Rosebrock Tracy R, Zeng Lirong, Brady Jennifer J, Abramovitch Robert B, Xiao Fangming, Martin Gregory B
Boyce Thompson Institute for Plant Research, Tower Road, Ithaca, New York 14853, USA.
Nature. 2007 Jul 19;448(7151):370-4. doi: 10.1038/nature05966.
Many bacterial pathogens of plants and animals use a type III secretion system to deliver diverse virulence-associated 'effector' proteins into the host cell. The mechanisms by which these effectors act are mostly unknown; however, they often promote disease by suppressing host immunity. One type III effector, AvrPtoB, expressed by the plant pathogen Pseudomonas syringae pv. tomato, has a carboxy-terminal domain that is an E3 ubiquitin ligase. Deletion of this domain allows an amino-terminal region of AvrPtoB (AvrPtoB(1-387)) to be detected by certain tomato varieties leading to immunity-associated programmed cell death. Here we show that a host kinase, Fen, physically interacts with AvrPtoB(1-387 )and is responsible for activating the plant immune response. The AvrPtoB E3 ligase specifically ubiquitinates Fen and promotes its degradation in a proteasome-dependent manner. This degradation leads to disease susceptibility in Fen-expressing tomato lines. Various wild species of tomato were found to exhibit immunity in response to AvrPtoB(1-387 )and not to full-length AvrPtoB. Thus, by acquiring an E3 ligase domain, AvrPtoB has thwarted a highly conserved host resistance mechanism.
许多动植物的细菌病原体利用III型分泌系统将多种与毒力相关的“效应子”蛋白输送到宿主细胞中。这些效应子发挥作用的机制大多未知;然而,它们通常通过抑制宿主免疫来促进疾病发生。一种由植物病原体丁香假单胞菌番茄致病变种表达的III型效应子AvrPtoB,具有一个作为E3泛素连接酶的羧基末端结构域。缺失该结构域会使某些番茄品种检测到AvrPtoB的氨基末端区域(AvrPtoB(1-387)),从而导致与免疫相关的程序性细胞死亡。在此我们表明,一种宿主激酶Fen与AvrPtoB(1-387)发生物理相互作用,并负责激活植物免疫反应。AvrPtoB E3连接酶特异性地将Fen泛素化,并以蛋白酶体依赖的方式促进其降解。这种降解导致表达Fen的番茄品系易患疾病。发现各种野生番茄品种对AvrPtoB(1-387)有免疫反应,而对全长AvrPtoB没有免疫反应。因此,通过获得一个E3连接酶结构域,AvrPtoB挫败了一种高度保守的宿主抗性机制。