Genot Baptiste, Lang Julien, Berriri Souha, Garmier Marie, Gilard Françoise, Pateyron Stéphanie, Haustraete Katrien, Van Der Straeten Dominique, Hirt Heribert, Colcombet Jean
Institute of Plant Sciences Paris Saclay, Centre National de la Recherche Scientifique, Institut National de Recherche Agronomique, Université Paris-Sud, Université Evry, Université Paris-Saclay, Paris Diderot, Sorbonne Paris-Cité, 91405 Orsay, France (B.G., J.L., S.B., M.G., F.G., S.P., H.H., J.C.).
Laboratory of Functional Plant Biology, Ghent University, B-9000 Ghent, Belgium (K.H., D.V.D.S.); and.
Plant Physiol. 2017 Jun;174(2):1238-1249. doi: 10.1104/pp.17.00378. Epub 2017 Apr 11.
Mitogen-activated protein kinases (MAPKs) are important regulators of plant immunity. Most of the knowledge about the function of these pathways is derived from loss-of-function approaches. Using a gain-of-function approach, we investigated the responses controlled by a constitutively active (CA) MPK3 in plants are dwarfed and display a massive derepression of defense genes associated with spontaneous cell death as well as the accumulation of reactive oxygen species, phytoalexins, and the stress-related hormones ethylene and salicylic acid (SA). Remarkably / and / lines, which are impaired in SA synthesis and ethylene signaling, respectively, retain most of the -associated phenotypes, indicating that the constitutive activity of MPK3 can bypass SA and ethylene signaling to activate defense responses. A comparative analysis of the molecular phenotypes of and autoimmunity suggested convergence between the MPK3- and MPK4-guarding modules. In support of this model, crosses with and , two known suppressors of , resulted in a partial reversion of the phenotypes. Overall, our data unravel a novel mechanism by which the MAPK signaling network contributes to a robust defense-response system.
丝裂原活化蛋白激酶（MAPKs）是植物免疫的重要调节因子。关于这些信号通路功能的大部分知识都来自功能缺失研究方法。我们采用功能获得研究方法，研究了组成型激活（CA）的MPK3所调控的反应。在植物中，CA-MPK3会导致植株矮小，并表现出与自发细胞死亡相关的防御基因大量去抑制，以及活性氧、植保素和应激相关激素乙烯和水杨酸（SA）的积累。值得注意的是，分别在SA合成和乙烯信号传导方面存在缺陷的突变体株系仍保留了大部分与CA-MPK3相关的表型，这表明MPK3的组成型活性可以绕过SA和乙烯信号传导来激活防御反应。对CA-MPK3和MPK4自身免疫分子表型的比较分析表明，MPK3和MPK4的保卫模块之间存在趋同现象。支持这一模型的是，CA-MPK3与两个已知的MPK4抑制子突变体杂交，导致CA-MPK3表型部分恢复。总体而言，我们的数据揭示了一种新机制，通过该机制，MAPK信号网络有助于构建一个强大的防御反应系统。
