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.

scholarly journals Compensatory Guaiacyl Lignin Biosynthesis at the Expense of Syringyl Lignin in 4CL1-Knockout Poplar

2020 ◽  
Vol 183 (1) ◽  
pp. 123-136 ◽  
Author(s):  
Chung-Jui Tsai ◽  
Peng Xu ◽  
Liang-Jiao Xue ◽  
Hao Hu ◽  
Batbayar Nyamdari ◽  
...  
Keyword(s):  
Lignin Biosynthesis ◽  
Syringyl Lignin ◽  
Guaiacyl Lignin

scholarly journals Phylogenetic Occurrence of the Phenylpropanoid Pathway and Lignin Biosynthesis in Plants

2021 ◽  
Vol 12 ◽  
Author(s):  
Tao Yao ◽  
Kai Feng ◽  
Meng Xie ◽  
Jaime Barros ◽  
Timothy J. Tschaplinski ◽  
...  
Keyword(s):  
Biosynthetic Pathway ◽  
Shikimate Pathway ◽  
Lignin Biosynthesis ◽  
Phenylpropanoid Pathway ◽  
Land Plant ◽  
Bioenergy Crops ◽  
Plant Colonization ◽  
Epsp Synthase ◽  
Syringyl Lignin ◽  
Lignin Biosynthetic Pathway

The phenylpropanoid pathway serves as a rich source of metabolites in plants and provides precursors for lignin biosynthesis. Lignin first appeared in tracheophytes and has been hypothesized to have played pivotal roles in land plant colonization. In this review, we summarize recent progress in defining the lignin biosynthetic pathway in lycophytes, monilophytes, gymnosperms, and angiosperms. In particular, we review the key structural genes involved in p-hydroxyphenyl-, guaiacyl-, and syringyl-lignin biosynthesis across plant taxa and consider and integrate new insights on major transcription factors, such as NACs and MYBs. We also review insight regarding a new transcriptional regulator, 5-enolpyruvylshikimate-3-phosphate (EPSP) synthase, canonically identified as a key enzyme in the shikimate pathway. We use several case studies, including EPSP synthase, to illustrate the evolution processes of gene duplication and neo-functionalization in lignin biosynthesis. This review provides new insights into the genetic engineering of the lignin biosynthetic pathway to overcome biomass recalcitrance in bioenergy crops.

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 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 Dimethyl-2-oxoglutarate improves redox balance and mitochondrial function in muscle pericytes of individuals with diabetes mellitus

Diabetologia ◽  
2020 ◽  
Vol 63 (10) ◽  
pp. 2205-2217 ◽  
Author(s):  
Ashton Faulkner ◽  
Anita Tamiato ◽  
William Cathery ◽  
Andrea Rampin ◽  
Carlo Maria Caravaggi ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Mitochondrial Function ◽  
Myogenic Differentiation ◽  
Tricarboxylic Acid Cycle ◽  
Antioxidant Properties ◽  
Vascular Complications ◽  
Redox Balance ◽  
Metabolic Enzyme ◽  
Antioxidant Systems ◽  
Limb Muscles

Abstract Aims/hypothesis Treatment of vascular complications of diabetes remains inadequate. We reported that muscle pericytes (MPs) from limb muscles of vascular patients with diabetes mellitus display elevated levels of oxidative stress causing a dysfunctional phenotype. Here, we investigated whether treatment with dimethyl-2-oxoglutarate (DM-2OG), a tricarboxylic acid cycle metabolite with antioxidant properties, can restore a healthy metabolic and functional phenotype. Methods MPs were isolated from limb muscles of diabetes patients with vascular disease (D-MPs) and from non-diabetic control participants (ND-MPs). Metabolic status was assessed in untreated and DM-2OG-treated (1 mmol/l) cells using an extracellular flux analyser and anion-exchange chromatography–mass spectrometry (IC-MS/MS). Redox status was measured using commercial kits and IC-MS/MS, with antioxidant and metabolic enzyme expression assessed by quantitative RT-PCR and western blotting. Myogenic differentiation and proliferation and pericyte–endothelial interaction were assessed as functional readouts. Results D-MPs showed mitochondrial dysfunction, suppressed glycolytic activity and reduced reactive oxygen species-buffering capacity, but no suppression of antioxidant systems when compared with ND-MP controls. DM-2OG supplementation improved redox balance and mitochondrial function, without affecting glycolysis or antioxidant systems. Nonetheless, this was not enough for treated D-MPs to regain the level of proliferation and myogenic differentiation of ND-MPs. Interestingly, DM-2OG exerted a positive effect on pericyte–endothelial cell interaction in the co-culture angiogenesis assay, independent of the diabetic status. Conclusions/interpretation These novel findings support the concept of using DM-2OG supplementation to improve pericyte redox balance and mitochondrial function, while concurrently allowing for enhanced pericyte–endothelial crosstalk. Such effects may help to prevent or slow down vasculopathy in skeletal muscles of people with diabetes.

scholarly journals Auranofin exerts broad-spectrum bactericidal activities by targeting thiol-redox homeostasis

2015 ◽  
Vol 112 (14) ◽  
pp. 4453-4458 ◽  
Author(s):  
Michael B. Harbut ◽  
Catherine Vilchèze ◽  
Xiaozhou Luo ◽  
Mary E. Hensler ◽  
Hui Guo ◽  
...  
Keyword(s):  
Redox Homeostasis ◽  
Thioredoxin Reductase ◽  
Redox Balance ◽  
Resistant Bacteria ◽  
Gram Positive ◽  
Antibiotic Resistant ◽  
Gram Positive Bacteria ◽  
Bactericidal Activities ◽  
Orally Bioavailable ◽  
Thiol Redox

Infections caused by antibiotic-resistant bacteria are a rising public health threat and make the identification of new antibiotics a priority. From a cell-based screen for bactericidal compounds againstMycobacterium tuberculosisunder nutrient-deprivation conditions we identified auranofin, an orally bioavailable FDA-approved antirheumatic drug, as having potent bactericidal activities against both replicating and nonreplicatingM. tuberculosis. We also found that auranofin is active against other Gram-positive bacteria, includingBacillus subtilisandEnterococcus faecalis, and drug-sensitive and drug-resistant strains ofEnterococcus faeciumandStaphylococcus aureus. Our biochemical studies showed that auranofin inhibits the bacterial thioredoxin reductase, a protein essential in many Gram-positive bacteria for maintaining the thiol-redox balance and protecting against reactive oxidative species. Auranofin decreases the reducing capacity of target bacteria, thereby sensitizing them to oxidative stress. Finally, auranofin was efficacious in a murine model of methicillin-resistantS. aureusinfection. These results suggest that the thioredoxin-mediated redox cascade of Gram-positive pathogens is a valid target for the development of antibacterial drugs, and that the existing clinical agent auranofin may be repurposed to aid in the treatment of several important antibiotic-resistant pathogens.

scholarly journals Coniferyl aldehyde 5-hydroxylation and methylation direct syringyl lignin biosynthesis in angiosperms

1999 ◽  
Vol 96 (16) ◽  
pp. 8955-8960 ◽  
Author(s):  
K. Osakabe ◽  
C. C. Tsao ◽  
L. Li ◽  
J. L. Popko ◽  
T. Umezawa ◽  
...  
Keyword(s):  
Lignin Biosynthesis ◽  
Syringyl Lignin

scholarly journals Nanoselenium Transformation And Inhibition of Cadmium Accumulation By Regulating The Lignin Biosynthetic Pathway And Plant Hormone Signal Transduction In Pepper Plants

2021 ◽  
Author(s):  
Dong Li ◽  
Chunran Zhou ◽  
Jinling Ma ◽  
Yangliu Wu ◽  
Lu Kang ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Cell Walls ◽  
Biosynthetic Pathway ◽  
Lignin Biosynthesis ◽  
Cadmium Accumulation ◽  
Protective Mechanism ◽  
Plant Signal Transduction ◽  
Lignin Biosynthetic Pathway ◽  
Pepper Plants

Abstract Selenium (Se) can promote the growth and resistance of agricultural crops as fertilizers, while the role of nano-selenium (nano-Se) against Cd remains unclear in pepper plants (Capsicum annuum L.). Biofortification with nano-Se observably restored Cd stress by decreasing the level of Cd in plant tissues and boosting the accumulation in biomass. The Se compounds transformed by nano-Se were primarily in the form of SeMet and MeSeCys in pepper tissues. Differential metabolites and the genes of plant signal transduction and lignin biosynthesis were measured by employing transcriptomics and determining target metabolites. The number of lignin-related genes (PAL, CAD, 4CL, and COMT) and contents of metabolites (sinapyl alcohol, phenylalanine, p-coumaryl alcohol, caffeyl alcohol, and coniferaldehyde) were remarkably enhanced by treatment with Cd1Se0.2, thus, maintaining the integrity of cell walls in the roots. It also enhanced signal transduction by plant hormones and responsive resistance by inducing the biosynthesis of genes (BZR1, LOX3, and NCDE1) and metabolites (brassinolide, abscisic acid, and jasmonic acid) in the roots and leaves. In general, this study can enable a better understanding of the protective mechanism of nano-Se in improving the capacity of plants to resist environmental stress.

Abstract 29: Chronic Stress Predisposes to Thrombosis by Abnormal Megakaryopiesis: Protective Effect of Apocynin

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Leonardo Sandrini ◽  
Alessandro Ieraci ◽  
Elisa Turra ◽  
Patrizia Amadio ◽  
Maurizio Popoli ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Nadph Oxidase ◽  
Chronic Stress ◽  
Redox Balance ◽  
Antioxidant Systems ◽  
Ros Generation ◽  
Reticulated Platelets ◽  
Stress Studies ◽  
Coronary Syndromes ◽  
Maturation State

Introduction: Psychological stress (e.g. anxiety and depression) has been identified as an important trigger of acute coronary syndromes (ACS), as a consequence of enhanced coagulation and of hyper-reactive platelets. Changes in redox balance, alteration of genes regulating antioxidant systems, including NADPH oxidase, and increased production of reactive oxygen species (ROS) have been measured in both chronic stress and ACS. However, the mechanisms by which chronic stress affects platelet activation and predisposes to thrombosis are not well known. Hypothesis: We hypothesized that Apocynin, an inhibitor of NADPH oxidase influences the alteration of megakaryopoiesis and activation of platelets induced by chronic stress in mice. Methods and Results: We show the NADPH/NADP + ratio in bone marrow (BM) of mice exposed to forced swimming for 4 days (5 min twice/day) is markedly reduced compared to control mice, and that Apocynin treatment (2.4 mg/ml in drinking water for 4 days) prevents this alteration. Chronic stress leads to an abnormal megakaryopoiesis increasing the number of BM megakaryocytes (MKs) and affecting circulating platelets. MKs of stressed mice show an advanced maturation state (e.g. nuclear/cytoplasmic ratios and expression of CD42d), and an enhanced ability to produce ROS. Interestingly, a higher number of large and reticulated platelets with marked functional activation (e.g. integrin α IIb β3 and P-selectin expression, and platelet/leukocyte aggregates) is detected after chronic stress. In addition, Apocynin prevents ROS MKs generation and decreases the total number of MKs without affecting the percentage of CD42d + cells. Finally, the inhibitor of NADPH oxidase activity reduces the hyper-activation of platelets and the enhanced susceptibility to FeCl3-induced arterial thrombosis in stressed mice. Conclusion: Apocynin treatment, reducing ROS generation in MKs, restores the physiological bone marrow megakaryopoiesis and platelet behaviour, and it prevents the detrimental effect of chronic stress on atherothrombosis. These data suggest a potential use of NADPH oxidase inhibitors in the occurrence of thrombosis associated with chronic stress. Studies in human will verify the clinical impact of these findings.

scholarly journals Energetics of Inhibition: Insights with a Computational Model of the Human GABAergic Neuron–Astrocyte Cellular Complex

2010 ◽  
Vol 30 (11) ◽  
pp. 1834-1846 ◽  
Author(s):  
Rossana Occhipinti ◽  
Erkki Somersalo ◽  
Daniela Calvetti
Keyword(s):  
Glucose Consumption ◽  
Compartment Model ◽  
Cell Types ◽  
Redox Balance ◽  
Gabaergic Neurons ◽  
Neuronal Uptake ◽  
Activity Levels ◽  
Inhibitory Neurotransmitter ◽  
Metabolic Coupling

We investigate metabolic interactions between astrocytes and GABAergic neurons at steady states corresponding to different activity levels using a six-compartment model and a new methodology based on Bayesian statistics. Many questions about the energetics of inhibition are still waiting for definite answers, including the role of glutamine and lactate effluxed by astrocytes as precursors for γ-aminobutyric acid (GABA), and whether metabolic coupling applies to the inhibitory neurotransmitter GABA. Our identification and quantification of metabolic pathways describing the interaction between GABAergic neurons and astrocytes in connection with the release of GABA makes a contribution to this important problem. Lactate released by astrocytes and its neuronal uptake is found to be coupled with neuronal activity, unlike glucose consumption, suggesting that in astrocytes, the metabolism of GABA does not require increased glycolytic activity. Negligible glutamine trafficking between the two cell types at steady state questions glutamine as a precursor of GABA, not excluding glutamine cycling as a transient dynamic phenomenon, or a prominent role of GABA reuptake. Redox balance is proposed as an explanation for elevated oxidative phosphorylation and adenosine triphosphate hydrolysis in astrocytes, decoupled from energy requirements.

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