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Abstract
背景回顾：Reactive oxygen species (ROS) production is a key event in modulating plant responses to hypoxia and post-hypoxia reoxygenation.
提出问题：However, the molecular mechanism by which hypoxia-associated ROS homeostasis is controlled remains largely unknown.
主要发现：Here, we showed that the calcium-dependent protein kinase CPK16 regulates plant hypoxia tolerance by phosphorylating the plasma membrane–anchored NADPH oxidase RESPIRATORY BURST OXIDASE HOMOLOG D (RBOHD) to regulate ROS production in Arabidopsis (Arabidopsis thaliana).
结果1-蛋白激活：In response to hypoxia or reoxygenation, CPK16 was activated through phosphorylation of its Ser274 residue.
结果2-过表达和敲除表型：The cpk16 knockout mutant displayed enhanced hypoxia tolerance, whereas CPK16-overexpressing (CPK16-OE) lines showed increased sensitivity to hypoxic stress. In agreement with these observations, hypoxia and reoxygenation both induced ROS accumulation in the rosettes of CPK16-OEs more strongly than in rosettes of the cpk16-1 mutant or the wild type.
结果3-CPK16-RBOHD互作：Moreover, CPK16 interacted with and phosphorylated the N terminus of RBOHD at four serine residues (Ser133, Ser148, Ser163, and Ser347) that were necessary for hypoxia- and reoxygenation-induced ROS accumulation.
结果4-RBOHD作用于CPK16下游：Furthermore, the hypoxia-tolerant phenotype of cpk16-1 was fully abolished in the cpk16 rbohd double mutant.
结论：Thus, we have uncovered a regulatory mechanism by which the CPK16–RBOHD module shapes ROS production during hypoxia and reoxygenation in Arabidopsis.
摘 要
活性氧物质（ROS）的产生是调控植物响应缺氧以及缺氧后复氧的关键事件。但是，缺氧相关的ROS内稳态受到何种分子机制的调控还不清楚。本文中，作者发现钙依赖性蛋白激酶CPK16通过磷酸化锚定于质膜的NADPH氧化酶RBOHD来调控ROS生成，从而作用于拟南芥的缺氧耐受性。在响应缺氧或者复氧时，CPK16通过磷酸化自身的Ser274残基从而被激活。cpk16敲除突变体的耐缺氧能力增强，而CPK16过表达株系则表现出对缺氧胁迫的敏感性增强。与这些观察一致的是，缺氧和复氧都会诱导CPK16-OE株系莲座叶中的ROS积累，且积累程度要远高于 cpk16-1突变体和野生型。此外，CPK16能够与RBOHD互作，并磷酸化RBOHD蛋白N端的4个丝氨酸残基（Ser133、Ser148、Ser163和Ser347），并且这些氨基酸残基的磷酸化对于缺氧或复氧诱导的ROS积累是必需的。另外，cpk16-1突变体的耐缺氧表型在cpk16 rbohd双突变体中不复存在。因此，本文揭示了一个由CPK16–RBOHD模块介导的调控机制，在拟南芥缺氧和复氧过程中调控ROS形成。
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