Abscisic acid plays a key role in the mechanism of photosynthetic and physiological response effect of Tetrabromobisphenol A on tobacco

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 O2·- 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.