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The activity of ferredoxin (Fd)-dependent cyclic electron flow (Fd-CEF) around photosystem I (PSI) was determined in intact leaves of Arabidopsis thaliana. The oxidation rate of Fd reduced by PSI (vFd) and photosynthetic linear electron flow activity are simultaneously measured under actinic light illumination. The vFd showed a curved response to the photosynthetic linear electron flow activity. In the lower range of photosynthetic linear flow activity with plastoquinone (PQ) in a highly reduced state, vFd clearly showed a linear relationship with photosynthetic linear electron flow activity. On the other hand, vFd increased sharply when photosynthetic linear electron flow activity became saturated with oxidized PQ as the net CO2 assimilation rate increased. That is, under higher photosynthesis conditions, we observed excess vFd resulting in electron flow over photosynthetic linear electron flow. The situation in which excess vFd was observed was consistent with the previous Fd-CEF model. Thus, excess vFd could be attributed to the in vivo activity of Fd-CEF. Furthermore, the excess vFd was also observed in NAD(P)H dehydrogenase-deficient mutants localized in the thylakoid membrane. The physiological significance of the excessive vFd was discussed.

We describe a new member of the class of mutants in Arabidopsis exhibiting high rates of cyclic electron flow around photosystem I (CEF), a light-driven process that produces ATP but not NADPH. High cyclic electron flow 2 ( hcef2 ) shows strongly increased CEF activity through the NADPH dehydrogenase complex (NDH), accompanied by increases in thylakoid proton motive force ( pmf ), activation of the photoprotective qE response, and the accumulation of H2O2. Surprisingly, hcef2 was mapped to a non-sense mutation in the TADA1 (tRNA adenosine deaminase arginine) locus, coding for a plastid targeted tRNA editing enzyme required for efficient codon recognition. Comparison of protein content from representative thylakoid complexes, the cytochrome bf complex, and the ATP synthase, suggests that inefficient translation of hcef2 leads to compromised complex assembly or stability leading to alterations in stoichiometries of major thylakoid complexes as well as their constituent subunits. Altered subunit stoichiometries for photosystem I, ratios and properties of cytochrome bf hemes, and the decay kinetics of the flash-induced thylakoid electric field suggest that these defect lead to accumulation of H2O2 in hcef2 , which we have previously shown leads to activation of NDH-related CEF. We observed similar increases in CEF, as well as increases in H2O2 accumulation, in other translation defective mutants. This suggests that loss of coordination in plastid protein levels lead to imbalances in photosynthetic energy balance that leads to an increase in CEF. These results taken together with a large body of previous observations, support a general model in which processes that lead to imbalances in chloroplast energetics result in the production of H2O2, which in turn activates CEF. This activation could be from either H2O2 acting as a redox signal, or by a secondary effect from H2O2 inducing a deficit in ATP.

Photosynthetic linear electron flow (LEF) produces ATP and NADPH, while cyclic electron flow (CEF) exclusively drives photophosphorylation to supply extra ATP. The fine-tuning of linear and cyclic electron transport levels allows photosynthetic organisms to balance light energy absorption with cellular energy requirements under constantly changing light conditions. As LEF and CEF share many electron transfer components, a key question is how the same individual structural units contribute to these two different functional modes. Here, we report the structural identification of a photosystem I (PSI)–light harvesting complex I (LHCI)–cytochrome (cyt) b₆f supercomplex isolated from the unicellular alga Chlamydomonas reinhardtii under anaerobic conditions, which induces CEF. This provides strong evidence for the model that enhanced CEF is induced by the formation of CEF supercomplexes, when stromal electron carriers are reduced, to generate additional ATP. The additional identification of PSI–LHCI–LHCII complexes is consistent with recent findings that both CEF enhancement and state transitions are triggered by similar conditions, but can occur independently from each other. Single molecule fluorescence correlation spectroscopy indicates a physical association between cyt b₆f and fluorescent chlorophyll containing PSI–LHCI supercomplexes. Single particle analysis identified top-view projections of the corresponding PSI–LHCI–cyt b₆f supercomplex. Based on molecular modeling and mass spectrometry analyses, we propose a model in which dissociation of LHCA2 and LHCA9 from PSI supports the formation of this CEF supercomplex. This is supported by the finding that a Δlhca2 knockout mutant has constitutively enhanced CEF.

This article is a Commentary on Storti et al. (2020), 228: 1316–1326.

It is just over 60 years since a cycle for the regeneration of the CO₂-acceptor used in photosynthesis was proposed. In this opinion paper, we revisit the origins of the Calvin–Benson cycle that occurred at the time that the hexose monophosphate shunt, now called the pentose phosphate pathway, was being worked out. Eventually the pentose phosphate pathway was separated into two branches, an oxidative branch and a non-oxidative branch. It is generally thought that the Calvin–Benson cycle is the reverse of the non-oxidative branch of the pentose phosphate pathway but we describe crucial differences and also propose that some carbon routinely passes through the oxidative branch of the pentose phosphate pathway. This creates a futile cycle but may help to stabilize photosynthesis. If it occurs it could explain a number of enigmas including the lack of complete labelling of the Calvin–Benson cycle intermediates when carbon isotopes are fed to photosynthesizing leaves.

Significance Cyclic electron flow around photosystem I (CEF) is critical for balancing the energy budget of photosynthesis, but its regulation is not well understood. Our results provide evidence that hydrogen peroxide, which is produced as a result of imbalances in chloroplast redox state, acts as a signaling agent to activate CEF in higher plants in vivo. Cyclic electron flow (CEF) around photosystem I is thought to balance the ATP/NADPH energy budget of photosynthesis, requiring that its rate be finely regulated. The mechanisms of this regulation are not well understood. We observed that mutants that exhibited constitutively high rates of CEF also showed elevated production of H ₂O ₂. We thus tested the hypothesis that CEF can be activated by H ₂O ₂ in vivo. CEF was strongly increased by H ₂O ₂ both by infiltration or in situ production by chloroplast-localized glycolate oxidase, implying that H ₂O ₂ can activate CEF either directly by redox modulation of key enzymes, or indirectly by affecting other photosynthetic processes. CEF appeared with a half time of about 20 min after exposure to H ₂O ₂, suggesting activation of previously expressed CEF-related machinery. H ₂O ₂-dependent CEF was not sensitive to antimycin A or loss of PGR5, indicating that increased CEF probably does not involve the PGR5-PGRL1 associated pathway. In contrast, the rise in CEF was not observed in a mutant deficient in the chloroplast NADPH:PQ reductase (NDH), supporting the involvement of this complex in CEF activated by H ₂O ₂. We propose that H ₂O ₂ is a missing link between environmental stress, metabolism, and redox regulation of CEF in higher plants.

Fluctuating light (FL) conditions particularly the diurnal alternation between shaded and high-light periods are intrinsic to intercropping systems and impose substantial regulatory challenges on crop photosynthesis. However, the cultivar-specific mechanisms underlying adaptation to such dynamic light environments remain largely unexplored. Here, we examined how the duration of midday high-light exposure modulates the coordination between cyclic electron flow (CEF) and non-photochemical quenching (NPQ) in two soybean cultivars grown under simulated intercropping light regimes. Plants were exposed to morning shade followed by either short (T30) or prolonged (T150, T200) midday high-light treatments. All treatments triggered common photoprotective responses, including increased energy dissipation (DIo/CSm, +18.7–22.3%) and reduced electron transport efficiency (ETo/CSm, −14.2–17.5%). Yet, the cultivars exhibited distinct photoregulatory strategies depending on light duration. The light-adapted cultivar ND12 rapidly established a proton gradient (ΔpH; 34.8% faster) and sustained higher PSII efficiency (ETRII, +41.5%) under brief high-light exposure, indicating a preemptive ΔpH priming mechanism. In contrast, the light-sensitive GX7 required extended high-light duration (T200) to induce CEF (+60.5%) and plastoquinone pool expansion (+22.0%), suggesting a delayed, duration-dependent adjustment strategy. These cultivar-specific responses ultimately enhanced photosynthetic performance by 34.8–52.4% under FL conditions. Our findings offer mechanistic insights into how midday light duration shapes genotype-dependent photosynthetic regulation, providing a physiological basis for optimizing light utilization in intercropping systems.

Plants experience low ambient temperature and low red to far-red ratios (L-R/FR) of light due to vegetative shading and longer twilight durations in cool seasons. Low temperature induce photoinhibition through inactivation of the photosynthetic apparatus, however, the role of light quality on photoprotection during cold stress remains poorly understood. Here, we report that L-R/FR significantly prevents the overreduction of the entire intersystem electron transfer chain and the limitation of photosystem I (PSI) acceptor side, eventually alleviating the cold-induced photoinhibition. During cold stress, L-R/FR activated cyclic electron flow (CEF), enhanced protonation of PSII subunit S (PsbS) and de-epoxidation state of the xanthophyll cycle, and promoted energy-dependent quenching (qE) component of non-photochemical quenching (NPQ), enzyme activity of Foyer-Halliwell-Asada cycle and D1 proteins accumulation. However, L-R/FR –induced photoprotection pathways were compromised in tomato PROTON GRADIENT REGULATION5 ( PGR5 ) and PGR5-LIKE PHOTOSYNTHETIC PHENOTYPE1A ( PGRL1A ) co-silenced plants and NADH DEHYDROGENASE-LIKE COMPLEX M ( NDHM ) -silenced plants during cold stress. Our results demonstrate that both PGR5/PGRL1- and NDH-dependent CEF mediate L-R/FR –induced cold tolerance by enhancing the thermal dissipation and the repair of photodamaged PSII, thereby mitigating the overreduction of electron carriers and the accumulation of reactive oxygen species. The study indicates that there is an anterograde link between photoreception and photoprotection in tomato plants during cold stress.

The molecular entity responsible for catalyzing ferredoxin (Fd)-dependent cyclic electron flow around photosystem I (Fd-CEF) remains unidentified. To reveal the in vivo molecular mechanism of Fd-CEF, evaluating ferredoxin reduction–oxidation kinetics proves to be a reliable indicator of Fd-CEF activity. Recent research has demonstrated that the expression of Fd-CEF activity is contingent upon the oxidation of plastoquinone. Moreover, chloroplast NAD(P)H dehydrogenase does not catalyze Fd-CEF in Arabidopsis thaliana. In this study, we analyzed the impact of reduced Fd on Fd-CEF activity by comparing wild-type and pgr5-deficient mutants (pgr5hope1). PGR5 has been proposed as the mediator of Fd-CEF, and pgr5hope1 exhibited a comparable CO2 assimilation rate and the same reduction–oxidation level of PQ as the wild type. However, P700 oxidation was suppressed with highly reduced Fd in pgr5hope1, unlike in the wild type. As anticipated, the Fd-CEF activity was enhanced in pgr5hope1 compared to the wild type, and its activity further increased with the oxidation of PQ due to the elevated CO2 assimilation rate. This in vivo research clearly demonstrates that the expression of Fd-CEF activity requires not only reduced Fd but also oxidized PQ. Importantly, PGR5 was found to not catalyze Fd-CEF, challenging previous assumptions about its role in this process.

In higher plants, moderate photoinhibition of photosystem II (PSII) leads to a stimulation of cyclic electron flow (CEF) at low light, which is accompanied by an increase in the P700 oxidation ratio. However, the specific role of CEF stimulation at low light is not well known. Furthermore, the mechanism underlying this increase in P700 oxidation ratio at low light is unclear. To address these questions, intact leaves of the shade-adapted plant were treated at 2258 μmol photons m s for 30 min to induce PSII photoinhibition. Before and after this high-light treatment, PSI and PSII activity, the energy quenching in PSII, the redox state of PSI and proton motive force ( ) at a low light of 54 μmol photons m s were determined at the steady state. After high-light treatment, electron flow through PSII (ETRII) significantly decreased but CEF was remarkably stimulated. The P700 oxidation ratio significantly increased but non-photochemical quenching changed negligibly. Concomitantly, the total decreased significantly and the proton gradient (ΔpH) across the thylakoid membrane remained stable. Furthermore, the P700 oxidation ratio was negatively correlated with the value of ETRII. These results suggest that upon PSII photoinhibition, CEF is stimulated to increase the ATP synthesis, facilitating the rapid repair of photodamaged PSII. The increase in P700 oxidation ratio at low light cannot be explained by the change in , but is primarily controlled by electron transfer from PSII.