真菌病毒SmEV1的水平传染机制研究及生防潜力评估

Sclerotinia blight, caused by Sclerotinia minor, is responsible for serious yield losses of some economic crops. Since no disease-resistant cultivars are available, control measures for sclerotinia diseases are mainly dependent upon application of fungicides. However, use of fungicides may have negative effects including formation of fungicide-resistance strains of S. minor, and fungicides residue. Therefore, a new method is urgently needed to control sclerotinia diseases. Mycoviruses is the new resource for control of sclerotinia diseases. But fungal vegetative incompatibility is the key factor that limits the wide utilization of mycoviruses to control fungal diseases. Our previous study showed that Sclerotinia minor endornavirus 1 (SmEV1) conferred hypovirulence on its host S. minor strain LC22. SmEV1 could be horizontally transmitted by hyphal anastomosis and not be restricted by mycelial compatibility group. Therefore, it is necessary to study the mechanisms of mycovirus overcome the vegetative incompatibility. In this project, we proposed to elucidate the mechanisms of SmEV1 transmission; to identify the SmEV1 genes which suppressed host vegetative incompatibility reaction, and to demonstrate the key genes related to incompatibility reaction in Sm using the transcriptome profiling. Meanwhile, ecological adaptability and biocontrol potential of SmEV1 were assessed by pot and field experiments. The results from this project will reveal the molecular mechanisms of endornavirus SmEV1 overcome the vegetative incompatibility, and will demonstrate the biocontrol potential of SmEV1. Furthermore, the results will be useful for initiation of novel strategies for control of sclerotinia diseases caused by Sm.

小核盘菌（Sclerotinia minor, Sm）引起多种经济作物菌核病。由于抗病品种缺乏，化学防治易产生农药残留和抗药性，急需研发防治Sm的新方法。真菌病毒是防治这一真菌的新型资源。然而，真菌菌丝不亲和性反应常常阻碍真菌病毒的水平传染，是限制其防病效果的关键因子。申请人前期研究发现Sm菌株LC22含有内源RNA病毒SmEV1。SmEV1能引起Sm致病力衰退，且其传染不受菌丝亲和群的限制。有必要对其水平传染机制开展专门研究。鉴此，本项目提出研究SmEV1的传染特性；明确SmEV1中参与抑制寄主不亲和反应的基因，通过转录组测序分析Sm被SmEV1感染前后的差异表达基因，筛选并鉴定Sm中不亲和反应关键基因；评估SmEV1的田间生态适应性和生防潜力。研究结果将揭示SmEV1水平传染不受菌丝亲和群限制的分子机制，并明确SmEV1防治Sm的潜力，为Sm菌核病防治提供理论依据和新生防资源。

小核盘菌（Sclerotinia minor, Sm）能引起多种经济作物菌核病。由于抗病品种缺乏，化学防治易产生农药残留和抗药性，急需研发防治Sm的新方法。真菌病毒是防治这一真菌的新型资源。然而，真菌菌丝不亲和性反应常常阻碍真菌病毒的水平传染，是限制其防病效果的关键因子。本项目系统研究了真菌病毒SmEV1的分子属性，明确了真菌病毒SmEV1是一个全新的内源RNA病毒；通过水平传染测定、垂直传染测定及跨种属传染测定，明确了病毒SmEV1与S. minor菌株的弱毒特性密切相关，且病毒能不受菌丝亲和群的限制在S. minor菌株中进行广泛的水平传染，也能通过菌核后代进行稳定的垂直传染，SmEV1还能通过原生质体融合从小核盘菌（S. minor）跨种传染给核盘菌（S. sclerotiorum）；进一步探究了SmEV1水平传染不受菌丝亲和群限制的分子机制，SmEV1的侵染诱导寄主小核盘菌过氧化氢酶基因上调表达，增强胞内过氧化氢酶活性，降低胞内H2O2浓度，可能抑制了寄主的营养体不亲和反应，从而导致SmEV1在小核盘菌不同菌丝亲和群菌株中水平传播不受限制；通过SmEV1 对莴苣菌核病的室内试验评价，明确了SmEV1对莴苣菌核病具有生防效果。项目取得的结果揭示了SmEV1水平传染不受菌丝亲和群限制的分子机制，明确了SmEV1防治Sm的潜力，为Sm菌核病防治提供理论依据和新生防资源。项目实施3年来发表SCI论文2篇，作学术会议报告2次（国际会议学术报告1次，国内会议学术1次），另外还参加了2次国内学术会议，博士后出站1名，培养专业技术人员2名。