The Kinase OsCPK4 Regulates a Buffering Mechanism That Fine-Tunes Innate Immunity
The Kinase OsCPK4 Regulates a Buffering Mechanism That Fine-Tunes Innate Immunity
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激酶 OsCPK4 调节缓冲机制，微调先天免疫
DOI：
10.1104/pp.17.01024
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发表时间：
2018
期刊：
影响因子：
7.4
通讯作者：
Sun Wenxian
中科院分区：
文献类型：
--
作者：
Wang Jiyang;Wang Shanzhi;Hu Ke;Yang Jun;Xin Xiaoyun;Zhou Wenqing;Fan Jiangbo;Cui Fuhao;Mou Baohui;Zhang Shiyong;Wang Guoliang;Sun Wenxian
钙依赖性蛋白激酶OsCPK4已被证明在水稻（Oryza sativa）的盐和干旱耐受性、植物生长和发育中起重要作用。然而，关于OsCPK4在水稻免疫中的作用的分子机制知之甚少。在这项研究中，我们证明了微生物相关分子模式引发的氧化爆发和致病相关基因表达在oscpk4突变体中显著增强。与野生型相比，这些突变系对细菌枯萎病和真菌瘟病的抗性更强，表明OsCPK4负调控水稻的先天免疫。OsCPK4被进一步鉴定与受体样细胞质激酶OsRLCK176相互作用。OsRLCK176的积累受OsCPK4的负调控。有趣的是，激酶死亡的OsCPK4比野生型蛋白更强烈地促进OsRLCK176的降解。OsCPK4和OsRLCK176相互磷酸化，形成一个反馈回路。此外，OsCPK4和OsRLCK176的激酶活性和磷酸化有助于OsRLCK176的稳定性。这些发现表明，激酶失活的OsCPK4促进OsRLCK176降解并限制植物防御，而激活OsCPK4-OsRLCK176磷酸化回路使OsRLCK176降解机制失效，从而增强植物免疫力。总的来说，该研究提出了一种由OsCPK4介导的新型防御缓冲机制，该机制可以微调水稻中微生物相关的分子模式触发的免疫。
The calcium-dependent protein kinase OsCPK4 has been demonstrated to play important roles in salt and drought tolerance, plant growth, and development in rice (Oryza sativa). However, little is known about molecular mechanisms underlying OsCPK4 function in rice immunity. In this study, we demonstrated that the generation of oxidative burst and pathogenesis-related gene expression triggered by microbe-associated molecular patterns were significantly enhanced in theoscpk4mutants. These mutant lines are more resistant to bacterial blight and fungal blast diseases than the wild-type plants, indicating that OsCPK4 negatively regulates innate immunity in rice. OsCPK4 was further identified to interact with a receptor-like cytoplasmic kinase OsRLCK176. OsRLCK176 accumulation is negatively regulated by OsCPK4. Interestingly, the kinase-dead OsCPK4 promotes OsRLCK176 degradation more strongly than the wild-type protein. OsCPK4 and OsRLCK176 mutually phosphorylate each other and form a feedback loop. Moreover, the kinase activity and phosphorylation of OsCPK4 and OsRLCK176 contribute to the stability of OsRLCK176. These findings indicate that the kinase-inactive OsCPK4 promotes OsRLCK176 degradation and restricts plant defenses, whereas the activation of OsCPK4-OsRLCK176 phosphorylation circuit invalidates the OsRLCK176 degradation machinery, thus enhancing plant immunity. Collectively, the study proposes a novel defense buffering mechanism mediated by OsCPK4, which fine-tunes microbe-associated molecular pattern-triggered immunity in rice.