Induction of phosphatidylinositol 3-kinase-mediated endocytosis by salt stress leads to intracellular production of reactive oxygen species and salt tolerance
Induction of phosphatidylinositol 3-kinase-mediated endocytosis by salt stress leads to intracellular production of reactive oxygen species and salt tolerance
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DOI：
10.1111/j.1365-313x.2007.03134.x
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发表时间：
2007-07-01
期刊：
影响因子：
7.2
通讯作者：
Levine, Alex
中科院分区：
文献类型：
--
作者：
Leshem, Yehoram;Seri, Lior;Levine, Alex
盐给植物细胞带来了直接的问题，如渗透胁迫、离子稳态受损和钠毒性，随后是由活性氧（ROS）的产生引起的二次氧化胁迫。在这里，我们分析了盐胁迫过程中ROS的产生。我们发现，盐胁迫触发质膜内化，导致内体内的ROS的生产。细胞内活性氧的产生是由NADPH氧化酶对离子胁迫而非渗透胁迫的反应。在磷脂酰肌醇（PtdIns）3-激酶（PI 3 K）突变体中，PI 3 K是动物和植物中囊泡运输的关键调节剂，并且通过渥曼青霉素（其是PI 3 K和PI 4K的特异性抑制剂）抑制内吞作用和ROS产生。内吞作用和ROS的产生被拯救的幼苗补充外源PtdIns 3-磷酸（PtdIns 3 P），较少与PtdIns 4P，但不与PtdIns（4，5）P-2。令人惊讶的是，尽管减少了氧化应激，突变体和渥曼青霉素处理的植物表现出对盐过度敏感的表型，这也是由NADPH氧化酶的自杀抑制剂diphenyleneiodonium处理引起的，表明ROS在耐盐性中的积极作用。总之，我们的结果表明，盐胁迫反应，例如质膜内吞作用增加和细胞内活性氧的产生，是由磷脂调节的信号通路协调的，并表明活性氧在耐盐反应的信号转导中发挥作用。
Salt imposes immediate problems for plant cells, such as osmotic stress, impaired ion homeostasis and sodium toxicity, followed by a secondary oxidative stress caused by generation of reactive oxygen species (ROS). Here, we analyzed the production of ROS during salt stress. We show that salt stress triggered plasma membrane internalization, resulting in the production of ROS within endosomes. The intracellular ROS were produced by NADPH oxidase in response to the ionic but not the osmotic stress. Both endocytosis and ROS production were suppressed in phosphatidylinositol (PtdIns) 3-kinase (PI3K) mutants, PI3K being a key regulator of vesicle trafficking in animals and plants, and by wortmannin, which is a specific inhibitor of PI3K and PI4K. Endocytosis and the production of ROS were rescued by supplementation of seedlings with exogenous PtdIns 3-phosphate (PtdIns3P), less with PtdIns4P, but not with PtdIns(4,5)P-2. Surprisingly, despite reduced oxidative stress, the mutants and the wortmannin-treated plants exhibited a phenotype overly sensitive to salt, as also resulted from treatment with diphenyleneiodonium, a suicide inhibitor of NADPH oxidase, suggesting a positive role for ROS in salt tolerance. In summary, our results show that salt stress responses, such as increased plasma membrane endocytosis and the intracellular production of ROS, are coordinated by phospholipid-regulated signaling pathways, and suggest that ROS act in the signal transduction of the salt tolerance response.