Pseudomonas syringae pv. tabaci (Pst), which is the pathogen responsible for tobacco wildfire disease, has received considerable attention in recent years. The objective of this study was to clarify the responses of photosystem I (PSI) and photosystem II (PSII) to Pst infection in tobacco leaves. The net photosynthetic rate (Pn) and carboxylation efficiency (CE) were inhibited by Pst infection. The normalized relative variable fluorescence at the K step (W k) and the relative variable fluorescence at the J step (V J) increased while the maximal quantum yield of PSII (F v/F m) and the density of Q A-reducing PSII reaction centers per cross section (RC/CSm) decreased, indicating that the reaction centers, and the donor and acceptor sides of PSII were all severely damaged after Pst infection. The PSI activity decreased as the infection progressed. Furthermore, we observed a considerable overall degradation of PsbO, D1, PsaA proteins and an over-accumulation of reactive oxygen species (ROS). Photoinhibition and photoinhibition-like damage were observed under light and dark conditions, respectively, after Pst infection of tobacco leaves. The damage was greater in the dark. ROS over-accumulation was not the primary cause of the photoinhibition and photoinhibition-like damage. The PsbO, D1 and PsaA proteins appear to be the targets during Pst infection under light and dark conditions.

Background: Glycine soja is a halophytic soybean native to saline soil in Yellow River Delta, China. Photosystem I (PSI) performance and the interaction between photosystem II (PSII) and PSI remain unclear in Glycine soja under salt stress. This study aimed to explore salt adaptability in Glycine soja in terms of photosystems coordination. Results: Potted Glycine soja was exposed to 300 mM NaCl for 9 days with a cultivated soybean, Glycine max, as control. Under salt stress, the maximal photochemical efficiency of PSII (Fv/Fm) and PSI (△MR/MR₀) were significantly decreased with the loss of PSI and PSII reaction center proteins in Glycine max, and greater PSI vulnerability was suggested by earlier decrease in △MR/MR₀ than Fv/Fm and depressed PSI oxidation in modulated 820 nm reflection transients. Inversely, PSI stability was defined in Glycine soja, as △MR/MR₀ and PSI reaction center protein abundance were not affected by salt stress. Consistently, chloroplast ultrastructure and leaf lipid peroxidation were not affected in Glycine soja under salt stress. Inhibition on electron flow at PSII acceptor side helped protect PSI by restricting electron flow to PSI and seemed as a positive response in Glycine soja due to its rapid recovery after salt stress. Reciprocally, PSI stability aided in preventing PSII photoinhibition, as the simulated feedback inhibition by PSI inactivation induced great decrease in Fv/Fm under salt stress. In contrast, PSI inactivation elevated PSII excitation pressure through inhibition on PSII acceptor side and accelerated PSII photoinhibition in Glycine max, according to the positive and negative correlation of △MR/MR₀ with efficiency that an electron moves beyond primary quinone and PSII excitation pressure respectively. Conclusion: Therefore, photosystems coordination depending on PSI stability and rapid response of PSII acceptor side contributed to defending salt-induced oxidative stress on photosynthetic apparatus in Glycine soja. Photosystems interaction should be considered as one of the salt adaptable mechanisms in this halophytic soybean.

Bisphenol A (BPA), a widely distributed pollutant, suppresses photosynthesis in leaves. In previous studies on higher plants, the plants were treated by BPA through irrigation to root. This method cannot distinguish whether the BPA directly suppresses photosynthesis in leaves, or indirectly influences photosynthesis through affecting the function of root. Here, only the leaves but not the roots of cucumber were infiltrated with BPA solution. The photosystem II and I (PSII, PSI) were insensitive to BPA under darkness. BPA aggravated the PSII but not the PSI photoinhibition under light. BPA also inhibited CO₂ assimilation, and the effect of BPA on PSII photoinhibition disappeared when the CO₂ assimilation was blocked. The H₂O₂ accumulated in BPA-treated leaves under light. And the BPA-caused PSII photoinhibition was prevented under low (2%) O₂. We also proved that the BPA-caused PSII photoinhibition depend on the turnover of D1 protein. In conclusion, this study proved that BPA could directly suppress photosynthesis in leaves, however, BPA does not damage PSII directly, but inhibits CO₂ assimilation and over-reduces the electron transport chain under light, which increases the production of reactive oxygen species (H₂O₂), the over-accumulated ROS inhibits the turnover of D1 protein and consequently aggravates PSII photoinhibition.