Suppression of a specific branch of mitogen-activated protein kinase (MAPK) signaling by bacterial AvrRpt2-like cysteine proteases: Mechanistic elucidation and application for MAPK studies.

细菌 AvrRpt2 样半胱氨酸蛋白酶抑制丝裂原激活蛋白激酶 (MAPK) 信号传导的特定分支：MAPK 研究的机制阐明和应用。

• 批准号: 327033184
• 负责人: Dr. Justin Lee
• 金额: --
• 依托单位: Abteilung Biochemie pflanzlicher Interaktionen
• 依托单位国家: 德国
• 项目类别: Research Grants
• 财政年份: 2016
• 资助国家: 德国
• 起止时间: 2015-12-31 至 2019-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/327033184?language=en
• 关键词: Suppression; specific; branch; mitogen; activated

Plants recognize conserved structures of pathogens during the infection process and activate defence reactions. One key signalling event is the activation of mitogen-activated protein kinases (MAPKs/MPKs). We recently reported a new function of a well-studied bacterial pathogenesis effector called AvrRpt2, where it blocked the pathogen-induced activation of specific MAPKs (i.e. inhibition of MPK4/MPK11 but not MPK3/MPK6). This novel function of blocking MPK4/MPK11 activation is conserved in homologs from a number of plant-associated and soil bacteria (that includes agronomically important phytopathogens like Ralstonia solanacearum, Erwinia amylovora and Acidovorax citrulli). Additionally, we also have preliminary findings that multiple transcription factors known to be important for stress regulation are destabilized or their expression is blocked by AvrRpt2. We propose that these may be novel virulence functions of AvrRpt2, which seem to be independent of previously known AvrRpt2 targets. In this proposal, we aim to elucidate the molecular mechanism for these processes. Since the cysteine protease activity of AvrRpt2 is essential for these functions, the AvrRpt2 cleaved substrates must be responsible for the observed effects on the MAPKs and transcription factors. Hence, we will use a proteomics-based method (called TAILs) to detect the novo N-termini of cleaved proteins in plants expressing AvrRpt2 and hence identify new in vivo AvrRpt2 substrates. Furthermore, we want to exploit the specific AvrRpt2-mediated interference with MPK4/MPK11 activation to bypass the constraints imposed by the extreme dwarf phenotype and lethality of the mpk4mpk11 double mutant and study signalling unique to these two MAPKs in healthy plants. The knowledge gleaned from the current study will advance the understanding of bacterial infection strategies and allow us to improve pest management schemes against pathogens.

植物在感染过程中识别病原体的保守结构并激活防御反应。一个关键的信号事件是有丝分裂原活化蛋白激酶（MAPKs/MPKs）的激活。我们最近报道了一种被广泛研究的细菌致病效应物AvrRpt2的新功能，它可以阻断病原体诱导的特定MAPKs的激活（即抑制MPK4/MPK11，但不抑制MPK3/MPK6）。这种阻断MPK4/MPK11激活的新功能在许多植物相关细菌和土壤细菌的同源物中是保守的（包括农学上重要的植物病原体，如Ralstonia solanacearum， Erwinia amylovora和Acidovorax citrulli）。此外，我们还初步发现，已知对应激调节重要的多种转录因子被AvrRpt2破坏稳定或其表达被阻断。我们认为这些可能是AvrRpt2新的毒力功能，似乎独立于先前已知的AvrRpt2靶点。在本文中，我们旨在阐明这些过程的分子机制。由于AvrRpt2的半胱氨酸蛋白酶活性对这些功能至关重要，因此AvrRpt2切割的底物必须负责观察到的对MAPKs和转录因子的影响。因此，我们将使用基于蛋白质组学的方法（称为TAILs）来检测表达AvrRpt2的植物中断裂蛋白的新n端，从而鉴定出新的体内AvrRpt2底物。此外，我们希望利用avrrpt2介导的MPK4/MPK11激活的特异性干扰，绕过mpk4mpk11双突变体的极端矮化表型和致病性所施加的限制，研究这两种mapk在健康植物中的独特信号传导。从目前的研究中收集到的知识将促进对细菌感染策略的理解，并使我们能够改进针对病原体的害虫管理方案。