Chi Yuan, Wang Chao, Wang Mengyun, Wan Di, Huang Feifei, Jiang Zhonghao, Crawford Bridget M, Vo-Dinh Tuan, Yuan Fang, Wu Feihua, Pei Zhen-Ming
College of Life Sciences, Zhejiang University, Hangzhou, China.
Department of Biology, Duke University, Durham, North Carolina, USA.
Plant Cell Environ. 2021 Dec;44(12):3563-3575. doi: 10.1111/pce.14186. Epub 2021 Sep 30.
The flagellin epitope flg22, a pathogen-associated molecular pattern (PAMP), binds to the receptor-like kinase FLAGELLIN SENSING2 (FLS2), and triggers Ca influx across the plasma membrane (PM). The flg22-induced increases in cytosolic Ca concentration ([Ca ] ) (FICA) play a crucial role in plant innate immunity. It's well established that the receptor FLS2 and reactive oxygen species (ROS) burst undergo sensitivity adaptation after flg22 stimulation, referred to as desensitization and resensitization, to prevent over responses to pathogens. However, whether FICA also mount adaptation mechanisms to ensure appropriate and efficient responses against pathogens remains poorly understood. Here, we analysed systematically [Ca ] increases upon two successive flg22 treatments, recorded and characterized rapid desensitization but slow resensitization of FICA in Arabidopsis thaliana. Pharmacological analyses showed that the rapid desensitization might be synergistically regulated by ligand-induced FLS2 endocytosis as well as the PM depolarization. The resensitization of FICA might require de novo FLS2 protein synthesis. FICA resensitization appeared significantly slower than FLS2 protein recovery, suggesting additional regulatory mechanisms of other components, such as flg22-related Ca permeable channels. Taken together, we have carefully defined the FICA sensitivity adaptation, which will facilitate further molecular and genetic dissection of the Ca -mediated adaptive mechanisms in PAMP-triggered immunity.
鞭毛蛋白表位flg22是一种病原体相关分子模式（PAMP），它与类受体激酶鞭毛蛋白感知2（FLS2）结合，并触发钙离子跨质膜（PM）内流。flg22诱导的胞质钙离子浓度（[Ca²⁺]）升高（FICA）在植物先天免疫中起关键作用。众所周知，受体FLS2和活性氧（ROS）爆发在flg22刺激后会经历敏感性适应，即脱敏和再敏化，以防止对病原体的过度反应。然而，FICA是否也会启动适应机制以确保对病原体做出适当而有效的反应，目前仍知之甚少。在此，我们系统分析了拟南芥在连续两次flg22处理后的[Ca²⁺]升高情况，记录并表征了FICA的快速脱敏但缓慢再敏化现象。药理学分析表明，快速脱敏可能由配体诱导的FLS2内吞作用以及质膜去极化协同调节。FICA的再敏化可能需要从头合成FLS2蛋白。FICA再敏化明显慢于FLS2蛋白恢复，这表明存在其他成分（如flg22相关的钙离子通透通道）的额外调节机制。综上所述，我们仔细定义了FICA敏感性适应，这将有助于进一步从分子和遗传学角度剖析PAMP触发免疫中钙离子介导的适应机制。
