How do oomycete and fungal effectors enter host plant cells?

卵菌和真菌效应子如何进入宿主植物细胞？

• 批准号: 0924861
• 负责人: Brett Tyler
• 金额: $ 50万
• 依托单位: Virginia Polytechnic Institute and State University
• 依托单位国家: 美国
• 项目类别: Standard Grant
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-09-01 至 2012-08-31
• 项目状态: 已结题
• 来源: https://www.nsf.gov/awardsearch/showAward?AWD_ID=0924861&HistoricalAwards=false
• 关键词: How; do; oomycete; fungal; effectors

Oomycete and fungal plant pathogens cause a number of very important diseases. Many of these pathogens can deliver proteins into the cytoplasm of their host cells to disable host immunity; these proteins are called effectors. The mechanism by which these proteins enter host cells is poorly understood. The investigators have shown that oomycete and fungal effector proteins can enter host cells without the aid of any pathogen-encoded machinery, but instead rely on short amino acid sequences in the N-termini called RXLR motifs. The investigators have discovered that the RXLR motifs can bind a class of membrane lipids called phosphoinositides. In this project, the investigators will test whether binding of the effectors to phosphoinositides is actually responsible for transferring the effectors into host cells. They will identify which host phosphoinositides are utilized by the effectors, and they will characterize the mechanism of binding. Finally they will test whether it is possible to block effector entry and so prevent disease. An extremely wide range of the most destructive plant pathogens, including those causing wheat rust, rice blast, grape powdery mildew and potato late blight depend on effectors. Understanding effector entry and determining how to block it would provide an entirely new approach to treating this broad class of diseases. Treatment of animal diseases caused by fungi, oomycetes and some parasites may also be treatable by this approach. This project will train two graduate students and provide summer research opportunities for multi-cultural undergraduate students.

卵菌和真菌植物病原体引起许多非常重要的疾病。这些病原体中的许多可以将蛋白质递送到其宿主细胞的细胞质中以使宿主免疫失效;这些蛋白质被称为效应物。这些蛋白质进入宿主细胞的机制知之甚少。研究人员已经表明，卵菌和真菌效应蛋白可以在没有任何病原体编码机制的帮助下进入宿主细胞，而是依赖于N末端称为RXLR基序的短氨基酸序列。研究人员发现，RXLR基序可以结合一类称为磷酸肌醇的膜脂质。在这个项目中，研究人员将测试效应物与磷酸肌醇的结合是否真的负责将效应物转移到宿主细胞中。他们将确定哪些宿主磷酸肌醇被效应器利用，并将表征结合机制。最后，他们将测试是否有可能阻止效应物进入，从而预防疾病。一个极其广泛的最具破坏性的植物病原体，包括那些导致小麦锈病，稻瘟病，葡萄白粉病和马铃薯晚疫病依赖于效应。了解效应子进入并确定如何阻止它将为治疗这一广泛类别的疾病提供一种全新的方法。这种方法也可以治疗由真菌、卵菌和一些寄生虫引起的动物疾病。该项目将培养两名研究生，并为多文化本科生提供暑期研究机会。