Hamdoun Safae, Liu Zhe, Gill Manroop, Yao Nan, Lu Hua
Department of Biological Sciences, University of Maryland Baltimore County, Baltimore, Maryland, United States of America.
State Key Laboratory of Biocontrol, Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou, P.R. China.
PLoS One. 2013 Dec 11;8(12):e83219. doi: 10.1371/journal.pone.0083219. eCollection 2013.
Plant-pathogen interactions involve sophisticated action and counteraction strategies from both parties. Plants can recognize pathogen derived molecules, such as conserved pathogen associated molecular patterns (PAMPs) and effector proteins, and subsequently activate PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI), respectively. However, pathogens can evade such recognitions and suppress host immunity with effectors, causing effector-triggered susceptibility (ETS). The differences among PTI, ETS, and ETI have not been completely understood. Toward a better understanding of PTI, ETS, and ETI, we systematically examined various defense-related phenotypes of Arabidopsis infected with different Pseudomonas syringae pv. maculicola ES4326 strains, using the virulence strain DG3 to induce ETS, the avirulence strain DG34 that expresses avrRpm1 (recognized by the resistance protein RPM1) to induce ETI, and HrcC(-) that lacks the type three secretion system to activate PTI. We found that plants infected with different strains displayed dynamic differences in the accumulation of the defense signaling molecule salicylic acid, expression of the defense marker gene PR1, cell death formation, and accumulation/localization of the reactive oxygen species, H2O2. The differences between PTI, ETS, and ETI are dependent on the doses of the strains used. These data support the quantitative nature of PTI, ETS, and ETI and they also reveal qualitative differences between PTI, ETS, and ETI. Interestingly, we observed the induction of large cells in the infected leaves, most obviously with HrcC(-) at later infection stages. The enlarged cells have increased DNA content, suggesting a possible activation of endoreplication. Consistent with strong induction of abnormal cell growth by HrcC(-), we found that the PTI elicitor flg22 also activates abnormal cell growth, depending on a functional flg22-receptor FLS2. Thus, our study has revealed a comprehensive picture of dynamic changes of defense phenotypes and cell fate determination during Arabidopsis-P. syringae interactions, contributing to a better understanding of plant defense mechanisms.
植物与病原体的相互作用涉及双方复杂的作用和反作用策略。植物能够识别病原体衍生的分子,如保守的病原体相关分子模式(PAMPs)和效应蛋白,随后分别激活PAMP触发的免疫(PTI)和效应蛋白触发的免疫(ETI)。然而,病原体能够逃避这种识别并用效应蛋白抑制宿主免疫,导致效应蛋白触发的感病性(ETS)。PTI、ETS和ETI之间的差异尚未完全明确。为了更好地理解PTI、ETS和ETI,我们系统地检测了用不同丁香假单胞菌番茄致病变种ES4326菌株感染的拟南芥的各种防御相关表型,使用致病菌株DG3诱导ETS,表达无毒基因avrRpm1(被抗性蛋白RPM1识别)的无毒菌株DG34诱导ETI,以及缺乏三型分泌系统的HrcC(-)激活PTI。我们发现,用不同菌株感染的植物在防御信号分子水杨酸的积累、防御标记基因PR1的表达、细胞死亡形成以及活性氧H2O2的积累/定位方面表现出动态差异。PTI、ETS和ETI之间的差异取决于所用菌株的剂量。这些数据支持了PTI、ETS和ETI的定量性质,同时也揭示了PTI、ETS和ETI之间的定性差异。有趣的是,我们观察到感染叶片中出现大细胞,在感染后期最明显的是HrcC(-)感染的情况。这些增大的细胞DNA含量增加,表明可能激活了核内复制。与HrcC(-)强烈诱导异常细胞生长一致,我们发现PTI激发子flg22也激活异常细胞生长,这依赖于功能性的flg22受体FLS2。因此,我们的研究揭示了拟南芥与丁香假单胞菌相互作用期间防御表型和细胞命运决定的动态变化的全貌,有助于更好地理解植物防御机制。