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.

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.

Physiological and proteomics responses of nitrogen assimilation and glutamine/glutamine family of amino acids metabolism in mulberry (Morus alba L.) leaves to NaCl and NaHCO3 stress.

In order to find out the response mechanism of nitrogen assimilation and glutamine/glutamine family of amino acids metabolism in mulberry (Morus alba L.) leaves under NaCl and NaHCO3 stress, and to reveal its role in salt alkali adaptation. The effects of the nitrogen metabolism of mulberry leaves were studied under 100 mmol L-1 NaCl and NaHCO3 stress.The results showed that the activity of NR and the content of TN and SP did not change significantly, the expression of NiR, Fd-NiR, Fd-NiR gene and theactivity of NiR increased significantly under NaCl stress, but nitrogen assimilation was inhibited under NaHCO3 stress. NaCl stress had no significant effect on the expression and activity of GS and GOGAT in mulberry leaves. Under NaHCO3 stress, the expression of Fd-GOGAT, Fd-GOGAT2, Fd-GOGAT gene, and the activity of GS and GOGAT were significantly decreased. NaCl stress can promote the accumulation of Pro, Put and Spd in mulberry leaves. The accumulation of Pro under NaHCO3 stress is greater than that under NaCl stress. NaCl stress also induced the up-regulation of GAD, GAD1 and GAD1 gene expression, so promoting the synthesis of GABA may be an adaptive mechanism for mulberry to cope with NaCl stress, but the expression of GAD did not change significantly and GAD gene expression lower than CK under NaHCO3 stress. Although both NaCl and NaHCO3 stress could promote the synthesis of GSH by up-regulation of GCLM expression, GSH under NaHCO3 stress was significantly higher than that under NaCl stress, the content of H2O2 was still significantly higher than that of NaCl stress, that means GSH may not play a key role in alleviating the oxidative damage in mulberry leaves caused by salt and alkali.

Toxic effects of heavy metal Cd and Zn on chlorophyll, carotenoid metabolism and photosynthetic function in tobacco leaves revealed by physiological and proteomics analysis.

To explore the mechanisms underlying the action of the heavy metals Cd and Zn on the photosynthetic function of plant leaves, the effects of 100 µmol L-1 Cd and 200 µmol L-1 Zn stress (the exposure concentrations of Cd and Zn in the culture medium were 2.24 mg kg-1 and 5.36 mg kg-1) on the chlorophyll and carotenoid contents as well as the photosynthetic function of tobacco leaves (Long Jiang 911) were studied. The key proteins in these physiological processes were quantitatively analyzed using a TMT-based proteomics approach. Cd stress was found to inhibit the expression of key enzymes during chlorophyll synthesis in leaves, resulting in a decrease of the Chl content. However, Zn stress did not significantly influence the chlorophyll content. Leaves adapted to Zn stress by upregulating CAO expression and increase the Chl b content. Although the Car content in leaves did not significantly change under either Cd or Zn stress, the expressions of ZE and VDE during Car metabolism decreased significantly under Cd stress. This was accompanied by damages to the xanthophyll cycle and the NPQ-dependent energy dissipation mechanism. In contrast, under Zn stress, leaves adapted to Zn stress by increasing the expression of VDE, thus improving NPQ. Under Cd stress, the expressions of three sets of proteins were significantly down-regulated, including PSII donor-side proteins (PPD3, PPD6, OEE1, OEE2-1, OEE2-2, OEE2-3, and OEE3-2), receptor-side proteins (D1, D2, CP43, CP47, Cyt b559α, Cyt b559ß, PsbL, PsbQ, PsbR, Psb27-H1, and Psb28), and core proteins of the PSI reaction center (psaA, psaB, psaC, psaD, psaE-A, PsaE-B, psaF, psaG, psaH-1, psaK, psaL, psaN, and psaOL). In comparison, only eight of the above proteins (PPD6, OEE3-2, PsbL, PsbQ, Psb27-H1, psaL, and psaOL) were significantly down-regulated by Zn stress. Under Cd stress, both the donor side and the receptor side of PSII were damaged, and PSII and PSI experienced severe photoinhibition. However, Zn stress did not decrease either PSII or PSI activities in tobacco leaves. In addition, the expression of electron transport-related proteins (cytb6/f complex, PC, Fd, and FNR), ATPase subunits, Rubisco subunits, and RCA decreased significantly in leaves under Cd stress. However, no significant changes were observed in any of these proteins under Zn stress. Although Cd stress was found to up-regulate the expressions of PGRL1A and PGRL1B and induce an increase of PGR5/PGRL1-CEF in tobacco leaves, NDH-CEF was significantly inhibited. Under Zn stress, the expressions of ndhH and PGRL1A in leaves were significantly up-regulated, but there were no significant changes in either NDH-CEF or PGR5/PGRL-CEF. Under Cd stress, the expressions of proteins related to Fd-dependent nitrogen metabolism and reactive oxygen species (ROS) scavenging processes (e.g., FTR, Fd-NiR, and Fd-GOGAT) were significantly down-regulated in leaves. However, no significant changes of any of the above proteins were identified under Zn stress. In summary, Cd stress could inhibit the synthesis of chlorophyll in tobacco leaves, significantly down-regulate the expressions of photosynthesis-related proteins or subunits, and suppress both the xanthophyll cycle and NDH-CEF process. The expressions of proteins related to the Fd-dependent nitrogen metabolism and ROS scavenging were also significantly down-regulated, which blocked the photosynthetic electron transport, thus resulting in severe photoinhibition of both PSII and PSI. However, Zn stress had little effect on the photosynthetic function of tobacco leaves.

Overexpression of Trx CDSP32 gene promotes chlorophyll synthesis and photosynthetic electron transfer and alleviates cadmium-induced photoinhibition of PSII and PSI in tobacco leaves.

Cadmium stress causes a decrease in chlorophyll content and inhibits photosynthesis in tobacco leaves. The role of thioredoxin-like protein CDSP32 expressed in plant chloroplasts is to alleviates the reduced enzymes expression involved in chlorophyll synthesis of tobacco leaves due to Cd exposure, effectively preventing chlorophyll degradation and promoting increased tobacco biomass. Overexpression of Trx CDSP32 can protect the oxygen-evolving complex on the PSII donor side and promote electron transfer on the PSII acceptor side of tobacco leaves under Cd stress. Trx CDSP32 not only significantly increase the PSI activity of tobacco leaves, but also alleviate cadmium-induced PSI photoinhibition. Although Trx CDSP32 has no significant effect on the expression of PC and FNR proteins in tobacco leaves under Cd stress, it can alleviate the decreased expression of protein subunits involved in photosynthetic electron transfer such as Cyt b6/f complex subunits, Fd, and ATP synthase subunits. Trx CDSP32 can promote the synthesis of chlorophyll, stabilize the electron transfer chain, and promote ATP synthase activity to alleviate cadmium-induced photoinhibition of PSII and PSI in tobacco leaves.