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破坏 MAMP 诱导的 MEKK1-MKK1/MKK2-MPK4 途径激活 TNL 免疫受体 SMN1/RPS6。

Disruption of the MAMP-Induced MEKK1-MKK1/MKK2-MPK4 Pathway Activates the TNL Immune Receptor SMN1/RPS6.

机构信息

Faculty and Graduate School of Agriculture, Kagawa University, 2393 Ikenobe, Miki-cho, Kita-gun, Kagawa, Japan.

United Graduate School of Agriculture, Ehime University, 3-5-7 Tarumi, Matsuyama, Ehime, Japan.

出版信息

Plant Cell Physiol. 2019 Apr 1;60(4):778-787. doi: 10.1093/pcp/pcy243.

DOI:10.1093/pcp/pcy243
PMID:30590768
Abstract

Mitogen-activated protein kinase (MAPK) pathways have a pivotal role in innate immunity signaling in plants. In Arabidopsis, the MAPK pathway that consists of MEKK1, MKK1/MKK2 and MPK4 is involved in pattern-triggered immunity signaling upstream of defense gene expression. This pathway is partly guarded by SUMM2, a nucleotide-binding domain leucine-rich repeat (NLR) protein, which is activated by disruption of the MAPK pathway. To identify other components required for the guard mechanism, here we developed a new mutant screening system utilizing a dwarf autoimmune line that overexpressed the N-terminal regulatory domain of MEKK1. Mutants with suppression of the dwarf, autoimmune phenotypes were identified, and one locus responsible for the phenotype was designated as suppressor of MEKK1N overexpression-induced dwarf 1 (SMN1). MutMap analysis revealed that SMN1 encodes the Toll/Interleukin-1 receptor (TIR)-class NLR protein RPS6, a previously identified resistant protein against bacterial pathogen Pseudomonas syringae pv. tomato expressing the HopA1 effector. Importantly, mutations in SMN1/RPS6 also partially suppressed the dwarf, autoimmune phenotypes of mekk1 and mpk4 plants. Our results suggest that the two structurally distinct NLR proteins, SMN1/RPS6 and SUMM2, monitor integrity of the MEKK1-MKK1/MKK2-MPK4 pathway.

摘要

丝裂原活化蛋白激酶(MAPK)途径在植物先天免疫信号转导中起着关键作用。在拟南芥中,由 MEKK1、MKK1/MKK2 和 MPK4 组成的 MAPK 途径参与防御基因表达上游的模式触发免疫信号转导。该途径部分受到 SUMM2 的保护,SUMM2 是一种核苷酸结合域富含亮氨酸重复(NLR)蛋白,它通过破坏 MAPK 途径而被激活。为了鉴定守卫机制所需的其他成分,我们在这里开发了一种新的突变筛选系统,该系统利用矮化自身免疫系来过度表达 MEKK1 的 N 端调节域。鉴定出抑制矮化、自身免疫表型的突变体,将一个负责表型的基因座命名为 MEKK1N 过表达诱导矮化 1(SMN1)的抑制子。MutMap 分析表明,SMN1 编码 Toll/白细胞介素-1 受体(TIR)类 NLR 蛋白 RPS6,这是一种先前鉴定的对表达 HopA1 效应物的细菌病原体丁香假单胞菌 pv。番茄的抗性蛋白。重要的是,SMN1/RPS6 中的突变也部分抑制了 mekk1 和 mpk4 植物的矮化、自身免疫表型。我们的结果表明,两种结构不同的 NLR 蛋白,SMN1/RPS6 和 SUMM2,监测 MEKK1-MKK1/MKK2-MPK4 途径的完整性。

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