Arabidopsis LONG-CHAIN BASE KINASE 1 (LCBK1) interacts with MEDEA, a component of PCR2 complex that negatively regulates immunity. LCBK1 phosphorylates phytosphingosine and thereby promotes stomatal immunity against bacterial pathogens. Arabidopsis polycomb-group repressor complex2 (PRC2) protein MEDEA (MEA) suppresses both pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). MEA represses the expression of RPS2 and thereby attenuates AvrRpt2 effector-mediated ETI. However, the mechanism of MEA-mediated PTI diminution was not known. By screening the Arabidopsis cDNA library using yeast-2-hybrid interaction, we identified LONG-CHAIN BASE KINASE1 (LCBK1) as an MEA-interacting protein. We found that lcbk1 mutants are susceptible to virulent bacterial pathogens, such as Pseudomonas syringae pv maculicola (Psm) and P. syringae pv tomato (Pst) but not the avirulent strain of Pst that carries AvrRpt2 effector. Pathogen inoculation induces LCBK1 expression, especially in guard cells. We found that LCBK1 has a positive regulatory role in stomatal closure after pathogen inoculation. WT plants close stomata within an hour of Pst inoculation or flg22 (a 22 amino acid peptide from bacterial flagellin protein that activates PTI) treatment, but not lcbk1 mutants. LCBK1 phosphorylates phytosphingosine (PHS). Exogenous application of phosphorylated PHS (PHS-P) induces stomatal closure and rescues loss-of-PTI phenotype of lcbk1 mutant plants. MEA overexpressing (MEA-Oex) plants are defective, whereas loss-of-function mea-6 mutants are hyperactive in PTI-induced stomatal closure. Exogenous application of PHS-P rescues loss-of-PTI in MEA-Oex plants. Results altogether demonstrate that LCBK1 is an interactor of MEA that positively regulates PTI-induced stomatal closure in Arabidopsis.

中文翻译：

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MEDEA 相互作用蛋白 LONG-CHAIN BASE KINASE 1 促进拟南芥的模式触发免疫。

拟南芥长链碱基激酶 1 (LCBK1) 与 MEDEA 相互作用，MEDEA 是负调控免疫的 PCR2 复合物的一个组成部分。LCBK1 磷酸化植物鞘氨醇，从而促进对细菌病原体的气孔免疫。拟南芥 polycomb-group 阻遏复合物 2 (PRC2) 蛋白 MEDEA (MEA) 抑制模式触发免疫 (PTI) 和效应触发免疫 (ETI)。MEA 抑制 RPS2 的表达，从而减弱 AvrRpt2 效应子介导的 ETI。然而，MEA 介导的 PTI 减少的机制尚不清楚。通过使用酵母-2-杂交相互作用筛选拟南芥 cDNA 文库，我们将长链碱基激酶 1 (LCBK1) 鉴定为 MEA 相互作用蛋白。我们发现 lcbk1 突变体对毒性细菌病原体敏感，例如 Pseudomonas syringae pv maculicola (Psm) 和 P. syringae pv 番茄 (Pst) 但不是携带 AvrRpt2 效应子的无毒 Pst 菌株。病原体接种诱导 LCBK1 表达，尤其是在保卫细胞中。我们发现LCB​​K1在病原体接种后对气孔关闭具有正向调节作用。WT 植物在接种 Pst 或 flg22（来自细菌鞭毛蛋白的 22 个氨基酸肽，可激活 PTI）处理后一小时内关闭气孔，但 lcbk1 突变体不关闭。LCBK1 磷酸化植物鞘氨醇 (PHS)。磷酸化 PHS (PHS-P) 的外源应用诱导气孔关闭并挽救 lcbk1 突变植物的 PTI 表型缺失。MEA 过表达 (MEA-Oex) 植物有缺陷，而功能丧失的 mea-6 突变体在 PTI 诱导的气孔关闭中过度活跃。PHS-P 的外源应用挽救了 MEA-Oex 工厂中 PTI 的损失。