Lv Feifei, Zhou Jun, Zeng Lizhang, Xing Da
MOE Key Laboratory of Laser Life Science and Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, China.
MOE Key Laboratory of Laser Life Science and Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, China
J Exp Bot. 2015 Aug;66(15):4719-32. doi: 10.1093/jxb/erv231. Epub 2015 May 21.
β-cyclocitral (β-CC), a volatile oxidized derivative of β-carotene, can upregulate the expression of defence genes to enhance excess light (EL) acclimation. However, the signalling cascades underlying this process remain unclear. In this study, salicylic acid (SA) is involved in alleviating damage to promote β-CC-enhanced EL acclimation. In early stages of EL illumination, β-CC pretreatment induced SA accumulation and impeded reactive oxygen species (ROS) production in the chloroplast. A comparative analysis of two SA synthesis pathways in Arabidopsis revealed that SA concentration mainly increased via the isochorismate synthase 1 (ICS1)-mediated isochorismate pathway, which depended on essential regulative function of enhanced disease susceptibility 1 (EDS1). Further results showed that, in the process of β-CC-enhanced EL acclimation, nuclear localization of nonexpressor of pathogenesis-related genes 1 (NPR1) was regulated by SA accumulation and NPR1 induced subsequent transcriptional reprogramming of gluthathione-S-transferase 5 (GST5) and GST13 implicated in detoxification. In summary, β-CC-induced SA synthesis contributes to EL acclimation response by decreasing ROS production in the chloroplast, promoting nuclear localization of NPR1, and upregulating GST transcriptional expression. This process is a possible molecular regulative mechanism of β-CC-enhanced EL acclimation.
β-环柠檬醛（β-CC）是β-胡萝卜素的一种挥发性氧化衍生物，可上调防御基因的表达以增强对过剩光（EL）的适应性。然而，这一过程背后的信号级联反应仍不清楚。在本研究中，水杨酸（SA）参与减轻损伤以促进β-CC增强的EL适应性。在EL光照的早期阶段，β-CC预处理诱导了SA积累，并抑制了叶绿体中活性氧（ROS）的产生。对拟南芥中两条SA合成途径的比较分析表明，SA浓度主要通过异分支酸合酶1（ICS1）介导的异分支酸途径增加，这依赖于增强的疾病易感性1（EDS1）的重要调节功能。进一步的结果表明，在β-CC增强的EL适应性过程中，病程相关基因非表达子1（NPR1）的核定位受SA积累的调节，并且NPR1诱导了随后参与解毒的谷胱甘肽-S-转移酶5（GST5）和GST13的转录重编程。总之，β-CC诱导的SA合成通过降低叶绿体中的ROS产生、促进NPR1的核定位以及上调GST转录表达，有助于EL适应性反应。这一过程是β-CC增强的EL适应性的一种可能的分子调节机制。
