Zhao Youfu, Thilmony Roger, Bender Carol L, Schaller Andreas, He Sheng Yang, Howe Gregg A
Department of Energy-Plant Research Laboratory, Michigan State University, East Lansing, MI 48824, USA.
Plant J. 2003 Nov;36(4):485-99. doi: 10.1046/j.1365-313x.2003.01895.x.
Pseudomonas syringae pv. tomato strain DC3000 (Pst DC3000) causes bacterial speck disease on tomato. The pathogenicity of Pst DC3000 depends on both the type III secretion system that delivers virulence effector proteins into host cells and the phytotoxin coronatine (COR), which is thought to mimic the action of the plant hormone jasmonic acid (JA). We found that a JA-insensitive mutant (jai1) of tomato was unresponsive to COR and highly resistant to Pst DC3000, whereas host genotypes that are defective in JA biosynthesis were as susceptible to Pst DC3000 as wild-type (WT) plants. Treatment of WT plants with exogenous methyl-JA (MeJA) complemented the virulence defect of a bacterial mutant deficient in COR production, but not a mutant defective in the type III secretion system. Analysis of host gene expression using cDNA microarrays revealed that COR works through Jai1 to induce the massive expression of JA and wound response genes that have been implicated in defense against herbivores. Concomitant with the induction of JA and wound response genes, the type III secretion system and COR repressed the expression of pathogenesis-related (PR) genes in Pst DC3000-infected WT plants. Resistance of jai1 plants to Pst DC3000 was correlated with a high level of PR gene expression and reduced expression of JA/wound response genes. These results indicate that COR promotes bacterial virulence by activating the host's JA signaling pathway, and further suggest that the type III secretion system might also modify host defense by targeting the JA signaling pathway in susceptible tomato plants.
丁香假单胞菌番茄致病变种DC3000（Pst DC3000）可引发番茄细菌性斑点病。Pst DC3000的致病性既取决于将毒力效应蛋白传递至宿主细胞的III型分泌系统，也取决于植物毒素冠菌素（COR），人们认为COR可模拟植物激素茉莉酸（JA）的作用。我们发现，番茄的JA不敏感突变体（jai1）对COR无反应，且对Pst DC3000具有高度抗性，而JA生物合成存在缺陷的宿主基因型对Pst DC3000的易感性与野生型（WT）植株相同。用外源甲基茉莉酸（MeJA）处理WT植株可弥补COR产生缺陷的细菌突变体的毒力缺陷，但不能弥补III型分泌系统缺陷的突变体的毒力缺陷。使用cDNA微阵列分析宿主基因表达发现，COR通过Jai1起作用，诱导大量与防御食草动物有关的JA和伤口反应基因表达。与JA和伤口反应基因的诱导同时发生的是，III型分泌系统和COR抑制了Pst DC3000感染的WT植株中病程相关（PR）基因的表达。jai1植株对Pst DC3000的抗性与高水平的PR基因表达以及JA/伤口反应基因表达降低相关。这些结果表明，COR通过激活宿主的JA信号通路促进细菌毒力，进一步表明III型分泌系统可能也通过靶向易感番茄植株中的JA信号通路来改变宿主防御。
