Gimenez-Ibanez Selena, Boter Marta, Ortigosa Andrés, García-Casado Gloria, Chini Andrea, Lewsey Mathew G, Ecker Joseph R, Ntoukakis Vardis, Solano Roberto
Plant Molecular Genetics Department, Centro Nacional de Biotecnología-CSIC (CNB-CSIC), Madrid, 28049, Spain.
Centre for AgriBioscience, Department of Animal, Plant and Soil Science, School of Life Science, La Trobe University, Bundoora, Victoria, 3086, Australia.
New Phytol. 2017 Feb;213(3):1378-1392. doi: 10.1111/nph.14354. Epub 2016 Dec 22.
Coronatine (COR) facilitates entry of bacteria into the plant apoplast by stimulating stomata opening. COR-induced signaling events at stomata remain unclear. We found that the COR and jasmonate isoleucine (JA-Ile) co-receptor JAZ2 is constitutively expressed in guard cells and modulates stomatal dynamics during bacterial invasion We analyzed tissue expression patterns of AtJAZ genes and measured stomata opening and pathogen resistance in loss- and gain-of-function mutants. Arabidopsis jaz2 mutants are partially impaired in pathogen-induced stomatal closing and more susceptible to Pseudomonas. Gain-of-function mutations in JAZ2 prevent stomatal reopening by COR and are highly resistant to bacterial penetration. The JAZ2 targets MYC2, MYC3 and MYC4 directly regulate the expression of ANAC19, ANAC55 and ANAC72 to modulate stomata aperture. Due to the antagonistic interactions between the salicylic acid (SA) and JA defense pathways, efforts to increase resistance to biotrophs result in enhanced susceptibility to necrotrophs, and vice versa. Remarkably, dominant jaz2Δjas mutants are resistant to Pseudomonas syringae but retain unaltered resistance against necrotrophs. Our results demonstrate the existence of a COI1-JAZ2-MYC2,3,4-ANAC19,55,72 module responsible for the regulation of stomatal aperture that is hijacked by bacterial COR to promote infection. They also provide novel strategies for crop protection against biotrophs without compromising resistance to necrotrophs.
冠菌素（COR）通过刺激气孔开放促进细菌进入植物质外体。COR在气孔处引发的信号转导事件尚不清楚。我们发现COR与茉莉酸异亮氨酸（JA-Ile）的共同受体JAZ2在保卫细胞中组成性表达，并在细菌入侵期间调节气孔动态。我们分析了拟南芥JAZ基因的组织表达模式，并测量了功能缺失和功能获得突变体中的气孔开放和病原体抗性。拟南芥jaz2突变体在病原体诱导的气孔关闭方面部分受损，并且对丁香假单胞菌更敏感。JAZ2的功能获得性突变阻止COR诱导的气孔重新开放，并且对细菌穿透具有高度抗性。JAZ2靶向MYC2、MYC3和MYC4直接调节ANAC19、ANAC55和ANAC72的表达以调节气孔孔径。由于水杨酸（SA）和JA防御途径之间的拮抗相互作用，增强对活体营养型病原体抗性的努力会导致对坏死营养型病原体的易感性增加，反之亦然。值得注意的是，显性jaz2Δjas突变体对丁香假单胞菌具有抗性，但对坏死营养型病原体的抗性保持不变。我们的结果表明存在一个COI1-JAZ2-MYC2,3,4-ANAC19,55,72模块，负责调节气孔孔径，该模块被细菌COR劫持以促进感染。它们还为作物保护提供了新策略，以抵御活体营养型病原体而不影响对坏死营养型病原体的抗性。
