Yanhui Che, Tongtong Yao, Hongrui Wang, Xiaoqian Liu, Zhe Zhang, Zihan Wang, Hongbo Zhang, Ye Yuan, Guoqiang He, Guangyu Sun, Huihui Zhang
Key Laboratory of Saline-alkali Vegetation Ecology Restoration, Ministry of Education, College of Life Sciences, Northeast Forestry University, Harbin 150040, China.
College of Resources and Environment, Northeast Agricultural University, Harbin, Heilongjiang, China.
J Hazard Mater. 2023 Apr 5;447:130792. doi: 10.1016/j.jhazmat.2023.130792. Epub 2023 Jan 13.
The toxicity of bromide to animals and microorganisms has been widely studied, but the mechanism by which bromide toxicity affects plants is rarely studied. This study used the bromophenol compound Tetrabromobisphenol A (TBBPA) as a representative of bromide to explore the physiological and molecular response mechanism of tobacco leaves to TBBPA. In addition, physiological determination, transcriptomics, weighted gene co-expression network analysis (WGCNA) analysis, and random forest prediction model were conducted. The findings from this study indicated that TBBPA limited the photoreaction process by destroying the light-catching antenna protein of tobacco leaves, the activity of the photosystem reaction centers (PSII and PSI), and the linear electron transport efficiency. TBBPA also reduced the rate of the Calvin-Benson cycle by inhibiting the activities of gene such as Rubisco, PGK, and TPI, and finally destroyed the photosynthesis process. Although cyclic electron transport was enhanced under stress conditions, it could not reverse the damage caused by TBBPA on photosynthesis. TBBPA exposure resulted in the accumulation of reactive oxygen species (ROS) in tobacco leaves, and the activities of Superoxide dismutase (SOD), Ascorbate peroxidase (APX), and Glutathione peroxidase (GPX) and their coding genes were significantly down-regulated. Although POD activity and proline (Pro) content were increased, they were insufficient to remove excess O free radicals to relieve ROS stress. WCGNA and random forest models predicted that the damage of TBBPA to the above processes in tobacco was closely related to the increase in abscisic acid (ABA) content. TBBPA affects the Calvin cycle by inducing ABA signal transduction and stomatal closure, which leads to a series of chain reactions, such as electron transport chain obstruction, excess of ROS, decrease in chlorophyll synthesis, and photosystem reaction center damage.
溴化物对动物和微生物的毒性已得到广泛研究，但溴化物毒性影响植物的机制却鲜有研究。本研究以溴酚化合物四溴双酚A（TBBPA）作为溴化物的代表，探讨烟叶对TBBPA的生理和分子响应机制。此外，还进行了生理测定、转录组学、加权基因共表达网络分析（WGCNA）以及随机森林预测模型分析。本研究结果表明，TBBPA通过破坏烟叶的捕光天线蛋白、光合系统反应中心（PSII和PSI）的活性以及线性电子传递效率，限制了光反应过程。TBBPA还通过抑制Rubisco、PGK和TPI等基因的活性，降低了卡尔文-本森循环的速率，最终破坏了光合作用过程。尽管在胁迫条件下循环电子传递增强，但它无法逆转TBBPA对光合作用造成的损害。TBBPA暴露导致烟叶中活性氧（ROS）积累，超氧化物歧化酶（SOD）、抗坏血酸过氧化物酶（APX）和谷胱甘肽过氧化物酶（GPX）的活性及其编码基因显著下调。尽管过氧化物酶（POD）活性和脯氨酸（Pro）含量增加，但它们不足以清除过量的氧自由基以缓解ROS胁迫。WCGNA和随机森林模型预测，TBBPA对烟草上述过程的损害与脱落酸（ABA）含量的增加密切相关。TBBPA通过诱导ABA信号转导和气孔关闭影响卡尔文循环，从而导致一系列连锁反应，如电子传递链受阻、ROS过量、叶绿素合成减少以及光合系统反应中心受损。
