Abstract：
Microbial plant pathogens deploy amphipathic cyclic lipopeptides to reduce surface tension in their environment. While plants can detect these molecules to activate cellular stress responses, the role of these lipopeptides or associated host responses in pathogenesis are not fully clear. The gramillin cyclic lipopeptide is produced by the Fusarium graminearum fungus and is a virulence factor and toxin in maize. Here, we show that gramillin promotes virulence and necrosis in both monocots and dicots by disrupting ion balance across membranes. Gramillin is a cation-conducting ionophore and causes plasma membrane depolarization. This disruption triggers cellular signaling, including a burst of reactive oxygen species (ROS), transcriptional reprogramming, and callose production. Gramillin-induced ROS depends on expression of host ILK1 and RBOHD genes, which promote fungal induction of virulence genes during infection and host susceptibility. We conclude that gramillin\'s ionophore activity targets plant membranes to coordinate attack by the F. graminearum fungus.
摘要：
微生物植物病原体部署两亲性环状脂肽以降低其环境中的表面张力。虽然植物可以检测到这些分子来激活细胞应激反应，这些脂肽或相关宿主反应在发病机制中的作用尚不完全清楚。禾本科青霉素环脂肽由禾本科镰刀菌真菌产生，是玉米中的毒力因子和毒素。这里,我们表明，gramillin通过破坏膜间的离子平衡来促进单子叶植物和双子叶植物的毒力和坏死。格拉姆林是阳离子传导离子载体，可引起质膜去极化。这种中断触发了蜂窝信号，包括活性氧（ROS）的爆发，转录重编程，和callose生产。格拉姆林诱导的ROS依赖于宿主ILK1和RBOHD基因的表达，在感染和宿主易感性过程中促进真菌对毒力基因的诱导。我们得出的结论是，gramillin的离子载体活性靶向植物膜，以协调F.graminearum真菌的攻击。
