The phytotoxicity of exposure to two polybrominated diphenyl ethers (BDE47 and BDE209) on photosynthesis and the response of the hormone signaling and ROS scavenging system in tobacco leaves

Abstract

To reveal the response and adaptative mechanism of plants to the organic pollutants PBDEs, physiological and transcriptomic techniques were used to study the effects of exposure to BDE47 and BDE209 on tobacco (Nicotiana tabacum L.) plant growth, physiological function and response of key genes. Exposure to both BDE47 and BDE209 inhibited the growth of tobacco plants. The number of down-regulated DEGs following exposure to BDE47 was significantly higher than that following exposure to BDE209. Enrichment analysis using the KEGG showed that BDE47 and BDE209 primarily affected tobacco leaf photosynthesis-antenna proteins, photosynthesis, plant hormone signal transduction and α-linolenic acid metabolism. BDE47 primarily inhibits the synthesis of Chl a, and BDE209 has a more significant impact on Chl b. Most photosynthesis-related DEGs were concentrated in PSII and PSI; the number of down-regulated DEGs in PSI was significantly higher than that in PSII, and the range in which the PSI activity was reduced was also higher than that of PSII, i.e., PSII and PSI (particularly PSI) were sensitive to the effects of exposure to BDE47 and BDE209 on photosynthesis. The increase of the ratio of regulatory energy dissipation played an important protective role in alleviating the photoinhibition of PSII. Exposure to BDE47 and BDE209 can lead to the accumulation of ROS in tobacco leaves, but correspondingly, the activities of antioxidant enzymes SOD, POD, CAT, APX and GPX and the up-regulated expression of their coding genes play an important role in preventing excessive oxidative damage. Exposure to BDE47 and BDE209 promoted the up-regulation of gene expression related to Pro synthesis. In particular, the Pro synthetic process of the Orn pathway was promoted. Exposure to BDE47 and BDE209 induced the up-regulated expression of genes related to the synthesis of ABA and JA, promoted the synthesis of ABA and JA, and activated ABA and JA signal transduction pathways. In conclusion, both BDE47 and BDE209 inhibit the synthesis of chlorophyll and hinder the process of light energy capture and electron transfer in tobacco leaves. BDE47 was more toxic than BDE209. However, tobacco leaves can also adapt to BDE47 and BDE209 by regulating the antioxidant system, accumulating Pro and initiating the hormone signal transduction process. The results of this study provide a theoretical basis for the phytotoxicity mechanism of PBDEs.