Investigation of Intercellular Salicylic Acid Accumulation during Compatible and Incompatible Arabidopsis-Pseudomonas syringae Interactions Using a Fast Neutron-Generated Mutant Allele of EDS5 Identified by Genetic Mapping and Whole-Genome Sequencing
Investigation of Intercellular Salicylic Acid Accumulation during Compatible and Incompatible Arabidopsis-Pseudomonas syringae Interactions Using a Fast Neutron-Generated Mutant Allele of EDS5 Identified by Genetic Mapping and Whole-Genome Sequencing
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DOI：
10.1371/journal.pone.0088608
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发表时间：
2014-03-04
期刊：
影响因子：
3.7
通讯作者：
Cameron, Robin K.
中科院分区：
文献类型：
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作者：
Carviel, Jessie L.;Wilson, Daniel C.;Cameron, Robin K.
一种用于鉴定快中子诱导的缺失突变的全基因组测序技术显示，iap 1 -1是EDS 5（eds 5 -5）的一个新等位基因。RPS 2-AvrRpt 2启动的效应触发免疫（ETI）在iap 1 -1/eds 5 -5中相对于植物内细菌水平和过敏反应受到损害，而细胞内和细胞间游离水杨酸（SA）的积累大大减少，表明SA在ETI期间作为细胞内信号分子和细胞间隙中的抗菌剂发挥作用。在野生型Col-0和强毒假单胞菌pv.番茄（Pst）细胞间游离SA积累较少，因此推测Pst抑制细胞间SA积累。当Col-0接种Pst的冠菌素缺陷菌株时，观察到细胞间SA的高水平积累，这表明Pst利用其植物毒素冠菌素抑制细胞间SA的积累。这项工作表明，SA在细胞间隙中的积累是基础/PAMP触发的免疫以及ETI的重要组成部分，病原体定植在细胞间隙。
A whole-genome sequencing technique developed to identify fast neutron-induced deletion mutations revealed that iap1-1 is a new allele of EDS5 (eds5-5). RPS2-AvrRpt2-initiated effector-triggered immunity (ETI) was compromised in iap1-1/eds5-5 with respect to in planta bacterial levels and the hypersensitive response, while intra-and intercellular free salicylic acid (SA) accumulation was greatly reduced, suggesting that SA contributes as both an intracellular signaling molecule and an antimicrobial agent in the intercellular space during ETI. During the compatible interaction between wild-type Col-0 and virulent Pseudomonas syringae pv. tomato (Pst), little intercellular free SA accumulated, which led to the hypothesis that Pst suppresses intercellular SA accumulation. When Col-0 was inoculated with a coronatine-deficient strain of Pst, high levels of intercellular SA accumulation were observed, suggesting that Pst suppresses intercellular SA accumulation using its phytotoxin coronatine. This work suggests that accumulation of SA in the intercellular space is an important component of basal/PAMP-triggered immunity as well as ETI to pathogens that colonize the intercellular space.