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The WY Domain of an RxLr Effector Drives Interactions with a Host Target Phosphatase to Mimic Host Regulatory Proteins and Promote Phytophthora infestans Infection
Molecular Plant-Microbe Interactions ( IF 3.5 ) Pub Date : 2024-03-28 , DOI: 10.1094/mpmi-08-23-0118-fi
Adam R. Bentham 1 , Wei Wang 2, 3 , Franziska Trusch 2, 3 , Freya A. Varden 1 , Paul R. J. Birch 2, 3 , Mark J. Banfield 1
Affiliation  

Plant pathogens manipulate the cellular environment of the host to facilitate infection and colonization that often lead to plant diseases. To accomplish this, many specialized pathogens secrete virulence proteins called effectors into the host cell, which subvert processes such as immune signaling, gene transcription, and host metabolism. Phytophthora infestans, the causative agent of potato late blight, employs an expanded repertoire of RxLR effectors with WY domains to manipulate the host through direct interaction with protein targets. However, our understanding of the molecular mechanisms underlying the interactions between WY effectors and their host targets remains limited. In this study, we performed a structural and biophysical characterization of the P. infestans WY effector Pi04314 in complex with the potato Protein Phosphatase 1-c (PP1c). We elucidate how Pi04314 uses a WY domain and a specialized C-terminal loop carrying a KVxF motif that interact with conserved surfaces on PP1c, known to be used by host regulatory proteins for guiding function. Through biophysical and in planta analyses, we demonstrate that Pi04314 WY or KVxF mutants lose their ability to bind PP1c. The loss of PP1c binding correlates with changes in PP1c nucleolar localization and a decrease in lesion size in plant infection assays. This study provides insights into the manipulation of plant hosts by pathogens, revealing how effectors exploit key regulatory interfaces in host proteins to modify their function and facilitate disease.

Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY 4.0 International license.



中文翻译:

RxLr 效应器的 WY 结构域驱动与宿主靶标磷酸酶的相互作用,以模拟宿主调节蛋白并促进致病疫霉感染

植物病原体操纵宿主的细胞环境以促进感染和定植,这通常会导致植物病害。为了实现这一目标,许多特殊的病原体将称为效应子的毒力蛋白分泌到宿主细胞中,从而破坏免疫信号、基因转录和宿主代谢等过程。致病疫霉是马铃薯晚疫病的病原体,它利用具有 WY 结构域的 RxLR 效应子的扩展库,通过与蛋白质靶点的直接相互作用来操纵宿主。然而,我们对 WY 效应器与其宿主靶标之间相互作用的分子机制的理解仍然有限。在这项研究中,我们对致病疫霉WY 效应子 Pi04314 与马铃薯蛋白磷酸酶 1-c (PP1c) 的复合物进行了结构和生物物理表征。我们阐明了 Pi04314 如何使用 WY 结构域和携带 KVxF 基序的特化 C 端环,该基序与 PP1c 上的保守表面相互作用,已知宿主调节蛋白使用其来指导功能。通过生物物理学和植物分析,我们证明 Pi04314 WY 或 KVxF 突变体失去了结合 PP1c 的能力。 PP1c 结合的丧失与 PP1c 核仁定位的变化和植物感染测定中病灶大小的减小相关。这项研究提供了对病原体对植物宿主的操纵的见解,揭示了效应器如何利用宿主蛋白中的关键调控界面来改变其功能并促进疾病。

版权所有 © 2024 作者。这是一篇根据 CC BY 4.0 国际许可证分发的开放获取文章。

更新日期:2024-03-28
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