Underwood William, Zhang Shuqun, He Sheng Y
Department of Energy-Plant Research Laboratory, Michigan State University, East Lansing, MI 48824, USA.
Plant J. 2007 Nov;52(4):658-72. doi: 10.1111/j.1365-313X.2007.03262.x. Epub 2007 Sep 18.
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.
细菌性病原菌丁香假单胞菌番茄致病变种（Pst）DC3000菌株可感染番茄和拟南芥植株，是研究细菌性病害分子基础的一个模型。Pst DC3000通过III型分泌系统（TTSS）向宿主细胞分泌一系列大多未被鉴定的效应蛋白。目前对于单个TTSS效应蛋白促进毒力的分子机制知之甚少。效应蛋白HopAO1与蛋白酪氨酸磷酸酶相似，包括一个保守的催化位点，并且在一些非宿主植物中可抑制过敏反应（HR）。尚不清楚HopAO1在宿主拟南芥中是否具有类似作用。在此，我们表明HopAO1在拟南芥中的转基因表达可抑制由Pst DC3000 hrpA突变体引发的胼胝质沉积，并使通常无致病性的hrpA突变体在叶片组织内繁殖。HopAO1还可抑制由病原体相关分子模式（PAMP）flg22诱导的对Pst DC3000的抗性。然而，HopAO1并不抑制由几个经典无毒基因触发的HR。这些结果表明，HopAO1主要靶向拟南芥中PAMP诱导的固有免疫。HopAO1的毒力功能依赖于完整的磷酸酶催化位点，因为表达催化无活性衍生物的转基因植物未表现出这些效应。有趣的是，催化无活性的HopAO1的表达对野生型HopAO1的功能具有显性负效应。对丝裂原活化蛋白激酶（MAPK）活性的分析表明，HopAO1靶向MAPK激活下游或与之无关的一个步骤。全基因组表达分析显示，在hrpA突变体感染的HopAO1转基因植物中，几个著名防御基因的表达受到抑制。
