农科院戴小枫研究组揭示病原操纵寄主先天免疫反应新机制
2017年3月28日，国际环境科学顶级期刊《Environmental Microbiology》上在线发表了中国农业科学院农产品加工研究所戴小枫研究组和美国加州大学戴维斯分校克里希那•苏巴拉奥教授研究组合作的一篇研究论文，研究报道了在黄萎病病原菌─大丽轮枝菌与寄主植物互作研究方面取得突破性进展。研究首次揭示大丽轮枝菌利用碳水化合物结合模块CBM1蛋白抑制先天免疫反应以促进病原侵染寄主的分子机制。博士研究生桂月晶和团队研究骨干陈捷胤为文章的共同第一作者，戴小枫研究员和美国加州大学戴维斯分校克里希那•苏巴拉奥教授为共同通讯作者。
病原与寄主植物长期共进化过程中，分泌的蛋白往往容易被寄主植物受体识别而激活先天免疫反应，限制了病原的侵染;为克服这一障碍，病原进化出相应的效应子来抑制先天免疫反应，从而实现病原对寄主植物的成功侵染。然而，上述机制在恶性土传病原真菌—大丽轮枝菌中一直未被发现，制约了人们对大丽轮枝菌与寄主植物互作机制的认识和黄萎病防控技术的研发。
加工所加工有害生物创新团队从大丽轮枝菌中鉴定出2个可诱导烟草先天免疫反应的糖苷水解酶GH12家族蛋白(VdEG1和VdEG3)。侵染寄主棉花时，2个蛋白依赖于酶活发挥毒力功能;侵染寄主烟草时，作为激发子不依赖于酶活被寄主受体识别而诱导先天免疫。进一步研究发现，两个蛋白诱导的先天免疫反应途径存在差异，VdEG1依赖于全长与跨膜受体蛋白复合体(LRR-RLPs/SOBIR1/BAK1)互作诱导免疫反应;而VdEG3利用63个氨基酸短肽与跨膜受体激酶复合体(LRR-RLKs/BAK1)互作诱导免疫反应。大丽轮枝菌为逃避寄主激发的先天免疫反应，进化出碳水化合物结合模块CBM1蛋白(VdCBM1)来抑制上述免疫反应，促进病原对寄主植物的侵染。此外，还发现VdEG3偶联的CBM1结构域具有抑制自身诱导先天免疫反应的特性。该研究首次发现了大丽轮枝菌CBM1蛋白具有抑制免疫反应的功能，揭示了CBM1与糖苷水解酶协同互作操控寄主先天免疫反应的分子机理，拓宽了研究人员对大丽轮枝菌与寄主植物互作机制的认识，为黄萎病防控技术研发提供了新的理论和策略。
原文链接：
Verticillium dahliae manipulates plant immunity by glycoside hydrolase 12 proteins in conjunction with carbohydrate-binding module 1
原文摘要：
Glycoside hydrolase 12 (GH12) proteins act as virulence factors and pathogen-associated molecular patterns (PAMPs) in oomycetes. However, the pathogenic mechanisms of fungal GH12 proteins have not been characterized. In this study, we demonstrated that two of the six GH12 proteins produced by the fungus Verticillium dahliae Vd991, VdEG1 and VdEG3 acted as PAMPs to trigger cell death and PAMP-triggered immunity (PTI) independent of their enzymatic activity in Nicotiana benthamiana. A 63-amino-acid peptide of VdEG3 was sufficient for cell death-inducing activity, but this was not the case for the corresponding peptide of VdEG1. Further study indicated that VdEG1 and VdEG3 trigger PTI in different ways: BAK1 is required for VdEG1- and VdEG3-triggered immunity, while SOBIR1 is specifically required for VdEG1-triggered immunity in N. benthamiana. Unlike oomycetes, which employ RXLR effectors to suppress host immunity, a carbohydrate-binding module family 1 (CBM1) protein domain suppressed GH12 protein-induced cell death. Furthermore, during infection of N. benthamiana and cotton, VdEG1 and VdEG3 acted as PAMPs and virulence factors, respectively indicative of host-dependent molecular functions. These results suggest that VdEG1 and VdEG3 associate differently with BAK1 and SOBIR1 receptor-like kinases to trigger immunity in N. benthamiana, and together with CBM1-containing proteins manipulate plant immunity.
作者：戴小枫
