Xiao Lin, Ma Wenna, Zhang Jiarong, Pu Xiaojun, Rengel Zed, Song Zhongbang, Chen Qi
Faculty of Life Science and Technology, Kunming University of Science and Technology, 650500, Kunming, China.
Faculty of Life Science and Technology, Kunming University of Science and Technology, 650500, Kunming, China; Yunnan Modern Professional Technology College, 675000, Chuxiong, China.
J Plant Physiol. 2023 May;284:153977. doi: 10.1016/j.jplph.2023.153977. Epub 2023 Mar 28.
Flavonols are well-known antioxidants that prevent stomatal closure via interfering with ROS signaling. Phytomelatonin regulates stomatal closure, but the signaling pathways are still largely unknown. Here, we investigated the role of flavonols in phytomelatonin-mediated stomatal closure in tobacco plants. The application of melatonin induced stomatal closure through NADPH oxidase-mediated ROS production. Transgenic tobacco plants overexpressing soybean GmSNAT1 (coding for serotonin N-acetyltransferase that catalyzes the penultimate step in phytomelatonin biosynthesis) had higher phytomelatonin concentration, accumulated more ROS in guard cells and were more sensitive to melatonin-induced stomatal closure than the wild-type plants, which was associated with the higher expression of PMTR1-homologous genes. Exogenous melatonin decreased flavonol concentrations in guard cells and the expression of flavonoid-related genes in wild-type and transgenic tobacco plants, and these inhibitory effects were more obvious in GmSNAT1-overexpressing plants than the wild type. However, the melatonin-mediated stomatal closure and ROS production were diminished by the application of kaempferol (a type of flavonol). Additionally, transgenic tobacco plants with increased expression of NtFLS (encoding flavonol synthase) were less sensitive to melatonin-induced stomatal closure. In conclusion, phytomelatonin hampers the biosynthesis of flavonols in guard cells, which results in high concentration of ROS and induces stomatal closure in tobacco plants.
黄酮醇是众所周知的抗氧化剂，可通过干扰活性氧信号传导来阻止气孔关闭。植物褪黑素调节气孔关闭，但其信号通路仍 largely 未知。在此，我们研究了黄酮醇在植物褪黑素介导的烟草植株气孔关闭中的作用。褪黑素的施用通过 NADPH 氧化酶介导的活性氧产生诱导气孔关闭。过表达大豆 GmSNAT1（编码催化植物褪黑素生物合成倒数第二步的血清素 N-乙酰转移酶）的转基因烟草植株具有更高的植物褪黑素浓度，保卫细胞中积累更多的活性氧，并且比野生型植株对褪黑素诱导的气孔关闭更敏感，这与 PMTR1 同源基因的高表达有关。外源褪黑素降低了野生型和转基因烟草植株保卫细胞中的黄酮醇浓度以及类黄酮相关基因的表达，并且这些抑制作用在过表达 GmSNAT1 的植株中比野生型更明显。然而，山奈酚（一种黄酮醇）的施用减弱了褪黑素介导的气孔关闭和活性氧产生。此外，NtFLS（编码黄酮醇合酶）表达增加的转基因烟草植株对褪黑素诱导的气孔关闭不太敏感。总之，植物褪黑素阻碍了保卫细胞中黄酮醇的生物合成，这导致活性氧浓度升高并诱导烟草植株气孔关闭。
