Cross-Microbial Protection via Priming a Conserved Immune Co-Receptor through Juxtamembrane Phosphorylation in Plants
Cross-Microbial Protection via Priming a Conserved Immune Co-Receptor through Juxtamembrane Phosphorylation in Plants
复制标题
通过植物近膜磷酸化启动保守的免疫共受体进行跨微生物保护
DOI：
10.1016/j.chom.2019.10.010
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发表时间：
2019-12-11
影响因子：
30.3
通讯作者：
Li, Jian-Feng
中科院分区：
文献类型：
--
作者：
Gong, Ben-Qiang;Guo, Jianhang;Li, Jian-Feng
生物体可以根据先前的经验对反复出现的压力做出强化反应。然而，在缺乏适应性免疫的植物中，免疫启动的分子基础仍然难以捉摸。在这里，我们报告说，细菌的挑战，可以准备植物真菌的攻击，诱导certainamembrane磷酸化的CERK1，在响应真菌激发子几丁质的信号传导不可或缺的辅助受体。这种磷酸化是由BAK1介导的，BAK1是一种响应多种激发子的信号传导共受体。BAK1与CERK1相互作用，BAK1的缺失降低了CERK1的启动磷酸化。CERK1的邻膜磷酸模拟突变赋予加速的几丁质反应和强化的真菌抗性而不触发组成性免疫，而邻膜磷酸缺陷突变减少细菌诱导的对真菌感染的保护。这些发现揭示了细胞表面免疫共受体之间的串扰可以引发防御，并证明植物受体样激酶的质膜磷酸化可以独立于激酶活化而发生，以将蛋白质置于引发状态。
Living organisms can be primed for potentiated responses to recurring stresses based on prior experience. However, the molecular basis of immune priming remains elusive in plants that lack adaptive immunity. Here, we report that bacterial challenges can prepare plants for fungal attacks by inducing juxtamembrane phosphorylation of CERK1, the coreceptor indispensable for signaling in response to the fungal elicitor chitin. This phosphorylation is mediated by BAK1, a co-receptor for signaling in response to multiple elicitors. BAK1 interacts with CERK1, and loss of BAK1 reduces priming phosphorylation of CERK1. Juxtamembrane phosphomimetic mutations of CERK1 confer accelerated chitin responses and fortified fungal resistance without triggering constitutive immunity, whereas juxtamembrane phosphodeficient mutations diminish bacteria-induced protection against fungal infection. These findings reveal that crosstalk between cell-surface immune co-receptors can prime defense and demonstrate that juxtamembrane phosphorylation of plant receptor-like kinases can occur independent of kinase activation to place the protein into a prime state.