Plant cell-surface-localized pattern recognition receptors (PRRs) recognize microbial patterns and activate pattern-triggered immunity (PTI). Typical PTI responses include reactive oxygen species (ROS) burst controlled by the NADPH oxidase RESPIRATORY BURST OXIDASE HOMOLOGUE D (RbohD) and activation of the mitogen-activated protein kinase (MAPK) cascade composed of MAPKKK3/5-MKK4/5-MPK3/6. However, the mechanisms through which PRRs regulate and coordinate these immune responses are not fully understood. Here, we showed that Arabidopsis thaliana OXIDATIVE SIGNAL-INDUCIBLE1 (OXI1), a kinase known to be activated by ROS, is involved in the LYK5-CERK1 receptor complex, which recognizes fungal cell wall-derived chitin. The oxi1 mutant exhibits enhanced susceptibility to various pathogens and reduced chitin-induced MAPK activation and ROS burst. We showed that chitin induces the phosphorylation of OXI1 in an RbohD-dependent manner. H2O2 and chitin treatment causes the oxidation of OXI1 at Cys104 and Cys205, which is essential for the kinase activity of OXI1. These oxidation sites are required for chitin-induced MAPK activation and disease resistance. Activated OXI1 directly phosphorylates MAPKKK5 to regulate MAPK activation. Additionally, OXI1 phosphorylates RbohD, suggesting that it may activate RbohD to promote ROS burst to further enhance the long-term MAPK activation. Together, our findings reveal a pathway linking PRR-mediated ROS production to MAPK activation through OXI1.

中文翻译：

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OXI1 激酶通过将微生物模式诱导的 ROS 爆发与 MAPK 激活联系起来来调节植物免疫


植物细胞表面定位模式识别受体 （PRR） 识别微生物模式并激活模式触发免疫 （PTI）。典型的 PTI 反应包括由 NADPH 氧化酶呼吸爆发氧化酶同源物 D （RbohD） 控制的活性氧 （ROS） 爆发和由 MAPKKK3/5-MKK4/5-MPK3/6 组成的丝裂原活化蛋白激酶 （MAPK） 级联反应的激活。然而，PRR 调节和协调这些免疫反应的机制尚不完全清楚。在这里，我们表明拟南芥氧化信号-INDUCIBLE1 （OXI1） 是一种已知被 ROS 激活的激酶，参与 LYK5-CERK1 受体复合物，该受体复合物识别真菌细胞壁衍生的几丁质。oxi1 突变体表现出对各种病原体的敏感性增强，并减少几丁质诱导的 MAPK 激活和 ROS 爆发。我们发现几丁质以 RbohD 依赖性方式诱导 OXI1 的磷酸化。H 2 O 2 和几丁质处理导致 OXI1 在 Cys104 和 Cys205 位点氧化，这对 OXI1 的激酶活性至关重要。这些氧化位点是几丁质诱导的 MAPK 激活和抗病性所必需的。活化的 OXI1 直接磷酸化 MAPKKK5 以调节 MAPK 活化。此外，OXI1 磷酸化 RbohD，表明它可能激活 RbohD 以促进 ROS 爆发，从而进一步增强长期 MAPK 激活。总之，我们的研究结果揭示了一条通过 OXI1 将 PRR 介导的 ROS 产生与 MAPK 激活联系起来的途径。