A Phytophthora infestans RXLR effector targets plant PP1c isoforms that promote late blight disease.
A Phytophthora infestans RXLR effector targets plant PP1c isoforms that promote late blight disease.
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DOI：
10.1038/ncomms10311
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发表时间：
2016-01-29
影响因子：
16.6
通讯作者：
Birch PRJ
中科院分区：
文献类型：
--
作者：
Boevink PC;Wang X;McLellan H;He Q;Naqvi S;Armstrong MR;Zhang W;Hein I;Gilroy EM;Tian Z;Birch PRJ
植物病原体传递效应子来改变宿主过程。了解效应器如何靶向和操纵宿主蛋白对于了解作物病害至关重要。在这里，我们发现 RXLR 效应子 Pi04314 在植物中的表达通过宿主细胞核中的活性增强致病疫霉在叶子上的定植，并减弱茉莉酸和水杨酸反应基因的诱导。 Pi04314 与三种宿主蛋白磷酸酶 1 催化 (PP1c) 同工型相互作用，导致它们从核仁重新定位到核质。 PP1c-1 的重新定位也会在感染期间发生，并且依赖于效应器中的 R/KVxF 基序。沉默 PP1c 同工型或过度表达磷酸酶死亡的 PP1c-1 突变体可减弱感染，表明宿主 PP1c 活性是疾病所必需的。此外，PP1c-1mut 的表达消除了植物内 Pi04314 表达介导的增强的叶片定植。我们认为 PP1c 同工型是与 Pi04314 形成全酶以促进晚疫病的易感因子。致病疫霉是植物晚疫病的病原体。这里 Boevink 等人。提供证据表明宿主蛋白磷酸酶是致病疫霉效应蛋白的靶标，并且是疾病发展所必需的。
Plant pathogens deliver effectors to alter host processes. Knowledge of how effectors target and manipulate host proteins is critical to understand crop disease. Here, we show that in planta expression of the RXLR effector Pi04314 enhances leaf colonization by Phytophthora infestans via activity in the host nucleus and attenuates induction of jasmonic and salicylic acid-responsive genes. Pi04314 interacts with three host protein phosphatase 1 catalytic (PP1c) isoforms, causing their re-localization from the nucleolus to the nucleoplasm. Re-localization of PP1c-1 also occurs during infection and is dependent on an R/KVxF motif in the effector. Silencing the PP1c isoforms or overexpression of a phosphatase-dead PP1c-1 mutant attenuates infection, demonstrating that host PP1c activity is required for disease. Moreover, expression of PP1c–1mut abolishes enhanced leaf colonization mediated by in planta Pi04314 expression. We argue that PP1c isoforms are susceptibility factors forming holoenzymes with Pi04314 to promote late blight disease. Phytophtora infestans is the causative agent of late blight disease in plants. Here Boevink et al. provide evidence that host protein phosphatases are targeted by a P. infestans effector protein and are required for disease development.