题目：植物抗病毒机制与抗病毒基因的人工设计

主讲：刘玉乐 教授（清华大学）

时间：11月12日（周四）10:20-11:20

地点：慧园4栋301

个人简介：

清华大学生命科学学院长聘教授、国家杰青。长期从事植物病毒和细胞自噬相关研究，在植物抗病免疫、病毒病理、病毒载体、细胞自噬方面做出了有国际影响的工作。发表SCI论文约130篇，以通讯或第一作者在Nature（2篇）、Cell（2篇）等刊物发表论文70余篇，SCI引用超过2.1万次，谷歌学术中被引超过3.5万次，自2014年每年均入选爱思唯尔(Elsevier)发布的中国高被引学者榜单，主编教材《生物化学》（2023年），是出任国际重要病毒学杂志Journal of Virology编辑的首位中国大陆本土科学家。

报告摘要：

Plants have evolved diverse antiviral defense mechanisms. We established a mechanistic link between Ca²⁺ signaling and antiviral RNA interference (RNAi), revealing a previously unknown pathway by which calcium signals activate antiviral immunity. We identified autophagy as a novel antiviral defense mechanism and elucidated the molecular basis of methyl salicylate-mediated airborne defense in plants. We developed a novel strategy for engineering broad-spectrum, durable, and complete disease resistance using protease-activated immune receptors. By incorporating conserved pathogen protease cleavage sites into autoactive nucleotide-binding leucine-rich repeat receptors (NLRs), we created synthetic immune receptors that are activated upon pathogen infection. A single engineered NLR conferred broad-spectrum and complete resistance to multiple potyviruses. This strategy provides a versatile platform for engineering resistance against diverse pathogens and potentially insect pests. We also elucidated the complete biosynthetic pathway of debneyol, a broad-spectrum antimicrobial phytoalexin. Debneyol is synthesized from farnesyl pyrophosphate through three sequential enzymatic reactions catalyzed by EAS, EAE, and EH1. We further identified MCD1 as a key regulatory factor that promotes debneyol biosynthesis by facilitating the EAS–EAE interaction and enhancing EAE activity. Increased MCD1 expression enhances resistance to fungal, viral, and bacterial pathogens. These discoveries establish a molecular framework for phytoalexin-mediated immunity and open new avenues for engineering broad-spectrum disease resistance and producing antimicrobial compounds through synthetic biology.