AvrPiz-t-mediated suppression of PAMP- and effector-triggered immunity in rice by targeting host ubiqiutin proteasome system

植物真菌病原体在世界范围内造成农作物生产的巨大产量损失。植物细菌和卵菌病原菌干扰宿主防御的分子机制已逐渐阐明。然而，对于真菌病原体，这些机制仍然知之甚少。稻瘟病是由稻瘟病菌（Magnaporthe）引起的水稻最具破坏性的病害。它是研究谷类作物中植物-真菌相互作用的研究人员的先进模式病理系统。M. Escherichia coli将一种名为AvrPiz-t的效应蛋白引入其宿主，在那里它引起免疫功能的广泛变化。这种效应子值得注意的是攻击植物免疫的两个组分，即对病原体保守分子模式的反应（PAMP触发的免疫或PTI）和对病原体的株系特异性免疫应答（效应子触发的免疫或ETI）。初步结果表明，AvrPiz-t代表了一种新的真菌效应器，与宿主相互作用？的泛素化系统的毒力和免疫诱导活性。特别是，它与三种称为泛素E3连接酶的水稻酶相互作用，以抑制它们的连接酶活性，从而降低宿主免疫反应的有效性。病原体的免疫抑制活性被这些相同的E3连接酶抵消，这些连接酶泛素化AvrPiz-t以标记其降解。该项目旨在从分子水平上了解AvrPiz-t如何与宿主蛋白相互作用以抑制宿主的先天免疫。具体目标是：（1）确定AvrPiz-t的干扰，降解，泛素化和PTI抑制机制;（2）确定E3连接酶在PTI和ETI调节中的功能;（3）使用遗传和生物化学方法深入了解E3连接酶与介导AvrPiz-t诱导的免疫应答的抗性蛋白之间的关系。该项目将为水稻和其他谷类作物的真菌病害控制提供新的见解。作为世界近50%人口的主食，该项目开发新的稻瘟病控制策略将影响许多发展中国家的粮食安全和社会稳定。此外，该项目将为一名博士后研究员和一名博士生提供广泛的培训机会，他们可能在未来继续研究这一重要疾病。

Fungal pathogens of plants cause tremendous yield losses in crop production worldwide. The molecular mechanisms underlying pathogen interference with host defenses have been gradually elucidated for plant bacterial and oomycete pathogens. However, these mechanisms are still poorly understood for fungal pathogens. Rice blast, caused by the fungus Magnaporthe oryzae, is the most devastating disease of rice. It serves as an advanced model pathosystem for researchers who study plant-fungal interactions in cereal crops. M. oryzae introduces an effector protein called AvrPiz-t into its host, where it causes widespread changes in immune function. This effector is noteworthy for attacking two components of plant immunity, the reaction to conserved molecular patterns of the pathogen (PAMP-triggered immunity or PTI) and strain-specific immune responses to pathogens (effector-triggered immunity or ETI). Preliminary results indicate that AvrPiz-t represents a novel fungal effector that interacts with the host?s ubiquitination system for both its virulence and immunity inducing activities. In particular, it interacts with three rice enzymes called ubiquitin E3 ligases to suppress their ligase activity and thereby reduce the effectiveness of the host's immune response. The immunosuppressive activity of the pathogen is countered by these same E3 ligases, which ubiquitinate AvrPiz-t to mark it for degradation. This project seeks to understand at the molecular level how AvrPiz-t interacts with host proteins to suppress the host's innate immunity. The specific goals are: (1) Determine the interference, degradation, ubiquitination and PTI suppression mechanisms of AvrPiz-t; (2) Identify the function of an E3 ligase in the regulation of PTI and ETI; and (3) Use genetic and biochemical approaches to gain insight into the relationship between this E3 ligase and the resistance protein that mediates the immune response induced by AvrPiz-t. The project will potentially provide new insights into fungal disease control in rice and other cereal crops. As the staple food for nearly 50% of the world's population, development of new rice blast control strategies from this project will affect food security and social stability in many developing countries. Moreover, this project will provide extensive training opportunities for a postdoctoral fellow and a PhD student who might continue to work on this important disease in the future.