Nucleoredoxin guards against oxidative stress by protecting antioxidant enzymes

Kneeshaw, Sophie; Keyani, Rumana; Delorme-Hinoux, Valérie; Imrie, Lisa; Loake, Gary J.; Bihan, Thierry Le; Reichheld, Jean‐Philippe; Spoel, Steven H.

doi:10.1073/pnas.1703344114

Cited by 104 publications

(56 citation statements)

References 43 publications

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“…These proteins belong to the redoxin superfamily of oxidoreductases, which functions in reduction of oxidized proteins under high cellular reactive oxygen species (ROS) conditions. Recently, it was shown that nucleoredoxin activity is required to maintain the integrity of antioxidative enzyme systems under redox dis‐balance . Thus, our data demonstrates that soybean pod‐wall immediately triggers the oxidative stress tolerance machinery under KI‐simulated terminal drought onset.…”

Section: Discussionmentioning

confidence: 52%

Pod‐wall proteomics provide novel insights into soybean seed‐filling process under chemical‐induced terminal drought stress

et al. 2018

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BACKGROUND: Drought is very detrimental when it occurs during the reproductive phase of soybeans, leading to considerable yield loss due to the disproportionate allocation of photo-assimilates to competing sinks. As pod walls are known to play a crucial role in regulating carbon partitioning during seed filling under stress conditions, the present study aims to analyze the stage-specific carbon allocation pattern during potassium iodide (KI)-simulated terminal drought, and to provide an insight into the pod-wall proteome responses during drought onset. RESULTS:A comparative proteomics approach was adopted to visualize the differential protein expression in soybean pod-wall at stage R5 (seed initiation). Sugar status was analyzed using high-performance liquid chromatography (HPLC) and biochemical methods. Potassium iodide-simulated terminal drought during reproductive stages 4, 5 and 6 (R4, R5, and R6) caused a significant decline in starch, total carbohydrate, and reducing sugar in the leaves; however, the pod-wall and seeds showed a reduction only in the total carbohydrate content, whereas starch and reducing sugar levels remained unchanged. A pod-wall proteome at stage R5 showed immediate induction of proteins belonging to stress signaling / regulation, protein folding / stabilization, redox-homeostasis, cellular energy, and carbon utilization and down-regulation of negative regulators of drought stress and protein degradation-related proteins. CONCLUSIONS: A KI spray effectively simulated terminal drought stress and caused around 50% yield loss when compared to controls. Our results indicate that, at the very onset of desiccation stress, the pod wall (stage R5) activates strong protective responses to maintain the carbon allocation to the surviving seeds.

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Section: Discussionmentioning

confidence: 52%

Pod‐wall proteomics provide novel insights into soybean seed‐filling process under chemical‐induced terminal drought stress

et al. 2018

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“…A cpk8 mutant had a somewhat higher H 2 O 2 level, as determined by DAB and fluorescein‐based probes. It is therefore likely that CAT activity can be modulated by a number of interactions and modifications, which could result in controlled H 2 O 2 release from peroxisomes (Costa et al ., ; Kneeshaw et al ., ).…”

Section: Control Of H2o2 Concentration: How and Where?mentioning

confidence: 97%

Hydrogen peroxide metabolism and functions in plants

2018

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1 I. Introduction 2 II. Measurement and imaging of H O 2 III. H O and O toxicity 3 IV. Production of H O : enzymes and subcellular locations 4 V. H O transport 9 VI. Control of H O concentration: how and where? 9 VII. Metabolic functions of H O 11 VIII. H O signalling 11 IX. Where next? 13 Acknowledgements 13 References 13 SUMMARY: Hydrogen peroxide (H O ) is produced, via superoxide and superoxide dismutase, by electron transport in chloroplasts and mitochondria, plasma membrane NADPH oxidases, peroxisomal oxidases, type III peroxidases and other apoplastic oxidases. Intracellular transport is facilitated by aquaporins and H O is removed by catalase, peroxiredoxin, glutathione peroxidase-like enzymes and ascorbate peroxidase, all of which have cell compartment-specific isoforms. Apoplastic H O influences cell expansion, development and defence by its involvement in type III peroxidase-mediated polymer cross-linking, lignification and, possibly, cell expansion via H O -derived hydroxyl radicals. Excess H O triggers chloroplast and peroxisome autophagy and programmed cell death. The role of H O in signalling, for example during acclimation to stress and pathogen defence, has received much attention, but the signal transduction mechanisms are poorly defined. H O oxidizes specific cysteine residues of target proteins to the sulfenic acid form and, similar to other organisms, this modification could initiate thiol-based redox relays and modify target enzymes, receptor kinases and transcription factors. Quantification of the sources and sinks of H O is being improved by the spatial and temporal resolution of genetically encoded H O sensors, such as HyPer and roGFP2-Orp1. These H O sensors, combined with the detection of specific proteins modified by H O , will allow a deeper understanding of its signalling roles.

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“…CNVs-based M-GWAS analysis identify the association between Bifidobacterium dentium and nucleoredoxin ( NXN ) with copy loss of 642 bp (chr17:898377-899018; P = 4.11 × 10 −6 ; Fig. 5B), and nucleoredoxin 1 as the oxidoreductase protects antioxidant enzymes such as catalase from ROS-induced oxidation in plant cells (Kneeshaw et al, 2017). In addition, NXN was significantly high expressed in normal tissue samples compared with colon adenocarcinoma (COAD) and rectum adenocarcinoma (READ) cases (Fig.…”

Section: Resultsmentioning

confidence: 99%

M-GWAS for the gut microbiome in Chinese adults illuminates on complex diseases

Liu

Tang

Huang

et al. 2019

Preprint

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SummaryThe gut microbiome has been established as a key environmental factor to health. Genetic influences on the gut microbiome have been reported, yet, doubts remain as to the significance of genetic associations. Here, we provide shotgun data for whole genome and whole metagenome from a Chinese cohort, identifying no less than 20% genetic contribution to the gut microbiota. Using common variants-, rare variants- and copy number variations (CNVs)-based association analyses, we identified abundant signals associated with the gut microbiome especially in metabolic, neurological and immunological functions. The controversial concept of enterotypes may have a genetic attribute, with the top 2 loci explaining 11% of the Prevotella-Bacteroides variances. Stratification according to gender led to the identification of differential associations in males and females. Genetically encoded responses to ectopic presence of oral bacteria in the gut appear to be a common theme in a number of diseases investigated by MWAS (Metagenome-wide association studies). Our two-stage M-GWAS (Microbiome genome-wide association studies) on a total of 1295 individuals unequivocally illustrates that neither microbiome nor GWAS studies could overlook one another in our quest for a better understanding of human health and diseases.HighlightsM-GWAS using high-depth whole genome identifies contributions from rare variants and CNVs.Gut microbial modules such as butyrate, amino acids, mucin degradation show genetic associations.Gender differential M-GWAS underscores differences in metabolic and psychological predispositions.Some of the MWAS markers for colorectal cancer and cardiometabolic diseases show genetic associations.

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Nucleoredoxin guards against oxidative stress by protecting antioxidant enzymes

Cited by 104 publications

References 43 publications

Pod‐wall proteomics provide novel insights into soybean seed‐filling process under chemical‐induced terminal drought stress

Pod‐wall proteomics provide novel insights into soybean seed‐filling process under chemical‐induced terminal drought stress

Hydrogen peroxide metabolism and functions in plants

M-GWAS for the gut microbiome in Chinese adults illuminates on complex diseases

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