Host Inhibition of a Bacterial Virulence Effector Triggers Immunity to Infection
Host Inhibition of a Bacterial Virulence Effector Triggers Immunity to Infection
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DOI：
10.1126/science.1169430
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发表时间：
2009-05-08
期刊：
影响因子：
56.9
通讯作者：
Rathjen, John P.
中科院分区：
文献类型：
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作者：
Ntoukakis, Vardis;Mucyn, Tatiana S.;Rathjen, John P.
植物病原细菌分泌效应蛋白，攻击寄主信号机制以抑制免疫。效应器可以被宿主识别，从而产生免疫力。一种这样的效应器是丁香假单胞菌的AvrPtoB，它通过E3连接酶结构域降解宿主蛋白激酶，如番茄Fen。与Fen高度相关的PTO激酶结合抗性蛋白PrF识别AvrPtoB。在这里，我们表明PTO对AvrPtoB介导的降解具有抵抗力，因为它使E3连接酶结构域失活。AvrPtoB泛素化催化裂隙内的Fen，导致其分解并丢失相关的PRF蛋白。PTO通过磷酸化和失活AvrPtoB E3结构域来避免这种情况。因此，病原菌毒力分子的失活是植物抗病的一种机制。
Plant pathogenic bacteria secrete effector proteins that attack the host signaling machinery to suppress immunity. Effectors can be recognized by hosts leading to immunity. One such effector is AvrPtoB of Pseudomonas syringae, which degrades host protein kinases, such as tomato Fen, through an E3 ligase domain. Pto kinase, which is highly related to Fen, recognizes AvrPtoB in conjunction with the resistance protein Prf. Here we show that Pto is resistant to AvrPtoB-mediated degradation because it inactivates the E3 ligase domain. AvrPtoB ubiquitinated Fen within the catalytic cleft, leading to its breakdown and loss of the associated Prf protein. Pto avoids this by phosphorylating and inactivating the AvrPtoB E3 domain. Thus, inactivation of a pathogen virulence molecule is one mechanism by which plants resist disease.