scholarly journals NTRC-dependent redox balance of 2-Cys peroxiredoxins is needed for optimal function of the photosynthetic apparatus

2017 ◽  
Vol 114 (45) ◽  
pp. 12069-12074 ◽  
Author(s):  
Juan Manuel Pérez-Ruiz ◽  
Belén Naranjo ◽  
Valle Ojeda ◽  
Manuel Guinea ◽  
Francisco Javier Cejudo
Keyword(s):  
Redox Regulation ◽  
Photosynthetic Apparatus ◽  
Reducing Power ◽  
Redox Balance ◽  
Light Energy ◽  
Energy Utilization ◽  
Antioxidant Systems ◽  
Redox Systems ◽  
Triple Mutant ◽  
Low Efficiency

Thiol-dependent redox regulation allows the rapid adaptation of chloroplast function to unpredictable changes in light intensity. Traditionally, it has been considered that chloroplast redox regulation relies on photosynthetically reduced ferredoxin (Fd), thioredoxins (Trxs), and an Fd-dependent Trx reductase (FTR), the Fd-FTR-Trxs system, which links redox regulation to light. More recently, a plastid-localized NADPH-dependent Trx reductase (NTR) with a joint Trx domain, termed NTRC, was identified. NTRC efficiently reduces 2-Cys peroxiredoxins (Prxs), thus having antioxidant function, but also participates in redox regulation of metabolic pathways previously established to be regulated by Trxs. Thus, the NTRC, 2-Cys Prxs, and Fd-FTR-Trxs redox systems may act concertedly, but the nature of the relationship between them is unknown. Here we show that decreased levels of 2-Cys Prxs suppress the phenotype of the Arabidopsis thaliana ntrc KO mutant. The excess of oxidized 2-Cys Prxs in NTRC-deficient plants drains reducing power from chloroplast Trxs, which results in low efficiency of light energy utilization and impaired redox regulation of Calvin–Benson cycle enzymes. Moreover, the dramatic phenotype of the ntrc-trxf1f2 triple mutant, lacking NTRC and f-type Trxs, was also suppressed by decreased 2-Cys Prxs contents, as the ntrc-trxf1f2-Δ2cp mutant partially recovered the efficiency of light energy utilization and exhibited WT rate of CO2 fixation and growth phenotype. The suppressor phenotype was not caused by compensatory effects of additional chloroplast antioxidant systems. It is proposed that the Fd-FTR-Trx and NTRC redox systems are linked by the redox balance of 2-Cys Prxs, which is crucial for chloroplast function.

Different strategies of acclimation of photosynthesis, electron transport and antioxidative activity in leaves of two cotton species to water deficit

2016 ◽  
Vol 43 (5) ◽  
pp. 448 ◽  
Author(s):  
Xiao-Ping Yi ◽  
Ya-Li Zhang ◽  
He-Sheng Yao ◽  
Hong-Hai Luo ◽  
Ling Gou ◽  
...  
Keyword(s):  
Electron Transport ◽  
Water Deficit ◽  
Heat Dissipation ◽  
Photosynthetic Apparatus ◽  
Light Energy ◽  
Photochemical Quenching ◽  
Antioxidant Systems ◽  
Mehler Reaction ◽  
Cotton Species ◽  
Excess Light

To better understand the adaptation mechanisms of the photosynthetic apparatus of cotton plants to water deficit conditions, the influence of water deficit on photosynthesis, chlorophyll a fluorescence and the activities of antioxidant systems were determined simultaneously in Gossypium hirsutum L. cv. Xinluzao 45 (upland cotton) and Gossypium barbadense L. cv. Xinhai 21 (pima cotton). Water deficit decreased photosynthesis in both cotton species, but did not decrease chlorophyll content or induce any sustained photoinhibition in either cotton species. Water deficit increased ETR/4 − AG, where ETR/4 estimates the linear photosynthetic electron flux and AG is the gross rate of carbon assimilation. The increase in ETR/4 − AG, which represents an increase in photorespiration and alternative electron fluxes, was particularly pronounced in Xinluzao 45. In Xinluzao 45, water deficit increased the activities of antioxidative enzymes, as well as the contents of reactive oxygen species (ROS), which are related to the Mehler reaction. In contrast, moderate water deficit particularly increased non-photochemical quenching (NPQ) in Xinhai 21. Our results suggest that Xinluzao 45 relied on enhanced electron transport such as photorespiration and the Mehler reaction to dissipate excess light energy under mild and moderate water deficit. Xinhai 21 used enhanced photorespiration for light energy utilisation under mild water deficit but, when subjected to moderate water deficit, possessed a high capacity for dissipating excess light energy via heat dissipation.

scholarly journals Insights into the function of NADPH thioredoxin reductase C (NTRC) based on identification of NTRC-interacting proteins in vivo

2019 ◽  
Vol 70 (20) ◽  
pp. 5787-5798 ◽  
Author(s):  
Maricruz González ◽  
Víctor Delgado-Requerey ◽  
Julia Ferrández ◽  
Antonio Serna ◽  
Francisco Javier Cejudo
Keyword(s):  
Redox Regulation ◽  
Fluorescent Protein ◽  
Affinity Purification ◽  
Photosynthetic Apparatus ◽  
Thioredoxin Reductase ◽  
Redox System ◽  
Negative Control ◽  
Bimolecular Fluorescence Complementation ◽  
Redox Systems

Abstract Redox regulation in heterotrophic organisms relies on NADPH, thioredoxins (TRXs), and an NADPH-dependent TRX reductase (NTR). In contrast, chloroplasts harbor two redox systems, one that uses photoreduced ferredoxin (Fd), an Fd-dependent TRX reductase (FTR), and TRXs, which links redox regulation to light, and NTRC, which allows the use of NADPH for redox regulation. It has been shown that NTRC-dependent regulation of 2-Cys peroxiredoxin (PRX) is critical for optimal function of the photosynthetic apparatus. Thus, the objective of the present study was the analysis of the interaction of NTRC and 2-Cys PRX in vivo and the identification of proteins interacting with them with the aim of identifying chloroplast processes regulated by this redox system. To assess this objective, we generated Arabidopsis thaliana plants expressing either an NTRC–tandem affinity purification (TAP)-Tag or a green fluorescent protein (GFP)–TAP-Tag, which served as a negative control. The presence of 2-Cys PRX and NTRC in complexes isolated from NTRC–TAP-Tag-expressing plants confirmed the interaction of these proteins in vivo. The identification of proteins co-purified in these complexes by MS revealed the relevance of the NTRC–2-Cys PRX system in the redox regulation of multiple chloroplast processes. The interaction of NTRC with selected targets was confirmed in vivo by bimolecular fluorescence complementation (BiFC) assays.

scholarly journals Over Expression of the Cyanobacterial Pgr5-Homologue Leads to Pseudoreversion in a Gene Coding for a Putative Esterase in Synechocystis 6803

Life ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 174
Author(s):  
Ketty Margulis ◽  
Hagit Zer ◽  
Hagar Lis ◽  
Hanan Schoffman ◽  
Omer Murik ◽  
...  
Keyword(s):  
Redox Regulation ◽  
Electron Flow ◽  
Photosynthetic Apparatus ◽  
Redox Balance ◽  
Synechocystis 6803 ◽  
Experimental Conditions ◽  
Direct Role ◽  
Transfer Rates ◽  
Gene Coding ◽  
Eukaryotic Phytoplankton

Pgr5 proteins play a major direct role in cyclic electron flow paths in plants and eukaryotic phytoplankton. The genomes of many cyanobacterial species code for Pgr5-like proteins but their function is still uncertain. Here, we present evidence that supports a link between the Synechocystis sp. PCC6803 Pgr5-like protein and the regulation of intracellular redox balance. The knockout strain, pgr5KO, did not display substantial phenotypic response under our experimental conditions, confirming results obtained in earlier studies. However, the overexpression strain, pgr5OE, accumulated 2.5-fold more chlorophyll than the wild type and displayed increased content of photosystems matching the chlorophyll increase. As a result, electron transfer rates through the photosynthetic apparatus of pgr5OE increased, as did the amount of energy stored as glycogen. While, under photoautotrophic conditions, this metabolic difference had only minor effects, under mixotrophic conditions, pgr5OE cultures collapsed. Interestingly, this specific phenotype of pgr5OE mutants displayed a tendency for reverting, and cultures which previously collapsed in the presence of glucose were now able to survive. DNA sequencing of a pgr5OE strain revealed a second site suppression mutation in slr1916, a putative esterase associated with redox regulation. The phenotype of the slr1916 knockout is very similar to that of the strain reported here and to that of the pmgA regulator knockout. These data demonstrate that, in Synechocystis 6803, there is strong selection against overexpression of the Pgr5-like protein. The pseudoreversion event in a gene involved in redox regulation suggests a connection of the Pgr5-like protein to this network.

scholarly journals Mitochondrial redox systems as central hubs in plant metabolism and signalling

2021 ◽  
Author(s):  
Olivier Van Aken
Keyword(s):  
Stress Responses ◽  
Plant Mitochondria ◽  
Nuclear Gene ◽  
Tca Cycle ◽  
Cellular Damage ◽  
Future Research ◽  
Antioxidant Systems ◽  
Plant Metabolism ◽  
Redox Systems ◽  
Glutathione Cycle

Abstract Plant mitochondria are indispensable for plant metabolism and are tightly integrated into cellular homeostasis. This review provides an update on the latest research concerning the organisation and operation of plant mitochondrial redox systems, and how they affect cellular metabolism and signalling, plant development and stress responses. New insights into the organisation and operation of mitochondrial energy systems such as the tricarboxylic acid (TCA) cycle and mitochondrial electron chain (mtETC) are discussed. The mtETC produces reactive oxygen and nitrogen species, which can act as signals or lead to cellular damage, and are thus efficiently removed by mitochondrial antioxidant systems, including Mn-superoxide dismutase, ascorbate-glutathione cycle and thioredoxin-dependent peroxidases. Plant mitochondria are tightly connected with photosynthesis, photorespiration and cytosolic metabolism, thereby providing redox-balancing. Mitochondrial proteins are targets of extensive post-translational modifications, but their functional significance and how they are added or removed remains unclear. To operate in sync with the whole cell, mitochondria can communicate their functional status via mitochondrial retrograde signalling to change nuclear gene expression, and several recent breakthroughs here are discussed. At a whole organism level, plant mitochondria thus play crucial roles from the first minutes after seed imbibition, supporting meristem activity, growth and fertility, until senescence of darkened and aged tissue. Finally, plant mitochondria are tightly integrated with cellular and organismal responses to environmental challenges such as drought, salinity, heat and submergence, but also threats posed by pathogens. Both the major recent advances and outstanding questions are reviewed, which may help future research efforts on plant mitochondria.

scholarly journals Physical Activity and Redox Balance in the Elderly: Signal Transduction Mechanisms

2021 ◽  
Vol 11 (5) ◽  
pp. 2228
Author(s):  
Daniela Galli ◽  
Cecilia Carubbi ◽  
Elena Masselli ◽  
Mauro Vaccarezza ◽  
Valentina Presta ◽  
...  
Keyword(s):  
Physical Activity ◽  
Molecular Mechanisms ◽  
Vascular Tissue ◽  
The Elderly ◽  
Redox Balance ◽  
Antioxidant Systems ◽  
Targeted Prevention ◽  
Individual Subject ◽  
Aged People ◽  
The Individual

Reactive Oxygen Species (ROS) are molecules naturally produced by cells. If their levels are too high, the cellular antioxidant machinery intervenes to bring back their quantity to physiological conditions. Since aging often induces malfunctioning in this machinery, ROS are considered an effective cause of age-associated diseases. Exercise stimulates ROS production on one side, and the antioxidant systems on the other side. The effects of exercise on oxidative stress markers have been shown in blood, vascular tissue, brain, cardiac and skeletal muscle, both in young and aged people. However, the intensity and volume of exercise and the individual subject characteristics are important to envisage future strategies to adequately personalize the balance of the oxidant/antioxidant environment. Here, we reviewed the literature that deals with the effects of physical activity on redox balance in young and aged people, with insights into the molecular mechanisms involved. Although many molecular pathways are involved, we are still far from a comprehensive view of the mechanisms that stand behind the effects of physical activity during aging. Although we believe that future precision medicine will be able to transform exercise administration from wellness to targeted prevention, as yet we admit that the topic is still in its infancy.

scholarly journals Determining the Rate-Limiting Step for Light-Responsive Redox Regulation in Chloroplasts

Antioxidants ◽  
2018 ◽  
Vol 7 (11) ◽  
pp. 153 ◽  
Author(s):  
Keisuke Yoshida ◽  
Toru Hisabori
Keyword(s):  
Redox Regulation ◽  
Reducing Power ◽  
Rubisco Activase ◽  
Power Transfer ◽  
Target Proteins ◽  
Rate Limiting Step ◽  
Limiting Step ◽  
Rate Limiting

Thiol-based redox regulation ensures light-responsive control of chloroplast functions. Light-derived signal is transferred in the form of reducing power from the photosynthetic electron transport chain to several redox-sensitive target proteins. Two types of protein, ferredoxin-thioredoxin reductase (FTR) and thioredoxin (Trx), are well recognized as the mediators of reducing power. However, it remains unclear which step in a series of redox-relay reactions is the critical bottleneck for determining the rate of target protein reduction. To address this, the redox behaviors of FTR, Trx, and target proteins were extensively characterized in vitro and in vivo. The FTR/Trx redox cascade was reconstituted in vitro using recombinant proteins from Arabidopsis. On the basis of this assay, we found that the FTR catalytic subunit and f-type Trx are rapidly reduced after the drive of reducing power transfer, irrespective of the presence or absence of their downstream target proteins. By contrast, three target proteins, fructose 1,6-bisphosphatase (FBPase), sedoheptulose 1,7-bisphosphatase (SBPase), and Rubisco activase (RCA) showed different reduction patterns; in particular, SBPase was reduced at a low rate. The in vivo study using Arabidopsis plants showed that the Trx family is commonly and rapidly reduced upon high light irradiation, whereas FBPase, SBPase, and RCA are differentially and slowly reduced. Both of these biochemical and physiological findings suggest that reducing power transfer from Trx to its target proteins is a rate-limiting step for chloroplast redox regulation, conferring distinct light-responsive redox behaviors on each of the targets.

scholarly journals Cell type-specific differences in redox regulation and proliferation after low UVA doses

2018 ◽  
Author(s):  
Sylwia Ciesielska ◽  
Patryk Bil ◽  
Karolina Gajda ◽  
Aleksandra Poterala-Hejmo ◽  
Dorota Hudy ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Redox Regulation ◽  
Cellular Proliferation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cell Type ◽  
Redox Systems ◽  
Human Colon Cancer ◽  
Cellular Redox ◽  
Hct116 Cells

AbstractUltraviolet A (UVA) radiation is harmful for living organisms but in low doses may stimulate cell proliferation. Our aim was to examine the relationships between exposure to different low UVA doses, cellular proliferation, and changes in cellular reactive oxygen species levels. In human colon cancer (HCT116) and melanoma (Me45) cells exposed to UVA doses comparable to environmental, the highest doses (30-50 kJ/m2) reduced clonogenic potential but some lower doses (1 and 10 kJ/m2) induced proliferation. This effect was cell type and dose specific. In both cell lines the levels of reactive oxygen species and nitric oxide fluctuated with dynamics which were influenced differently by UVA; in Me45 cells decreased proliferation accompanied the changes in the dynamics of H2O2 while in HCT116 cells those of superoxide. Genes coding for proteins engaged in redox systems were expressed differently in each cell line; transcripts for thioredoxin, peroxiredoxin and glutathione peroxidase showed higher expression in HCT116 cells whereas those for glutathione transferases and copper chaperone were more abundant in Me45 cells. We conclude that these two cell types utilize different pathways for regulating their redox status. Many mechanisms engaged in maintaining cellular redox balance have been described. Here we show that the different cellular responses to a stimulus such as a specific dose of UVA may be consequences of the use of different redox control pathways. Assays of superoxide and hydrogen peroxide level changes after exposure to UVA may clarify mechanisms of cellular redox regulation and help in understanding responses to stressing factors.

scholarly journals Sepsis, mitochondrial failure and multiple organ dysfunction

2014 ◽  
Vol 37 (2) ◽  
pp. 58 ◽  
Author(s):  
Josefina Duran-Bedolla ◽  
Marco A Montes de Oca-Sandoval ◽  
Vianey Saldaña-Navor ◽  
José A Villalobos-Silva ◽  
Maria Carmen Rodriguez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Organ Dysfunction ◽  
Physiological State ◽  
Redox Balance ◽  
Multiple Organ ◽  
Reactive Species ◽  
Systemic Inflammatory Response ◽  
Antioxidant Systems ◽  
Multiple Organ Dysfunction

Purpose: The purpose of this review is to consider the state of oxidative stress, failure of the antioxidant systems and mitochondrial failure as the main physiopathological mechanisms leading to multiple organ dysfunction during sepsis. Principal findings: Sepsis is a clinical syndrome caused by a severe infection that triggers an exaggerated inflammatory response. Involved in the pathogenesis of sepsis are the activation of inflammatory, immune, hormonal, metabolic and bioenergetic responses. One of the pivotal factors in these processes is the increase of reactive species accompanied by the failure of the antioxidant systems, leading to a state of irreversible oxidative stress and mitochondrial failure. In a physiological state, reactive species and antioxidant systems are in redox balance. The loss of this balance during both chronic and infectious diseases leads to a state of oxidative stress, which is considered to be the greatest promoter of a systemic inflammatory response. The loss of the redox balance, together with a systemic inflammatory response during sepsis, can lead to progressive and irreversible mitochondrial failure, energy depletion, hypoxia, septic shock, severe sepsis, multiple organ dysfunction and death of the patient. Conclusion: Knowledge of the molecular processes associated with the development of oxidative stress should facilitate the development of effective therapies and better prognosis for patients with sepsis and organ dysfunction.

scholarly journals Compensatory guaiacyl lignin biosynthesis at the expense of syringyl lignin in 4CL1-knockout poplar

2019 ◽  
Author(s):  
Chung-Jui Tsai ◽  
Peng Xu ◽  
Liang-Jiao Xue ◽  
Hao Hu ◽  
Batbayar Nyamdari ◽  
...  
Keyword(s):  
Lignin Biosynthesis ◽  
Redox Balance ◽  
Antioxidant Systems ◽  
Activity Levels ◽  
Sulfur Assimilation ◽  
Syringyl Lignin ◽  
Metabolic Adaptations ◽  
Thiol Redox ◽  
Guaiacyl Lignin ◽  
Lignin Biosynthetic Pathway

AbstractThe lignin biosynthetic pathway is highly conserved in angiosperms, yet pathway manipulations give rise to a variety of taxon-specific outcomes. Knockout of lignin-associated 4-coumarate:CoA ligases (4CLs) in herbaceous species mainly reduces guaiacyl (G) lignin and enhances cell wall saccharification. Here we show that CRISPR-knockout of 4CL1 in Populus tremula × alba preferentially reduced syringyl (S) lignin, with negligible effects on biomass recalcitrance. Concordant with reduced S-lignin was downregulation of ferulate 5-hydroxylases (F5Hs). Lignification was largely sustained by 4CL5, a low-affinity paralog of 4CL1 typically with only minor xylem expression or activity. Levels of caffeate, the preferred substrate of 4CL5, increased in line with significant upregulation of caffeoyl shikimate esterase1. Upregulation of caffeoyl-CoA O-methyltransferase1 and downregulation of F5Hs are consistent with preferential funneling of 4CL5 products toward G-lignin biosynthesis at the expense of S-lignin. Thus, transcriptional and metabolic adaptations to 4CL1-knockout appear to have enabled 4CL5 catalysis at a level sufficient to sustain lignification. Finally, genes involved in sulfur assimilation, the glutathione-ascorbate cycle and various antioxidant systems were upregulated in the mutants, suggesting cascading responses to perturbed thioesterification in lignin biosynthesis.One sentence summaryKnockout of lignin-associated 4CL1 in Populus reveals a 4CL5-dependent, caffeate-modulated compensatory pathway for lignification with links to thiol redox balance and sulfur assimilation.

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