Hendrix Sophie, Iven Verena, Eekhout Thomas, Huybrechts Michiel, Pecqueur Ingeborg, Horemans Nele, Keunen Els, De Veylder Lieven, Vangronsveld Jaco, Cuypers Ann
Environmental Biology, Centre for Environmental Sciences, Hasselt University, Diepenbeek, Belgium.
Department of Plant Biotechnology and Bioinformatics, Ghent University, Ghent, Belgium.
Front Plant Sci. 2020 Apr 3;11:366. doi: 10.3389/fpls.2020.00366. eCollection 2020.
Cadmium (Cd) exposure causes an oxidative challenge and inhibits cell cycle progression, ultimately impacting plant growth. Stress-induced effects on the cell cycle are often a consequence of activation of the DNA damage response (DDR). The main aim of this study was to investigate the role of the transcription factor SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1) and three downstream cyclin-dependent kinase inhibitors of the SIAMESE-RELATED (SMR) family in the Cd-induced DDR and oxidative challenge in leaves of . Effects of Cd on plant growth, cell cycle regulation and the expression of DDR genes were highly similar between the wildtype and mutant. In contrast, mutant leaves displayed a much lower Cd sensitivity within the experimental time-frame and significantly less pronounced upregulations of DDR-related genes, indicating the involvement of SOG1 in the Cd-induced DDR. Cadmium-induced responses related to the oxidative challenge were disturbed in the mutant, as indicated by delayed Cd-induced increases of hydrogen peroxide and glutathione concentrations and lower upregulations of oxidative stress-related genes. In conclusion, our results attribute a novel role to SOG1 in regulating the oxidative stress response and connect oxidative stress to the DDR in Cd-exposed plants.
镉（Cd）暴露会引发氧化应激并抑制细胞周期进程，最终影响植物生长。应激对细胞周期的影响通常是DNA损伤反应（DDR）激活的结果。本研究的主要目的是探究转录因子γ反应抑制因子1（SOG1）以及暹罗相关（SMR）家族的三种下游细胞周期蛋白依赖性激酶抑制剂在镉诱导的DDR及叶片氧化应激中的作用。镉对植物生长、细胞周期调控以及DDR基因表达的影响在野生型和突变体之间高度相似。相比之下，突变体叶片在实验时间范围内对镉的敏感性要低得多，DDR相关基因的上调也明显不那么显著，这表明SOG1参与了镉诱导的DDR。突变体中与氧化应激相关的镉诱导反应受到干扰，这表现为镉诱导的过氧化氢和谷胱甘肽浓度增加延迟以及氧化应激相关基因的上调较低。总之，我们的结果赋予了SOG1在调节氧化应激反应中的新作用，并将氧化应激与镉暴露植物中的DDR联系起来。
