SA促进种子萌发在高盐度下通过调节抗氧化活性，通过信号串扰与GA。
Potential roles of salicylic acid (SA) on seed germination have been explored in many plant species. However, it is still controversial how SA regulates seed germination, mainly because the results have been somewhat variable, depending on plant genotypes used and experimental conditions employed. We found that SA promotes seed germination under high salinity in Arabidopsis. Seed germination of the sid2 mutant, which has a defect in SA biosynthesis, is hypersensitive to high salinity, but the inhibitory effects are reduced in the presence of physiological concentrations of SA. Abiotic stresses, including high salinity, impose oxidative stress on plants. Endogenous contents of H2O2 are higher in the sid2 mutant seeds. However, exogenous application of SA reduces endogenous level of reactive oxygen species (ROS), indicating that SA is involved in plant responses to ROS-mediated damage under abiotic stress conditions. Gibberellic acid (GA), a plant hormone closely associated with seed germination, also reverses the inhibitory effects of high salinity on seed germination and seedling establishment. Under high salinity, GA stimulates SA biosynthesis by inducing the SID2 gene. Notably, SA also induces genes encoding GA biosynthetic enzymes. These observations indicate that SA promotes seed germination under high salinity by modulating antioxidant activity through signaling crosstalks with GA.