The Arabidopsis ZED1 pseudokinase is required for ZAR1-mediated immunity induced by the Pseudomonas syringae type III effector HopZ1a
The Arabidopsis ZED1 pseudokinase is required for ZAR1-mediated immunity induced by the Pseudomonas syringae type III effector HopZ1a
复制标题
DOI：
10.1073/pnas.1315520110
复制
发表时间：
2013-11-12
影响因子：
11.1
通讯作者：
Desveaux, Darrell
中科院分区：
文献类型：
--
作者：
Lewis, Jennifer D.;Lee, Amy Huei-Yi;Desveaux, Darrell
植物和动物病原菌可以通过将III型分泌效应蛋白（T3 SE）注射到宿主细胞中来抑制宿主免疫。然而，如果宿主已经进化出识别特定T3 SE的存在或活性的手段，则T3 SE也可以引发宿主免疫。在动物和植物病原体中发现的多样化的YopJ/HopZ/AvrRxv T3 SE超家族提供了T3 SE发挥这种双重作用的例子。T3 SE HopZ 1a是由植物病原体假单胞菌携带的乙酰转移酶，当在拟南芥中被核苷酸结合富含亮氨酸重复序列（NB-LRR）蛋白ZAR 1识别时，其增强效应子触发的免疫（ETI）。然而，识别HopZ 1a并不需要任何已知的ETI相关基因。使用正向遗传学方法，我们确定了一个独特的ETI相关基因，这是必不可少的ZAR 1介导的免疫。hopZ-ETI缺陷1（zed 1）突变体在识别HopZ 1a时特异性受损，但不识别其他不相关的T3 SE或模式识别受体（PRR）触发的免疫。ZED 1直接与HopZ 1a和ZAR 1相互作用，并通过HopZ 1a在苏氨酸125和177上乙酰化。ZED 1是一种非功能性激酶，形成拟南芥中小基因组激酶簇的一部分。我们假设ZED 1作为诱饵将HopZ 1a引诱到ZAR 1抗性复合物，导致ETI激活。
Plant and animal pathogenic bacteria can suppress host immunity by injecting type III secreted effector (T3SE) proteins into host cells. However, T3SEs can also elicit host immunity if the host has evolved a means to recognize the presence or activity of specific T3SEs. The diverse YopJ/HopZ/AvrRxv T3SE superfamily, which is found in both animal and plant pathogens, provides examples of T3SEs playing this dual role. The T3SE HopZ1a is an acetyltransferase carried by the phytopathogen Pseudomonas syringae that elicits effector-triggered immunity (ETI) when recognized in Arabidopsis thaliana by the nucleotide-binding leucine-rich repeat (NB-LRR) protein ZAR1. However, recognition of HopZ1a does not require any known ETI-related genes. Using a forward genetics approach, we identify a unique ETI-associated gene that is essential for ZAR1-mediated immunity. The hopZ-ETI-deficient1 (zed1) mutant is specifically impaired in the recognition of HopZ1a, but not the recognition of other unrelated T3SEs or in pattern recognition receptor (PRR)-triggered immunity. ZED1 directly interacts with both HopZ1a and ZAR1 and is acetylated on threonines 125 and 177 by HopZ1a. ZED1 is a nonfunctional kinase that forms part of small genomic cluster of kinases in Arabidopsis. We hypothesize that ZED1 acts as a decoy to lure HopZ1a to the ZAR1-resistance complex, resulting in ETI activation.