The Pseudomonas syringae type III effector tyrosine phosphatase HopAO1 suppresses innate immunity in Arabidopsis thaliana.
The Pseudomonas syringae type III effector tyrosine phosphatase HopAO1 suppresses innate immunity in Arabidopsis thaliana.
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DOI：
10.1111/j.1365-313x.2007.03262.x
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发表时间：
2007-09
期刊：
影响因子：
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通讯作者：
William Underwood;Shuqun Zhang;S. He
中科院分区：
文献类型：
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作者：
William Underwood;Shuqun Zhang;S. He
细菌性病原菌丁香假单胞菌致病变种（Pseudomonas syringae pv.番茄（Pst）菌株DC 3000感染番茄和拟南芥属植物，并且是用于研究细菌疾病的分子基础的模型。Pst DC3000通过III型分泌系统（TTSS）分泌一系列基本上未表征的效应蛋白进入宿主细胞。目前对个体TTSS效应物促进毒力的分子机制知之甚少。HopAO1与蛋白酪氨酸磷酸酶具有相似性，包括一个保守的催化位点，并抑制一些非宿主植物的过敏反应（HR）。HopAO1是否在宿主拟南芥中具有类似的作用尚不清楚。在这里，我们表明，HopAO1在拟南芥中的转基因表达抑制胼胝质沉积引起的Pst DC3000 hrpA突变体，并允许正常的非致病性hrpA突变体在叶组织内繁殖。HopAO1还抑制由flg22（病原体相关分子模式（PAMP））诱导的对Pst DC3000的抗性。然而，HopAO1不抑制由几个经典无毒基因触发的HR。这些结果表明HopAO1主要靶向PAMP诱导的拟南芥先天免疫。HopAO1的毒力功能依赖于完整的磷酸酶催化位点，因为表达催化失活衍生物的转基因植物不显示这些作用。有趣的是，无催化活性的HopAO1的表达对野生型HopAO1的功能具有显性负效应。丝裂原活化蛋白激酶（MAPK）活性的分析表明，HopAO1的目标下游或独立的MAPK激活的步骤。全基因组表达分析表明，几个众所周知的防御基因的表达被抑制在hrpA突变体感染的HopAO1转基因植物。
The bacterial pathogen Pseudomonas syringae pv. tomato (Pst) strain DC3000 infects tomato and Arabidopsis plants, and is a model for studying the molecular basis of bacterial disease. Pst DC3000 secretes a battery of largely uncharacterized effector proteins into host cells via a type-III secretion system (TTSS). Little is currently known about the molecular mechanisms by which individual TTSS effectors promote virulence. The effector HopAO1 has similarity to protein tyrosine phosphatases, including a conserved catalytic site, and suppresses the hypersensitive response (HR) in some non-host plants. Whether HopAO1 has a similar effect in the host Arabidopsis is not clear. Here, we show that transgenic expression of HopAO1 in Arabidopsis suppresses callose deposition elicited by the Pst DC3000 hrpA mutant, and allows the normally non-pathogenic hrpA mutant to multiply within the leaf tissue. HopAO1 also suppresses resistance to Pst DC3000 induced by flg22, a pathogen-associated molecular pattern (PAMP). However, HopAO1 does not suppress the HR triggered by several classical avirulence genes. These results suggest that HopAO1 targets primarily PAMP-induced innate immunity in Arabidopsis. The virulence function of HopAO1 is dependent on an intact phosphatase catalytic site, as transgenic plants expressing a catalytically inactive derivative do not show these effects. Intriguingly, expression of the catalytically inactive HopAO1 has a dominant-negative effect on the function of the wild-type HopAO1. Analysis of mitogen-activated protein kinase (MAPK) activity suggests that HopAO1 targets a step downstream or independent of MAPK activation. Genome-wide expression analysis revealed that expression of several well-known defense genes was suppressed in hrpA mutant-infected HopAO1 transgenic plants.