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Major research on photosynthesis has been carried out under steady light. However, in the natural environment, steady light is rare, and light intensity is always changing. Changing light affects (usually reduces) photosynthetic carbon assimilation and causes decreases in biomass and yield. Ecologists first observed the importance of changing light for plant growth in the understory; other researchers noticed that changing light in the crop canopy also seriously affects yield. Here, we review the effects of environmental and non-environmental factors on dynamic photosynthetic carbon assimilation under changing light in higher plants. In general, dynamic photosynthesis is more sensitive to environmental and non-environmental factors than steady photosynthesis, and dynamic photosynthesis is more diverse than steady photosynthesis. Finally, we discuss the challenges of photosynthetic research under changing light.

Abstract Background Plants are always exposed to dynamic light. The photosynthetic light use efficiency of leaves is lower in dynamic light than in uniform irradiance. Research on the influence of environmental factors on dynamic photosynthesis is very limited. Nitrogen is critical for plants, especially for photosynthesis. Low nitrogen (LN) decreases ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) and thus limits photosynthesis. The decrease in Rubisco also delays photosynthetic induction in LN leaves; therefore, we hypothesized that the difference of photosynthetic CO2 fixation between uniform and dynamic light will be greater in LN leaves compared to leaves with sufficient nitrogen supply. Results To test this hypothesis, soybean plants were grown under low or high nitrogen (HN), and the photosynthetic gas exchange, enzyme activity and protein amount in leaves were measured under uniform and dynamic light. Unexpectedly, dynamic light caused less photosynthetic suppression, rather than more, in LN leaves than in HN leaves. The underlying mechanism was also clarified. Short low-light (LL) intervals did not affect Rubisco activity but clearly deactivated fructose-1,6-bisphosphatase (FBPase) and sedoheptulose-1,7-bisphosphatase (SBPase), indicating that photosynthetic induction after a LL interval depends on the reactivation of FBPase and SBPase rather than Rubisco. In LN leaves, the amount of Rubisco decreased more than FBPase and SBPase, so FBPase and SBPase were present in relative excess. A lower fraction of FBPase and SBPase needs to be activated in LN leaves for photosynthesis recovery during the high-light phase of dynamic light. Therefore, photosynthetic recovery is faster in LN leaves than in HN leaves, which relieves the photosynthetic suppression caused by dynamic light in LN leaves. Conclusions Contrary to our expectations, dynamic light caused less photosynthetic suppression, rather than more, in LN leaves than in HN leaves of soybean. This is the first report of a stress condition alleviating the photosynthetic suppression caused by dynamic light.

Pseudomonas syringae pv. tabaci (Pst) is a hemibiotrophic bacterial pathogen responsible for tobacco wildfire disease. Although considerable research has been conducted on the tobacco plant's tolerance to Pst, the role of light in the responses of the photosystems to Pst infection is poorly understood. This study aimed to elucidate the underlying mechanisms of the reduced photosystem damage in tobacco leaves due to Pst infection under light conditions. Compared to dark conditions, Pst infection under light conditions resulted in less chlorophyll degradation and a smaller decline in photosynthetic function. Although the maximal quantum yield of photosystem II (PSII) and the activity of the photosystem I (PSI) complex decreased as Pst infection progressed, damage to PSI and PSII after infection was reduced under light conditions compared to dark conditions. Pst was 17-fold more abundant in tobacco leaves under dark compared to light conditions at 3 days post inoculation (dpi). Additionally, H2O2 accumulated to a high level in tobacco leaves after Pst infection under light conditions; although to a lesser extent, H2O2 accumulation was also significant under dark conditions. Pretreatment with H2O2 alleviated chlorotic lesions and decreased Pst abundance in tobacco leaves at 3 dpi under dark conditions. MV pretreatment had the same effects under light conditions, whereas 3-(3,4-dichlorophenyl)-1,1-dimethylurea pretreatment aggravated chlorotic lesions and increased the Pst population. These results indicate that chlorotic symptoms and the size of the bacterial population are each negatively correlated with H2O2 accumulation. In other words, light appears to suppress the Pst population in tobacco leaves through the accumulation of H2O2 during infection. [ABSTRACT FROM AUTHOR]

Background: 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. Results: The net photosynthetic rate (Pn) and carboxylation efficiency (CE) were inhibited by Pst infection. The normalized relative variable fluorescence at the K step (Wk) and the relative variable fluorescence at the J step (VJ) increased while the maximal quantum yield of PSII (Fv/Fm) and the density of QA-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). Conclusions: 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. [ABSTRACT FROM AUTHOR]

The development of PSII tolerance to stress and photoprotection mechanisms during leaf growth has been widely studied, however, knowledge about PSI photoinhibition and interaction between PSI and PSII under stress during leaf growth is still lacking. This study showed that during the chilling-light treatment, the photoinhibitions of PSI and PSII were more severe in young leaves than in fully-expanded leaves of cucumber, but the inhibition of CO2 assimilation and the accumulation of reactive oxygen species (ROS) were similar in leaves at different development stages. During the chilling-light treatment, PSII photoinhibition was positive correlated to PSI photoinhibition in leaves, however, this correlation no longer existed in leaves pretreated with DCMU, an inhibitor of electron transport from PSII to PSI. Although the photoinhibitions of PSII and PSI in young leaves were more severe, the sensitivity of PSII to excitation pressure was lower in young leaves. The above results demonstrate that, the lower chilling-light tolerance of photosystems in young leaves was due to the higher sensitivity of PSI to ROS and the higher PSII excitation pressure caused by PSI photoinhibition in young leaves, rather than the difference of ROS content and sensitivity of PSII to excitation pressure between the young and fully-expanded leaves. [ABSTRACT FROM AUTHOR]

The purpose of this study was to explore how the mitochondrial AOX (alternative oxidase) pathway alleviates photoinhibition in Rumex K-1 leaves. Inhibition of the AOX pathway decreased the initial activity of NADP-malate dehydrogenase (EC 1.1.1.82, NADP-MDH) and the pool size of photosynthetic end electron acceptors, resulting in an over-reduction of the photosystem I (PSI) acceptor side. The over-reduction of the PSI acceptor side further inhibited electron transport from the photosystem II (PSII) reaction centers to the PSII acceptor side as indicated by an increase in Vj (the relative variable fluorescence at J-step), causing an imbalance between photosynthetic light absorption and energy utilization per active reaction center (RC) under high light, which led to the over-excitation of the PSII reaction centers. The over-reduction of the PSI acceptor side and the over-excitation of the PSII reaction centers enhanced the accumulation of reactive oxygen species (ROS), which inhibited the repair of the photodamaged PSII. However, the inhibition of the AOX pathway did not change the level of photoinhibition under high light in the presence of the chloroplast D1 protein synthesis inhibitor chloramphenicol, indicating that the inhibition of the AOX pathway did not accelerate the photodamage to PSII directly. All these results suggest that the AOX pathway plays an important role in the protection of plants against photoinhibition by minimizing the inhibition of the repair of the photodamaged PSII through preventing the over-production of ROS. [ABSTRACT FROM AUTHOR]

Alternaria alternata has received considerable attention in current literature and most of the studies are focused on its pathogenic effects on plant chloroplasts, but little is known about the characteristics of programmed cell death (PCD) induced by metabolic products (MP) of A. alternata, the effects of the MP on mitochondrial respiration and its relation to PCD. The purpose of this study was to explore the mechanism of MP-induced PCD in non-green tobacco BY-2 cells and to explore the role of mitochondrial inhibitory processes in the PCD of tobacco BY-2 cells. MP treatment led to significant cell death that was proven to be PCD by the concurrent cytoplasm shrinkage, chromatin condensation and DNA laddering observed in the cells. Moreover, MP treatment resulted in the overproduction of reactive oxygen species (ROS), rapid ATP depletion and a respiratory decline in the tobacco BY-2 cells. It was concluded that the direct inhibition of the mitochondrial electron transport chain (ETC), alternative pathway (AOX) capacity and catalase (CAT) activity by the MP might be the main contributors to the MP-induced ROS burst observed in tobacco BY-2 cells. The addition of adenosine together with the MP significantly inhibited ATP depletion without preventing PCD; however, when the cells were treated with the MP plus CAT, ROS overproduction was blocked and PCD did not occur. The data presented here demonstrate that the ROS burst played an important role in MP-induced PCD in the tobacco BY-2 cells. [ABSTRACT FROM AUTHOR]