Institute of Ecology and Evolutionary Biology, National Taiwan University, Taipei, Taiwan; Institute of Plant Biology, National Taiwan University, Taipei, Taiwan; Molecular and Biological Agricultural Sciences Program, Taiwan International Graduate Program, Academia Sinica, Taipei, Taiwan.
Research Center for Chinese Herbal Medicine, Graduate Institute of Healthy Industry Technology, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, Taiwan.
Plant Sci. 2024 Jun;343:112071. doi: 10.1016/j.plantsci.2024.112071. Epub 2024 Mar 19.
The S-locus lectin receptor kinases (G-LecRKs) have been suggested as receptors for microbe/damage-associated molecular patterns (MAMPs/DAMPs) and to be involved in the pathogen defense responses, but the functions of most G-LecRKs in biotic stress response have not been characterized. Here, we identified a member of this family, G-LecRK-I.2, that positively regulates flg22- and Pseudomonas syringae pv. tomato (Pst) DC3000-induced stomatal closure. G-LecRK-I.2 was rapidly phosphorylated under flg22 treatment and could interact with the FLS2/BAK1 complex. Two T-DNA insertion lines, glecrk-i.2-1 and glecrk-i.2-2, had lower levels of reactive oxygen species (ROS) and nitric oxide (NO) production in guard cells, as compared with the wild-type Col-0, under Pst DC3000 infection. Also, the immunity marker genes CBP60g and PR1 were induced at lower levels under Pst DC3000 hrcC infection in glecrk-i.2-1 and glecrk-i.2-2. The GUS reporter system also revealed that G-LecRK-I.2 was expressed only in guard cells. We also found that G-LecRK-I.2 could interact H-ATPase AHA1 to regulate H-ATPase activity in the guard cells. Taken together, our results show that G-LecRK-I.2 plays an important role in regulating stomatal closure under flg22 and Pst DC3000 treatments and in ROS and NO signaling specifically in guard cells.
S 基因座凝集素受体激酶（G-LecRKs）被认为是微生物/损伤相关分子模式（MAMPs/DAMPs）的受体，并参与病原体防御反应，但大多数 G-LecRKs 在生物胁迫反应中的功能尚未得到表征。在这里，我们鉴定了该家族的一个成员，G-LecRK-I.2，它正向调控 flg22 和丁香假单胞菌 pv。番茄（Pst）DC3000 诱导的气孔关闭。G-LecRK-I.2 在 flg22 处理下迅速磷酸化，并能与 FLS2/BAK1 复合物相互作用。两个 T-DNA 插入系，glecrk-i.2-1 和 glecrk-i.2-2，与野生型 Col-0 相比，在 Pst DC3000 感染下，保卫细胞中活性氧（ROS）和一氧化氮（NO）的产生水平较低。此外，在 glecrk-i.2-1 和 glecrk-i.2-2 中，免疫标记基因 CBP60g 和 PR1 的诱导水平也较低，而在 Pst DC3000 hrcC 感染下。GUS 报告系统还表明，G-LecRK-I.2 仅在保卫细胞中表达。我们还发现 G-LecRK-I.2 可以与 H-ATPase AHA1 相互作用，以调节保卫细胞中的 H-ATPase 活性。总之，我们的结果表明，G-LecRK-I.2 在 flg22 和 Pst DC3000 处理下调节气孔关闭以及在保卫细胞中特异性调节 ROS 和 NO 信号转导中起重要作用。
