Polybrominated diphenyl ethers (PBDEs) are ubiquitously distributed persistent organic pollutants (POPs) in marine environments. Phytoplankton are the entrance of PBDEs entering to biotic environments from abiotic environments, while the responding mechanisms of phytoplankton to PBDEs have not been full established. Therefore, we chose the model diatom Thalassiosira pseudonana in this study, by integrating whole transcriptome analysis with physiological-biochemical data, to reveal the molecular responding mechanisms of T. pseudonana to the toxicity of BDE-47. Our results indicated the changes of genes expressions correlated to the physiological-biochemical changes, and there were multiple molecular mechanisms of T. pseudonana responding to the toxicity of BDE-47: Gene expressions evidence explained the suppression of light reaction and proved the occurrence of cellular oxidative stress; In the meanwhile, up-regulations of genes in pathways involving carbon metabolisms happened, including the Calvin cycle, glycolysis, TCA cycle, fatty acid synthesis, and triacylglycerol synthesis; Lastly, DNA damage was found and three outcome including DNA repair, cell cycle arrest and programmed cell death (PCD) happened, which could finally inhibit the cell division and population growth of T. pseudonana. This study presented the most complete molecular responding mechanisms of phytoplankton cells to PBDEs, and provided valuable information of various PBDEs-sensitive genes with multiple functions for further research involving organic pollutants and phytoplankton.

多溴二苯醚（PBDEs）是海洋环境中普遍分布的持久性有机污染物（POPs）。浮游植物是多溴二苯醚从非生物环境进入生物环境的入口，而浮游植物对多溴二苯醚的反应机制尚未完全建立。因此，在本研究中，我们通过将整个转录组分析与生理生化数据相结合，选择了模型硅藻Thalassiosira pseudonana，以揭示拟南芥对BDE-47毒性的分子响应机制。我们的研究结果表明基因表达的变化与生理生化变化有关，并且假单胞菌存在多种分子机制。对BDE-47的毒性反应：基因表达的证据解释了光反应的抑制，并证明了细胞氧化应激的发生。同时，涉及碳代谢的途径中的基因发生了上调，包括加尔文循环，糖酵解，TCA循环，脂肪酸合成和三酰基甘油合成。最后，发现了DNA损伤，并发生了DNA修复，细胞周期停滞和程序性细胞死亡（PCD）三项结果，这些结果最终可以抑制拟南芥的细胞分裂和种群增长。。这项研究提出了最完整的浮游植物细胞对PBDEs的分子反应机制，并为各种对PBDEs敏感的具有多种功能的基因提供了有价值的信息，以进一步研究有机污染物和浮游植物。