组蛋白修饰因子调控植物病毒感染的分子机理

组蛋白甲基化和泛素化是决定染色质构象与基因转录状态的关键因素，它由组蛋白甲基化酶/泛素化酶与去甲基化酶/去泛素化酶动态调控。DNA病毒在宿主细胞复制过程中形成微小染色体结构，也受以染色质为模板的表观遗传机制调控。我们前期研究发现组蛋白去甲基化酶jmj24突变体对双生病毒不敏感，JMJ24与病毒蛋白AC2互作并增强其稳定性，通过IP-MS等技术我们发现去泛素化酶UBP12/13与特异病毒蛋白互作，本项目将利用蛋白质质谱及生化与分子遗传手段对JMJ24和UBP12/13在植物病毒感染过程的分子机理进行深入研究：1）JMJ24及UBP12/13响应病毒感染的遗传基础；2）JMJ24及UBP12/13调控病毒蛋白AC2稳定性或者病毒核小体组蛋白修饰的生化遗传机理；3）JMJ24及UBP12/13调控病毒感染的功能普遍性。本研究将深化我们对植物病毒与宿主的相互作用的了解，为病毒防御提供新的策略。

Histone methylation (or ubiquitination), which is dynamically regulated by histone methylases (or ubiquitinases) and histone demethylases (or deubiquitinases), is a key determinant of chromatin configuration to control transcriptional competency. DNA viruses form minichromosomes when they replicated in host cells, which are regulated by chromatin-based epigenetic machinery. We have found that JMJ24, a putative histone demethylase, interacted with and stabilized a viral protein AC2, and the jmj24 mutant resistant to virus infection in a preliminary investigation. We also found that viral protein interact with deubiquitinase UBP12/13. In this project we will investigate the molecular mechanisms of JMJ24 and UBP12/13 in regulation of plant virus infection with Mass Spectrometer, biochemistry and molecular genetics technology: 1) Genetic pathways by which the JMJ24 and UBP12/13 in response to virus infection; 2) Investigation molecular mechanisms of JMJ24 and UBP12/13 to stabilize virus protein or control histone modifications of viral minichromosomes; 3) The generality of JMJ24 and UBP12/13 in regulation of virus infection. From the study, we will get more knowledge on the molecular mechanisms of virus-host interactions and find new strategy to control viral diseases.