National Institute of Biological Sciences, Zhongguancun Life Science Park, Beijing, People's Republic of China.
Cell Host Microbe. 2012 Mar 15;11(3):253-63. doi: 10.1016/j.chom.2012.01.015.
Pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) serves as a primary plant defense response against microbial pathogens, with MEKK1, MKK1/MKK2, and MPK4 functioning as a MAP kinase cascade downstream of PAMP receptors. Plant Resistance (R) proteins sense specific pathogen effectors to initiate a second defense mechanism, termed effector-triggered immunity (ETI). In a screen for suppressors of the mkk1 mkk2 autoimmune phenotype, we identify the nucleotide-binding leucine-rich repeat (NB-LRR) protein SUMM2 and find that the MEKK1-MKK1/MKK2-MPK4 cascade negatively regulates SUMM2-mediated immunity. Further, the MEKK1-MKK1/MKK2-MPK4 cascade positively regulates basal defense targeted by the Pseudomonas syringae pathogenic effector HopAI1, which inhibits MPK4 kinase activity. Inactivation of MPK4 by HopAI1 results in activation of SUMM2-mediated defense responses. Our data suggest that SUMM2 is an R protein that becomes active when the MEKK1-MKK1/MKK2-MPK4 cascade is disrupted by pathogens, supporting the hypothesis that R proteins evolved to protect plants when microbial effectors suppress basal resistance.
病原体相关分子模式（PAMP）触发的免疫（PTI）是植物抵抗微生物病原体的主要防御反应，其中 MEKK1、MKK1/MKK2 和 MPK4 作为 PAMP 受体下游的 MAP 激酶级联反应发挥作用。植物抗性（R）蛋白感知特定的病原体效应子，启动第二种防御机制，称为效应子触发的免疫（ETI）。在筛选 mkk1 mkk2 自身免疫表型的抑制剂时，我们鉴定了核苷酸结合富含亮氨酸重复（NB-LRR）蛋白 SUMM2，并发现 MEKK1-MKK1/MKK2-MPK4 级联反应负调控 SUMM2 介导的免疫。此外，MEKK1-MKK1/MKK2-MPK4 级联反应正向调控 Pseudomonas syringae 致病效应因子 HopAI1 靶向的基础防御，HopAI1 抑制 MPK4 激酶活性。HopAI1 通过失活 MPK4 导致 SUMM2 介导的防御反应被激活。我们的数据表明，SUMM2 是一种 R 蛋白，当 MEKK1-MKK1/MKK2-MPK4 级联反应被病原体破坏时，它会变得活跃，这支持了这样一种假设，即 R 蛋白在微生物效应子抑制基础抗性时进化而来，以保护植物。
