Ministry of Education Key Laboratory of Laser Life Science and Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, China.
Plant Physiol. 2012 Oct;160(2):1081-96. doi: 10.1104/pp.112.201798. Epub 2012 Aug 27.
The perception of lipopolysaccharides (LPS) by plant cells can lead to nitric oxide (NO) production and defense gene induction. However, the signaling cascades underlying these cellular responses have not yet been resolved. This work investigated the biosynthetic origin of NO and the role of NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1 (NPR1) to gain insight into the mechanism involved in LPS-induced resistance of Arabidopsis (Arabidopsis thaliana). Analysis of inhibitors and mutants showed that LPS-induced NO synthesis was mainly mediated by an arginine-utilizing source of NO generation. Furthermore, LPS-induced NO caused transcript accumulation of alternative oxidase genes and increased antioxidant enzyme activity, which enhanced antioxidant capacity and modulated redox state. We also analyzed the subcellular localization of NPR1 to identify the mechanism for protein-modulated plant innate immunity triggered by LPS. LPS-activated defense responses, including callose deposition and defense-related gene expression, were found to be regulated through an NPR1-dependent pathway. In summary, a significant NO synthesis induced by LPS contributes to the LPS-induced defense responses by up-regulation of defense genes and modulation of cellular redox state. Moreover, NPR1 plays an important role in LPS-triggered plant innate immunity.
植物细胞对脂多糖 (LPS) 的感知会导致一氧化氮 (NO) 的产生和防御基因的诱导。然而，这些细胞反应背后的信号级联尚未得到解决。本研究调查了 NO 的生物合成起源以及非表达病原体相关基因 1 (NPR1) 的作用，以深入了解 LPS 诱导拟南芥 (Arabidopsis thaliana) 抗性的机制。抑制剂和突变体的分析表明，LPS 诱导的 NO 合成主要是由精氨酸利用的 NO 生成源介导的。此外，LPS 诱导的 NO 导致交替氧化酶基因的转录积累，并增加抗氧化酶活性，从而增强抗氧化能力并调节氧化还原状态。我们还分析了 NPR1 的亚细胞定位，以确定 LPS 触发的蛋白调节植物先天免疫的机制。发现包括胼胝质沉积和防御相关基因表达在内的 LPS 激活的防御反应是通过 NPR1 依赖的途径进行调节的。总之，LPS 诱导的大量 NO 合成通过上调防御基因和调节细胞氧化还原状态来促进 LPS 诱导的防御反应。此外，NPR1 在 LPS 触发的植物先天免疫中发挥重要作用。
