Apoplastic cysteine proteases as inducers of plant defense and their inhibition by microbial effectors

质外体半胱氨酸蛋白酶作为植物防御诱导剂及其受微生物效应子的抑制

• 批准号: 244021783
• 负责人: Professor Dr. Gunther Döhlemann
• 金额: --
• 依托单位: Lehrstuhl Terrestrische Mikrobiologie
• 依托单位国家: 德国
• 项目类别: Research Grants
• 资助国家: 德国
• 项目状态: 未结题
• 来源: https://gepris.dfg.de/gepris/projekt/244021783?language=en
• 关键词: Apoplastic; cysteine; proteases; inducers; plant

The outcome of plant-microbe interactions is determined by the interplay of the microbial virulence repertoire with the plant immune system. In maize, the pathogenic fungus Ustilago maydis modulates host immunity to establish a biotrophic interaction and cause smut disease. Important hubs for the coordination of plant defence are papain-like cysteine proteases (PLCPs). Our previous work showed that these enzmes are crucial for the activation of salicylic acid (SA)-dependent defenses in maize leaves. During U. maydis infection, the activity of maize PLCPs is modulated by both the host plant via the cystatin CC9, as well as by the fungal effector protein Pit2. During the first phase of this project, we identified a novel, PLCP-release peptide signal (Zip1) which activates SA-mediated immunity. We showed that a fungal effector protein (Pit2) blocks the PLCP-mediated defense mechanism by acting as a molecular mimicry molecule, which releases a cross-kingdom conserved inhibitor peptide (cMIP). We observed an organ-specific, SA-mediated activation of PLCPs in roots, and found that root endophytic bacteria secrete inhibitors of root PLCPs. Based on these findings, we will focus on two main aspects:1) Zip1 signaling and its evolutionary conservation.This part of the project aims to gain mechanistic understanding on the activation of SA-signaling by Zip1. We will address the following questions: How is PROZIP1 localized and how is it processed to release apoplastic Zip1? What is the receptor for Zip1? Is Zip1 signaling specific to maize, or is this mechanismconserved in other plant species? 2) Organ specificity in PLCP-induced SA defense and its suppression in microbial root interactions. This part of the project aims to understand the molecular basis of organ-specific, PLCP-activated SA signaling, as well as to characterize the role of PLCP-inhibitors in the root microbiome. Our major goals are i) the biochemical and functional characterization of root-specific apoplastic PLCPs and their inhibitors; ii) to investigate root-specific SA signaling networks with an emphasis on the role of organ-specific PLCPs, and iii) to study the role of bacterial PLCP inhibitors for the establishment of the root-microbe interactions.

植物-微生物相互作用的结果由微生物毒力库与植物免疫系统的相互作用决定。在玉米中，致病真菌玉米黑粉菌调节宿主免疫力以建立活体营养相互作用并引起黑穗病。协调植物防御的重要枢纽是木瓜蛋白酶样半胱氨酸蛋白酶（PLCP）。我们以前的工作表明，这些酶是至关重要的激活水杨酸（SA）依赖的防御玉米叶片。在美国期间。在玉米感染中，玉米PLCP的活性由宿主植物通过半胱氨酸蛋白酶抑制剂CC 9以及真菌效应蛋白Pit 2调节。在该项目的第一阶段，我们确定了一种新的PLCP释放肽信号（Zip 1），它激活SA介导的免疫。我们发现，真菌效应蛋白（Pit 2）通过作为分子模拟分子，释放跨王国保守抑制肽（cMIP），阻断PLCP介导的防御机制。我们观察到一个器官特异性，SA介导的激活PLCPs在根中，并发现根内生细菌分泌根PLCPs的抑制剂。基于这些发现，我们将集中在两个主要方面：1）Zip 1信号及其进化保守性，这部分项目的目的是获得Zip 1激活SA信号的机制。我们将解决以下问题：PROZIP 1是如何本地化的，它是如何处理释放质外体Zip 1？Zip 1的受体是什么？ Zip 1信号是玉米特有的，还是在其他植物物种中保守的？ 2)PLCP诱导SA防御的器官特异性及其在微生物根相互作用中的抑制。该项目的这一部分旨在了解器官特异性PLCP激活SA信号传导的分子基础，以及表征PLCP抑制剂在根微生物组中的作用。我们的主要目标是i）根特异性质外体PLCP及其抑制剂的生物化学和功能表征; ii）调查根特异性SA信号网络，强调器官特异性PLCP的作用;和iii）研究细菌PLCP抑制剂在建立根-微生物相互作用中的作用。