Abstract：
Stomatal immunity plays an important role during bacterial pathogen invasion. Abscisic acid (ABA) induces plants to close their stomata and halt pathogen invasion, but many bacterial pathogens secrete phytotoxin coronatine (COR) to antagonize ABA signaling and reopen the stomata to promote infection at early stage of invasion. However, the underlining mechanism is not clear. SAD2 is an importin β family protein, and the sad2 mutant shows hypersensitivity to ABA. We discovered ABI1, which negatively regulated ABA signaling and reduced plant sensitivity to ABA, was accumulated in the plant nucleus after COR treatment. This event required SAD2 to import ABI1 to the plant nucleus. Abolition of SAD2 undermined ABI1 accumulation. Our study answers the long-standing question of how bacterial COR antagonizes ABA signaling and reopens plant stomata during pathogen invasion.
摘要：
气孔免疫在细菌病原体入侵中起着重要作用。脱落酸（ABA）诱导植物关闭气孔并阻止病原体入侵，但是许多细菌病原体分泌植物毒素冠状蛋白（COR）来拮抗ABA信号并重新打开气孔以促进入侵早期的感染。然而,强调机制尚不清楚。SAD2是一种输入蛋白β家族蛋白，sad2突变体对ABA表现出超敏反应。我们发现ABI1负调控ABA信号并降低植物对ABA的敏感性,COR处理后在植物核中积累。此事件需要SAD2将ABI1导入植物核。SAD2的废除破坏了ABI1的积累。我们的研究回答了长期以来的问题，即细菌COR如何在病原体入侵期间拮抗ABA信号并重新打开植物气孔。
