Phosphorylation-Mediated Inactivation of C3H14 by MPK4 Enhances Bacterial-Triggered Immunity in Arabidopsis
Phosphorylation-Mediated Inactivation of C3H14 by MPK4 Enhances Bacterial-Triggered Immunity in Arabidopsis
复制标题
MPK4 磷酸化介导的 C3H14 失活增强拟南芥细菌引发的免疫
DOI：
10.1093/plphys/kiac300
复制
发表时间：
2022
期刊：
影响因子：
7.4
通讯作者：
Gongke Zhou
中科院分区：
文献类型：
--
作者：
Dian Wang;Guohua Chai;Li Xu;Kangkang Yang;Yamei Zhuang;Aiguo Yang;Shengyi Liu;Yingzhen Kong;Gongke Zhou
摘要：对病原体相关分子模式 (PAMP) 的感知会触发丝裂原激活蛋白 (MAP) 激酶 4 (MPK4) 介导的磷酸化并诱导下游转录重编程，但人们对 MPK4 防御途径的机制知之甚少。在这里，我们发现 MPK4 磷酸化介导的 CCCH 蛋白 C3H14 失活可以正向调节拟南芥 (Arabidopsis thaliana) 的免疫反应。与野生型植物相比，C3H14 及其旁系同源物 C3H15 的功能丧失突变导致受感染叶片对 Pst DC3000 的防御增强，并产生系统获得性抗性 (SAR)，而 C3H14 或 C3H15 过度表达增强了对该病原体的易感性，但无法诱导 SAR。 C3H14 在 PAMP 触发的免疫 (PTI) 和 SAR 中的功能依赖于 MPK4 介导的磷酸化。用 Pst DC3000 或鞭毛蛋白肽 flg22 进行攻击可增强细胞质中 MPK4 对 C3H14 的磷酸化，从而缓解 C3H14 抑制的 PTI 相关基因的表达，并减弱 C3H14 激活的其靶标 NIM1-INTERACTING1 (NIMIN1) 和 NIMIN2（SAR 的两个负调节因子）的表达。水杨酸 (SA) 影响免疫中的 MPK4-C3H14-NIMIN1/2 级联，但 C3H14-NIMIN1/2 级联介导的 SA 信号传导独立于 MPK4 磷酸化。我们的研究表明 C3H14 可能是 MPK4 防御信号通路的负向成分。
Abstract Perception of pathogen-associated molecular patterns (PAMPs) triggers mitogen-activated protein (MAP) kinase 4 (MPK4)-mediated phosphorylation and induces downstream transcriptional reprogramming, but the mechanisms of the MPK4 defense pathway are poorly understood. Here, we showed that phosphorylation-mediated inactivation of the CCCH protein C3H14 by MPK4 positively regulates the immune response in Arabidopsis (Arabidopsis thaliana). Compared with wild-type plants, loss-of-function mutations in C3H14 and its paralog C3H15 resulted in enhanced defense against Pst DC3000 in infected leaves and the development of systemic acquired resistance (SAR), whereas C3H14 or C3H15 overexpression enhanced susceptibility to this pathogen and failed to induce SAR. The functions of C3H14 in PAMP-triggered immunity (PTI) and SAR were dependent on MPK4-mediated phosphorylation. Challenge with Pst DC3000 or the flagellin peptide flg22 enhanced the phosphorylation of C3H14 by MPK4 in the cytoplasm, relieving C3H14-inhibited expression of PTI-related genes and attenuating C3H14-activated expression of its targets NIM1-INTERACTING1 (NIMIN1) and NIMIN2, two negative regulators of SAR. Salicylic acid (SA) affected the MPK4–C3H14–NIMIN1/2 cascades in immunity, but SA signaling mediated by the C3H14-NIMIN1/2 cascades was independent of MPK4 phosphorylation. Our study suggests that C3H14 might be a negative component of the MPK4 defense signaling pathway.