作为一种保守的细胞内降解途径, 自噬在动物病毒和植物病毒侵染过程中通常能够发挥防御作用。前期, 我们首次发现植物RNA病毒的侵染抑制了自噬的发生,大麦条纹花叶病毒 (BSMV) 编码的多功能蛋白γb与自噬通路的关键蛋白ATG7在体内和体外直接互作,竞争性地干扰了ATG7和ATG8的互作,从而抑制了自噬介导的抗病毒作用,进而促进了BSMV的侵染。在此基础上,我们新发现BSMV复制酶γa的表达能抑制自噬小泡的降解,筛选并验证了液泡氢离子ATP酶B2亚基 (VAB2) 与γa蛋白互作。因此,本申请项目拟以VAB2与γa互作为切入点,重点深入分析γa蛋白抑制自噬活性的分子机制,解析同一种病毒的不同蛋白 (γa和γb) 抑制寄主自噬的不同策略。研究结果将有助于深入理解植物RNA病毒侵染与寄主自噬之间的相互关系并为寄主防御与病毒反防御的博弈提供新的科学证据。

Autophagy is a eukaryotic mechanism that removes damaged or unwanted cellular materials, and is a conserved defense strategy against virus infection. Recently, we have reported that the multifunctional γb protein from Barley stripe mosaic virus (BSMV) could suppress plant autophagy pathway by competitively interacting with the autophagy key factor ATG7 and promote BSMV infection. Upon this, we have confirmed that the expression of BSMV RNA-dependent RNA polymerase γa could inhibit autophagy. We also found that the host factor vacuolar-type H+-ATPase subunit B2 (VAB2) interacted with BSMV γa protein. Based on these data, the relationship between γa protein and autophagy will be further analyzed, thus illustrating the roles of VAB2-γa interaction played in the inhibition of autophagy and the accumulation of autophagosomes as well as the different autophagy-inhibition strategies by γa and γb. These results would reveal the relationship between plant RNA virus and autophagy pathway and provide new insights into the host defense and virus counter-defense arm race.