番茄抗病基因Tm-2(2)介导病毒抗性的分子机制研究

Plant viral disease is important for agricultural production. Studies on molecular mechanisms of virus resistance are the important foundation of disease resistance breeding. Most plant virus resistance genes, like tomato Tm-2 (2) gene, belong to CC-NBS-LRR type of resistance genes. However, little is known about their antiviral mechanisms. Tm-2 (2) gene confers plant resistance against tomato mosaic virus and tobacco mosaic virus, and has been used for almost 50 years and is still widely used in agricultural production because Tm-2(2)-mediated resistance is very durable. Recently, we developed the new system to study Tm-2(2)-mediated virus resistance in Nicotiana benthamiana, and found that J-domain protein MIP1s and chloroplast protein Rubisco small subunit are involved in Tm-2(2)-mediated virus resistance. On this basis, in this project, we plan to deeply study how Tm-2(2) mediates plant resistance against viruses , and how the resistance is regulated, by identifying plant host factors that interact with Tm-2(2) and/or its corresponding virus-encoded avirulence protein, and by identifying microRNAs whose expression are regulated by Tm-2(2)-mediated virus resistance. This study will deepen the understanding of the molecular mechanisms of virus resistance mediated by the main type of viral resistance gene, and will provide the molecular basis for plant disease control.

植物病毒病是重要的植物病害，对农业生产造成巨大损失。对植物抗病毒分子机制的研究有助于植物抗病育种。大多数植物病毒抗性基因与番茄Tm-2(2)基因类似，属于CC-NBS-LRR类型的抗病基因，然而，对该类病毒抗性基因抗病毒的机制了解很少。Tm-2(2)基因抗番茄花叶病毒和烟草花叶病毒，抗性非常持久，应用已近50年，仍在农业生产中广泛应用。最近，我们发展了可以在本生烟草中研究Tm-2(2)基因抗病毒的新系统，并发现J结构域蛋白MIP1和叶绿体蛋白Rubisco小亚基参与Tm-2(2)基因抗病毒。本项目在此基础上，拟从与病毒抗性蛋白Tm-2(2)或对应的无毒蛋白相互作用的植物蛋白，以及表达受病毒抗性调控的microRNA入手，深入研究Tm-2(2)如何介导植物对病毒产生抗性，以及抗性如何被调控。本研究将加深对主要类型的病毒抗性基因抗病毒分子机制的理解，为持久地控制植物病害提供分子依据。

番茄Tm-22基因是一个抗病毒基因，被长期应用于农业生产中。Tm-22编码一个含有CC结构域的NLR蛋白，其通过识别烟草花叶病毒或番茄花叶病毒的运动蛋白激活植物对病毒的极端抗性。本研究阐明了Tm-22定位于细胞质膜，并在在细胞质膜上发挥功能，其发挥作用不依赖于病毒运动蛋白的胞间连丝定位。发现其中CC结构域是信号结构域、NB-ARC结构域在CC结构域的激活中发挥了重要作用。Tm-22的分子内部结构域间存在相互作用。在识别MP之后，被激活的Tm-22分子之间可以形成寡聚体，其寡聚化过程可能依赖于NBS结构域。寡聚化的Tm-22需通过CC结构域激活下游抗病反应。当CC结构域与细胞质膜定位信号融合后，其可以诱导细胞死亡。发现多个寄主因子参与病毒抗性，并阐明了部分分子机制。