Induction of phosphatidylinositol 3-kinase-mediated endocytosis by salt stress leads to intracellular production of reactive oxygen species and salt tolerance.

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 Here, we analyzed the production of during salt stress. We show that salt stress triggered plasma membrane internalization, resulting in the production of duanyu1670 within endosomes. The intracellular duanyu1670 were produced by NADPH oxidase in response to the ionic but not the osmotic stress. Both endocytosis and duanyu1670 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 duanyu1670 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 duanyu1670 in salt tolerance. In summary, our results show that salt stress responses, such as increased plasma membrane endocytosis and the intracellular production of are coordinated by phospholipid-regulated signaling pathways, and suggest that duanyu1670 act in the signal transduction of the salt tolerance response.

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