南方水稻黑条矮缩病毒调控水稻对介体引诱能力的蛋白鉴定及作用机理

Over the past few years, Southern rice black-streaked dwarf virus (SRBSDV) has caused serious loss in rice production. Our previous study found that SRBSDV infection could increase the attractiveness of rice to the vector white-backed planthopper, which facilitates the virus transmission from infected plants to nonviruliferous insect vector, and promotes the spread of virus infection. This project is conducted to elucidate the mechanism for this phenomenon: Starting from the virus encoding proteins, using our existed transgenic plants which express the SRBSDV encoding proteins, identify the key protein of SRSBDV which enhance the vector attraction of the infected rice plants; Analyze the changes of transcriptome and metabolome of the transgenic plants which express the key protein of SRBSDV, unravel the effects of SRBSDV key protein on secondary metabolism of rice; Screen the host interaction factors of SRBSDV key protein through protein interaction technologies, investigate how the interaction affect secondary metabolism and vector attraction of rice. The expected results will unravel the molecular mechanism how SRBSDV regulates secondary metabolism of rice thus affecting the vector white-backed planthopper attraction, and will provide a deeper theoretical basis for the control of virus disease and the improvement of rice varieties.

近年来南方水稻黑条矮缩病毒(Southern rice black-streaked dwarf virus，SRBSDV)对我国及周边国家的水稻生产造成了严重危害。我们前期的研究发现，SRBSDV侵染能增强感病水稻对无毒白背飞虱的引诱能力，促进无毒介体从病株上获毒而有利于病毒的传播和扩散。本项目拟对该现象开展深入研究：从病毒编码的各个蛋白着手，利用表达SRBSDV编码蛋白的转基因水稻，鉴定病毒增强水稻对无毒介体引诱能力的关键蛋白；对表达病毒关键蛋白的转基因水稻进行转录组和代谢组分析，解析病毒蛋白对感病水稻次生代谢的影响；通过蛋白质互作技术筛选与病毒关键蛋白互作的寄主因子，研究病毒蛋白与寄主因子的互作对水稻次生代谢及对介体引诱能力的影响，在分子水平上解析病毒通过调控水稻次生代谢从而影响介体选择偏好性的具体机制，为有效控制病害的传播流行和水稻品种的改良提供更深入的理论依据。

南方水稻黑条矮缩病毒（Southern rice black-streaked dwarf virus，SRBSDV）侵染能增强感病水稻对无毒白背飞虱的引诱能力，促进无毒介体从病株上获毒而有利于病毒的传播和扩散。本项目对该现象开展深入研究：从病毒编码的各个蛋白着手，利用表达SRBSDV编码蛋白的转基因水稻，鉴定病毒编码的P6是增强水稻对无毒介体引诱能力的关键蛋白；通过免疫共沉淀技术筛选与病毒编码P6蛋白互作的寄主因子，发现P6蛋白能够和水稻乙烯信号通路的关键转录因子OsEIL2发生直接互作，并通过酵母双杂交、GST Pull-down、BiFC等手段证实了互作真实存在；进一步对P6和OsEIL2的互作方式开展研究，发现P6通过竞争性结合破坏OsEIL2的二聚体形成，从而抑制OsEIL2的转录活性，进而提高对介体白背飞虱的引诱能力。本研究在分子水平上解析病毒通过调控水稻乙烯信号转导从而影响介体选择偏好性的具体机制，为有效控制病害的传播流行和水稻品种的改良提供更深入的理论依据。该项目发表论文5篇，申请专利2项，培养学生5名。