Small RNA介导的DNA甲基化调控的水稻草矮病毒致病机制

Rice is an essential food crop which can support the living for half of the world’s population. However, diseases caused by a wide variety of rice viruses have resulted in enormous losses for the rice production, posing a direct threat on the national food security. Rice grassy stunt virus (RGSV), a single-strand RNA virus, will not only damage the production of the infected rice, it will also make total crop failure of rice. At present, we still don’t know the pathogenesis mechanism induced by RGSV in rice. We previously found that rice 24 nt small RNA as well as the transcription and expression of Pol VI gene, is highly repressed by RGSV infection. The genome-wide DNA methylation level is significantly reduced in the RGSV infection rice plants. Further work has revealed that RGSV-encoding P3 interacted with Pol VI to regulate DNA methylation of rice genome and facilitate virus infection and symptom development. This project is for the purpose of building a new virus pathogenic mechanism in which RNA virus will participate in regulating the epigenetic modification to affect the growth and development of the rice, thus finally providing a theoretical basis to prevent and control this virus disease.

水稻是维持世界过半人口生存的重要粮食作物，而由各种水稻病毒引起的病害却对水稻产量造成巨大损失，对国家粮食安全构成直接威胁。水稻草矮病毒（RGSV），一个单链RNA病毒，侵染水稻后造成严重减产，甚至绝收。目前，对于RGSV如何诱导水稻发病尚不清楚。我们前期研究发现，RGSV的侵染显著抑制了水稻内源24nt Small RNA的产生和Pol VI基因的转录和表达；水稻全基因组甲基化水平显著降低。深入研究揭示RGSV 编码的P3蛋白通过与Pol VI的互作从而调控DNA甲基化水平，进而参与病毒致病过程。该项目为建立RNA病毒参与调控植物表观遗传修饰，影响水稻生长发育的一种新的病毒致病机制，为有效进行该病毒病害的防控提供理论依据。

泛素蛋白酶系统（UPS）是真核生物功能蛋白翻译后的重要调控机制，其在水稻与病毒互作中的功能尚不清楚。本研究发现布尼亚病毒科负义单链RNA病毒水稻草矮病毒（RGSV）编码致病蛋白P3，导致水稻植株矮化和分蘖增多等病害症状。无论RGSV的侵染还是P3的稳定表达都引起RNA聚合酶IV（Pol Ⅳ）亚基Nuclear RNA Polymerase D1a（OsNRPD1a）的降解，破坏了依赖于RNA的 DNA甲基化通路（RdDM）。进一步研究发现，P3诱导并与E3泛素连接酶P3IP1互作，对OsNRPD1a经UPS降解。将P3IP1超量表达或者OsNRPD1a沉默表达后，水稻植株呈现矮化、分蘖增多的农艺性状。本研究首次揭示了P3IP1和OsNRPD1a在水稻发育、水稻与病毒互作中的功能，解析了单链RNA病毒调控P3IP1降解OsNRPD1a从而作用于RdDM通路的致病机制，丰富了病毒致病机制的理论，为抗病毒设计育种提供了新的编辑靶标，对培育抗病毒水稻具有重要的潜在应用价值。