Identification of Pseudomonas syringae type III effectors that can suppress programmed cell death in plants and yeast
Identification of Pseudomonas syringae type III effectors that can suppress programmed cell death in plants and yeast
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DOI：
10.1046/j.1365-313x.2003.01982.x
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发表时间：
2004-02-01
期刊：
影响因子：
7.2
通讯作者：
Alfano, JR
中科院分区：
文献类型：
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作者：
Jamir, Y;Guo, M;Alfano, JR
丁香假单胞菌致病变种番茄DC3000 III型分泌系统（TTSS）是植物上细菌致病性和引发过敏反应（HR）所必需的，过敏反应是发生在抗性植物上的程序性细胞死亡（PCD）。粘粒pHIR11使得非病原体能够引起依赖于TTSS和效应子HopPsyA的HR。我们使用pHIR11来确定效应子HopPtoE、无毒AvrPphE（Pto）、AvrPpiB1（Pto）、AvrPtoB和HopPtoF可以抑制烟草和拟南芥上的HopPsyA依赖性HR。混合接种物和农杆菌介导的瞬时表达实验证实，抑制作用发生在植物细胞内。除AvrPpiB1（Pto）外，这些抑制子抑制烟草病程相关（PR）基因PR1a的表达。DC3000抑制突变体引起了增强的HR与这些突变体缺乏HR抑制一致。此外，HopPtoG被确定为一个抑制剂的基础上，由hopPtoG突变体产生的增强的HR。值得注意的是，这些蛋白质的功能是抑制促凋亡蛋白Bax诱导植物和酵母中PCD的能力，表明这些效应物以跨界方式作为抗PCD蛋白质发挥作用。抑制PCD的效应子的高比例表明，抑制植物免疫是DC3000效应子的主要作用之一，也是烟草赤星病菌发病机制的核心要求。
The Pseudomonas syringae pv. tomato DC3000 type III secretion system (TTSS) is required for bacterial pathogenicity on plants and elicitation of the hypersensitive response (HR), a programmed cell death (PCD) that occurs on resistant plants. Cosmid pHIR11 enables non-pathogens to elicit an HR dependent upon the TTSS and the effector HopPsyA. We used pHIR11 to determine that effectors HopPtoE, avirulence AvrPphE(Pto), AvrPpiB1(Pto), AvrPtoB, and HopPtoF could suppress a HopPsyA-dependent HR on tobacco and Arabidopsis. Mixed inoculum and Agrobacterium-mediated transient expression experiments confirmed that suppressor action occurred within plant cells. These suppressors, with the exception of AvrPpiB1(Pto), inhibited the expression of the tobacco pathogenesis-related (PR) gene PR1a. DC3000 suppressor mutants elicited an enhanced HR consistent with these mutants lacking an HR suppressor. Additionally, HopPtoG was identified as a suppressor on the basis of an enhanced HR produced by a hopPtoG mutant. Remarkably, these proteins functioned to inhibit the ability of the pro-apoptotic protein, Bax to induce PCD in plants and yeast, indicating that these effectors function as anti-PCD proteins in a trans-kingdom manner. The high proportion of effectors that suppress PCD suggests that suppressing plant immunity is one of the primary roles for DC3000 effectors and a central requirement for P. syringae pathogenesis.