一种细菌效应物通过劫持钙调蛋白来靶向植物微管网络。

A Bacterial Effector Co-opts Calmodulin to Target the Plant Microtubule Network.

机构信息

Center for Plant Science Innovation, University of Nebraska, Lincoln, NE 68588-0660, USA; Department of Plant Pathology, University of Nebraska, Lincoln, NE 68588-0722, USA.

Center for Plant Science Innovation, University of Nebraska, Lincoln, NE 68588-0660, USA; School of Biological Sciences, University of Nebraska, Lincoln, NE 68588-0118, USA.

出版信息

Cell Host Microbe. 2016 Jan 13;19(1):67-78. doi: 10.1016/j.chom.2015.12.007.

DOI:10.1016/j.chom.2015.12.007

PMID:26764598

Abstract

The bacterial pathogen Pseudomonas syringae depends on effector proteins secreted by its type III secretion system for the pathogenesis of plants. The majority of these effector proteins are known suppressors of immunity, but their plant targets remain elusive. Using Arabidopsis thaliana as a model host, we report that the HopE1 effector uses the host calcium sensor, calmodulin (CaM), as a co-factor to target the microtubule-associated protein 65 (MAP65), an important component of the microtubule network. HopE1 interacted with MAP65 in a CaM-dependent manner, resulting in MAP65-GFP dissociation from microtubules. Transgenic Arabidopsis expressing HopE1 had reduced secretion of the immunity protein PR-1 compared to wild-type plants. Additionally, Arabidopsis map65-1 mutants were immune deficient and were more susceptible to P. syringae. Our results suggest a virulence strategy in which a pathogen effector is activated by host calmodulin to target MAP65 and the microtubule network, thereby inhibiting cell wall-based extracellular immunity.

摘要

植物病原菌丁香假单胞菌依赖其 III 型分泌系统分泌的效应蛋白来引发植物发病。这些效应蛋白大多数是已知的免疫抑制剂，但它们的植物靶标仍难以捉摸。我们以拟南芥为模型宿主，报告称 HopE1 效应物利用宿主钙传感器钙调蛋白 (CaM) 作为辅助因子来靶向微管相关蛋白 65 (MAP65)，MAP65 是微管网络的重要组成部分。HopE1 以 CaM 依赖的方式与 MAP65 相互作用，导致 MAP65-GFP 从微管上解离。与野生型植物相比，表达 HopE1 的转基因拟南芥中免疫蛋白 PR-1 的分泌减少。此外，map65-1 拟南芥突变体对丁香假单胞菌的敏感性增加。我们的研究结果表明，一种病原体效应物被宿主钙调蛋白激活，以靶向 MAP65 和微管网络，从而抑制基于细胞壁的细胞外免疫，这是一种毒力策略。