Exogenous application of nitric oxide donors regulates short-term flooding stress in soybean

Short-term water submergence to soybean (Glycine max L.) create hypoxic conditions hindering plant growth and productivity. Nitric oxide (NO) is considered a stress-signalling and stress-evading molecule, however, little is known about its role during flooding stress. We elucidated the role of sodium nitroprusside (SNP) and S-nitroso L-cysteine (CySNO) as NO donor in modulation of flooding stress-related bio-chemicals and genetic determinants of associated nitrosative stress to Daewon and Pungsannamul soybean cultivars after 3 h and 6 h of flooding stress. The results showed that exogenous SNP and CysNO induced glutathione activity and reduced the resulting superoxide anion contents during short-term flooding in Pungsannamul soybean. The exo- SNP and CysNO triggered the endogenous S-nitrosothiols, and resulted in elevated abscisic acid (ABA) contents in both soybean cultivars overtime. To know the role of ABA and NO related genes in short-term flooding stress, the mRNA expression of S-nitrosoglutathione reductase (GSNOR1), NO overproducer1 (NOX1) and nitrate reductase (NR), Timing of CAB expression1 (TOC1), and ABA-receptor (ABAR) were assessed. The transcripts accumulation of GSNOR1, NOX1, and NR being responsible for NO homeostasis, were significantly high in response to early or later phases of flooding stress. ABAR and TOC1 showed a decrease in transcript accumulation in both soybean plants treated with exogenous SNP and CySNO. The exo- SNP and CySNO could impinge a variety of biochemical and transcriptional programs that can mitigate the negative effects of short-term flooding stress in soybean.

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Gibberellin application ameliorates the adverse impact of short-term flooding on Glycine max L.

Biochemical Journal ◽

10.1042/bcj20180534 ◽

2018 ◽

Vol 475 (18) ◽

pp. 2893-2905 ◽

Cited By ~ 4

Author(s):

Muhammad Aaqil Khan ◽

Muhammad Hamayun ◽

Amjad Iqbal ◽

Sumera Afzal Khan ◽

Anwar Hussain ◽

...

Keyword(s):

Jasmonic Acid ◽

No Production ◽

Genetic Determinants ◽

Short Term ◽

Chlorophyll Contents ◽

Flooding Stress ◽

Hypoxic Conditions ◽

Glycine Max L ◽

Soybean Plants

Flooding is an abiotic stress that creates hypoxic conditions triggered by redox potential leading to restricted growth and grain yield in plants. In the current study, we have investigated the effect of exogenous gibberellins (GA4+7) on soybean under flooding stress. A regulatory role of GAs on biochemical changes in soybean plants [including chlorophyll contents, endogenous bioactive GA1 and GA4, endogenous jasmonic acid (JA) and abscisic acid (ABA)] has been elucidated after 3 and 6 h of flooding stress. The modulation of stress-related bio-chemicals and their genetic determinants [for instance, ABA (Timing of CAB expression1—TOC1, ABA-receptor—ABAR) and NO (S-nitrosoglutathione reductase—GSNOR1, NO overproducer1—NOX, and nitrite reductase—NR)] in response to short-term flooding stress were also explored. The current study showed that exogenous GAs rescued chlorophyll contents, enhanced endogenous bioactive GA1 and GA4 levels, endogenous jasmonic acid (JA) and checked the rate of ABA biosynthesis under short-term flooding. The exo-GAs induced the glutathione activity and reduced the resulting superoxide anion contents during short-term flooding in Pungsannamul soybean. Exo-GAs also triggered the endogenous S-nitrosothiols (precursor for increased NO production) that have been decreased over the time. Moreover, the exo-GAs could impinge a variety of biochemical and transcriptional programs that are ameliorative to plant growth during short-term flooding stress. The presence of GA1 and GA4 also confirms the presence of both C13-hydroxylation pathway and non-C13-hydroxylation pathway in soybean, respectively.

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N-acetyl ornithine deacetylase is a moonlighting protein and is involved in the adaptation of Entamoeba histolytica to nitrosative stress

Scientific Reports ◽

10.1038/srep36323 ◽

2016 ◽

Vol 6 (1) ◽

Cited By ~ 9

Author(s):

Preeti Shahi ◽

Meirav Trebicz-Geffen ◽

Shruti Nagaraja ◽

Rivka Hertz ◽

Sharon Alterzon-Baumel ◽

...

Keyword(s):

Nitric Oxide ◽

Entamoeba Histolytica ◽

Detrimental Effect ◽

Nitrosative Stress ◽

Metabolic Enzyme ◽

Rna Seq ◽

No Donor ◽

Moonlighting Protein ◽

Insight Into

Abstract Adaptation of the Entamoeba histolytica parasite to toxic levels of nitric oxide (NO) that are produced by phagocytes may be essential for the establishment of chronic amebiasis and the parasite’s survival in its host. In order to obtain insight into the mechanism of E. histolytica’s adaptation to NO, E. histolytica trophozoites were progressively adapted to increasing concentrations of the NO donor drug, S-nitrosoglutathione (GSNO) up to a concentration of 110 μM. The transcriptome of NO adapted trophozoites (NAT) was investigated by RNA sequencing (RNA-seq). N-acetyl ornithine deacetylase (NAOD) was among the 208 genes that were upregulated in NAT. NAOD catalyzes the deacetylation of N-acetyl-L-ornithine to yield ornithine and acetate. Here, we report that NAOD contributes to the better adaptation of the parasite to nitrosative stress (NS) and that this function does not depend on NAOD catalytic activity. We also demonstrated that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is detrimental to E. histolytica exposed to NS and that this detrimental effect is neutralized by NAOD or by a catalytically inactive NAOD (mNAOD). These results establish NAOD as a moonlighting protein, and highlight the unexpected role of this metabolic enzyme in the adaptation of the parasite to NS.

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Differential expression of AtWAKL10 in response to nitric oxide suggests a putative role in biotic and abiotic stress responses

PeerJ ◽

10.7717/peerj.7383 ◽

2019 ◽

Vol 7 ◽

pp. e7383

Author(s):

Phearom Bot ◽

Bong-Gyu Mun ◽

Qari Muhammad Imran ◽

Adil Hussain ◽

Sang-Uk Lee ◽

...

Keyword(s):

Nitric Oxide ◽

Abiotic Stress ◽

Pseudomonas Syringae ◽

Stress Responses ◽

Abiotic Stresses ◽

Nitrosative Stress ◽

Abiotic Stress Tolerance ◽

Biotic And Abiotic Stress ◽

Transcript Accumulation

Plant defense against pathogens and abiotic stresses is regulated differentially by communicating signal transduction pathways in which nitric oxide (NO) plays a key role. Here, we show the biological role of Arabidopsis thaliana wall-associated kinase (AtWAK) Like10 (AtWAKL10) that exhibits greater than a 100-fold change in transcript accumulation in response to the NO donor S-nitroso-L-cysteine (CysNO), identified from high throughput RNA-seq based transcriptome analysis. Loss of AtWAKL10 function showed a similar phenotype to wild type (WT) with, however, less branching. The growth of atwakl10 on media supplemented with oxidative or nitrosative stress resulted in differential results with improved growth following treatment with CysNO but reduced growth in response to S-nitrosoglutatione (GSNO) and methyl-viologen. Further, atwakl10 plants exhibited increased susceptibility to virulent Pseudomonas syringae pv tomato (Pst) DC3000 with a significant increase in pathogen growth and decrease in PR1 transcript accumulation compared to WT overtime. Similar results were found in response to Pst DC3000 avrB, resulting in increased cell death as shown by increased electrolyte leakage in atwakl10. Furthermore, atwakl10 also showed increased reactive oxygen species accumulation following Pst DC3000 avrB inoculation. Promoter analysis of AtWAKL10 showed transcription factor (TF) binding sites for biotic and abiotic stress-related TFs. Further investigation into the role of AtWAKL10 in abiotic stresses showed that following two weeks water-withholding drought condition most of the atwakl10 plants got wilted; however, the majority (60%) of these plants recovered following re-watering. In contrast, in response to salinity stress, atwakl10 showed reduced germination under 150 mM salt stress compared to WT, suggesting that NO-induced AtWAKL10 differentially regulates different abiotic stresses. Taken together, this study further elucidates the importance of NO-induced changes in gene expression and their role in plant biotic and abiotic stress tolerance.

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Role of Nitric Oxide in Short-term and Prolonged Effects of Angiotensin II on Renal Hemodynamics

Hypertension ◽

10.1161/01.hyp.27.5.1173 ◽

1996 ◽

Vol 27 (5) ◽

pp. 1173-1179 ◽

Cited By ~ 52

Author(s):

Xiaolin Deng ◽

William J. Welch ◽

Christopher S. Wilcox

Keyword(s):

Nitric Oxide ◽

Angiotensin Ii ◽

Renal Hemodynamics ◽

Short Term

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Florigen governs shoot regeneration

Scientific Reports ◽

10.1038/s41598-021-93180-1 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Yaarit Kutsher ◽

Michal Fisler ◽

Adi Faigenboim ◽

Moshe Reuveni

Keyword(s):

Nitric Oxide ◽

Shoot Regeneration ◽

Ectopic Expression ◽

Flowering Plants ◽

Regeneration Capacity ◽

No Donor ◽

Tobacco Leaves ◽

Age Related ◽

Delayed Flowering

AbstractIt is widely known that during the reproductive stage (flowering), plants do not root well. Most protocols of shoot regeneration in plants utilize juvenile tissue. Adding these two realities together encouraged us to study the role of florigen in shoot regeneration. Mature tobacco tissue that expresses the endogenous tobacco florigen mRNA regenerates poorly, while juvenile tissue that does not express the florigen regenerates shoots well. Inhibition of Nitric Oxide (NO) synthesis reduced shoot regeneration as well as promoted flowering and increased tobacco florigen level. In contrast, the addition of NO (by way of NO donor) to the tissue increased regeneration, delayed flowering, reduced tobacco florigen mRNA. Ectopic expression of florigen genes in tobacco or tomato decreased regeneration capacity significantly. Overexpression pear PcFT2 gene increased regeneration capacity. During regeneration, florigen mRNA was not changed. We conclude that florigen presence in mature tobacco leaves reduces roots and shoots regeneration and is the possible reason for the age-related decrease in regeneration capacity.

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Effect of time and vascular pressure on permeability and cyclic nucleotides in ischemic lungs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2000.279.5.h2077 ◽

2000 ◽

Vol 279 (5) ◽

pp. H2077-H2084 ◽

Cited By ~ 8

Author(s):

David B. Pearse ◽

Patrice M. Becker

Keyword(s):

Nitric Oxide ◽

High Pressure ◽

Reflection Coefficient ◽

Cyclic Nucleotides ◽

Fluid Flux ◽

No Donor ◽

Independent Mechanism ◽

Dependent Mechanism ◽

Intravascular Pressure

We previously found that increased intravascular pressure decreased ischemic lung injury by a nitric oxide (NO)-dependent mechanism (Becker PM, Buchanan W, and Sylvester JT. J Appl Physiol 84: 803–808, 1998). To determine the role of cyclic nucleotides in this response, we measured the reflection coefficient for albumin (ςalb), fluid flux ( J˙), cGMP, and cAMP in ferret lungs subjected to either 45 min (“short”; n = 7) or 180 min (“long”) of ventilated ischemia. Long ischemic lungs had “low” (1–2 mmHg, n = 8) or “high” (7–8 mmHg, n = 6) vascular pressure. Other long low lungs were treated with the NO donor ( Z)-1-[ N-(3-ammoniopropyl)- N-( n-propyl)amino]diazen-1-ium-1,2-diolate (PAPA-NONOate; 5 × 10−4 M, n = 6) or 8-bromo-cGMP (5 × 10−4 M, n = 6). Compared with short ischemia, long low ischemia decreased ςalb (0.23 ± 0.04 vs. 0.73 ± 0.08; P < 0.05) and increased J˙ (1.93 ± 0.26 vs. 0.58 ± 0.22 ml · min−1 · 100 g−1; P < 0.05). High pressure prevented these changes. Lung cGMP decreased by 66% in long compared with short ischemia. Lung cAMP did not change. PAPA-NONOate and 8-bromo-cGMP increased lung cGMP, but only 8-bromo-cGMP decreased permeability. These results suggest that ischemic vascular injury was, in part, mediated by a decrease in cGMP. Increased vascular pressure prevented injury by a cGMP-independent mechanism that could not be mimicked by administration of exogenous NO.

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Abstract 16720: Cytoglobin Regulates Cardiovascular Function and Vessel Tone by Controlling the Rate of Vascular Nitric Oxide Metabolism

Circulation ◽

10.1161/circ.130.suppl_2.16720 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Xiaoping Liu ◽

Mohamed A El-Mahdy ◽

Raed S Ismail ◽

Sean Little ◽

Le T Thuy ◽

...

Keyword(s):

Nitric Oxide ◽

Vascular Wall ◽

No Donor ◽

Nitric Oxide Metabolism ◽

No Consumption ◽

Potent Vasodilator ◽

Inner Diameter ◽

The Difference ◽

Synthase Inhibitor

Cytoglobin (Cygb) can effectively metabolize nitric oxide (NO), a potent vasodilator, in the presence of oxygen and reductants. Cygb in the vascular wall may affect cardiovascular functions by changing the rate of NO metabolism. In this study, we directly tested the vascular role of Cygb using Cygb knockout (Cygb-/-) mice. The mean blood pressure of Cygb-/- and C57BL/6 wild type (WT) mice was 65.3 ± 1.9 mmHg and 93.7 ± 1.5 mmHg, respectively (n=10). Using echocardiography, we observed that cardiac output (CO) was increased in Cygb-/- mice compared to WT with values of 29.8 ± 3.9 vs 17.7 ± 0.9 ml/min. The systemic vascular resistance (SVR) of Cygb-/- mice was decreased by ~60% vs that of WT mice (Fig. 1). Further, the inner diameter (id) of aorta of Cygb-/- mice was dilated compared to WT with values of 2.2 ± 0.1 mm vs 1.5 ± 0.05 mm (n=5), respectively. After treatment with the NO synthase inhibitor L-NAME, no difference in the aortic id remained between Cygb-/- (1.55 ± 0.03 mm) and WT (1.49 ± 0.02 mm) mice, indicating that the NO pathway is responsible for the difference in vascular inner diameters and tone. Myograph experiments show that the aortic vasodilation response of Cygb-/- mice is much more sensitive to acetylcholine (Ach) or the NO donor nitroprusside (SNP) (EC50 shifts from 13 nM and 2.9 nM (WT mice) to 0.33 nM and 0.16 nM (Cygb-/-) for Ach and SNP, respectively). Using NO electrodes to measure the rate of NO consumption by SMCs and quantitative imunoblotting to estimate Cygb content in RSMCs-AR and Cygb knockdown RSMCs, we observed that 90% of NO consumption by RSMCs-AR is caused by the intracellular Cygb. Our results indicate that Cygb deficiency in the vascular wall of Cygb-/- mice greatly reduces the rate of NO metabolism and increases vascular NO concentration, resulting in vasodilation, increase in vessel lumen diameter, and decrease in SVR. These results demonstrate that Cygb regulates cardiac function and vessel tone by controlling the rate of vascular NO metabolism.

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Role of nitric oxide in gut ischemia-reperfusion-induced hepatic microvascular dysfunction

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1997.273.5.g1007 ◽

1997 ◽

Vol 273 (5) ◽

pp. G1007-G1013 ◽

Cited By ~ 4

Author(s):

Yoshinori Horie ◽

Robert Wolf ◽

D. Neil Granger

Keyword(s):

Nitric Oxide ◽

Important Determinant ◽

Leukocyte Adhesion ◽

Ischemia Reperfusion ◽

Protective Action ◽

Microvascular Dysfunction ◽

Artery Occlusion ◽

No Donor ◽

Synthase Inhibitor

The overall objective of this study was to assess the contribution of an altered bioavailability of nitric oxide (NO) to the leukocyte adhesion and hypoxic stress elicited in the liver by gut ischemia-reperfusion (I/R). The accumulation of leukocytes, number of nonperfused sinusoids (NPS), and NADH autofluorescence were monitored (by intravital microscopy) in mouse liver after 15 min of superior mesenteric artery occlusion and 60 min of reperfusion. Leukostasis, NPS, and NADH autofluorescence (indicating hypoxia) were all increased in the liver at 60 min after gut I/R. The NO synthase inhibitor N G-monomethyl-l-arginine (l-NMMA) exaggerated the liver leukostasis elicited by gut I/R, responses that were prevented by coadministration of l-arginine. The NO donor diethylenetriamine-NO (DETA-NO) andl-arginine were both effective in attenuating the gut I/R-induced leukostasis and increased NADH autofluorescence, whereas neither DETA nord-arginine exerted a protective action. These findings indicate that NO is an important determinant of the liver leukostasis, impaired sinusoidal perfusion, and tissue hypoxia elicited by gut I/R.

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Nitric oxide-induced cardioprotection in cultured rat ventricular myocytes

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2000.278.4.h1211 ◽

2000 ◽

Vol 278 (4) ◽

pp. H1211-H1217 ◽

Cited By ~ 57

Author(s):

Roby D. Rakhit ◽

Richard J. Edwards ◽

James W. Mockridge ◽

Anwar R. Baydoun ◽

Amanda W. Wyatt ◽

...

Keyword(s):

Nitric Oxide ◽

Ventricular Myocytes ◽

Culture Conditions ◽

Neonatal Rat ◽

No Donor ◽

Rat Ventricular Myocytes ◽

Kinase C ◽

Neonatal Rat Ventricular Myocytes ◽

Oxide Synthase

The aim of this study was to investigate the role of nitric oxide (NO) in a cellular model of early preconditioning (PC) in cultured neonatal rat ventricular myocytes. Cardiomyocytes “preconditioned” with 90 min of stimulated ischemia (SI) followed by 30 min reoxygenation in normal culture conditions were protected against subsequent 6 h of SI. PC was blocked by N G-monomethyl-l-arginine monoacetate but not by dexamethasone pretreatment. Inducible nitric oxide synthase (NOS) protein expression was not detected during PC ischemia. Pretreatment (90 min) with the NO donor S-nitroso- N-acetyl-l,l-penicillamine (SNAP) mimicked PC, resulting in significant protection. SNAP-triggered protection was completely abolished by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) but was unaffected by chelerythrine or the presence of glibenclamide and 5-hydroxydecanoate. With the use of RIA, SNAP treatment increased cGMP levels, which were blocked by ODQ. Hence, NO is implicated as a trigger in this model of early PC via activation of a constitutive NOS isoform. After exposure to SNAP, the mechanism of cardioprotection is cGMP dependent but independent of protein kinase C or ATP-sensitive K+ channels. This differs from the proposed mechanism of NO-induced cardioprotection in late PC.

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Comprehensive Analyses of Nitric Oxide-Induced Plant Stem Cell-Related Genes in Arabidopsis thaliana

Genes ◽

10.3390/genes10030190 ◽

2019 ◽

Vol 10 (3) ◽

pp. 190

Author(s):

Muhammad Shahid ◽

Qari Imran ◽

Adil Hussain ◽

Murtaza Khan ◽

Sang Lee ◽

...

Keyword(s):

Nitric Oxide ◽

Stem Cell ◽

Nitrosative Stress ◽

High Reliability ◽

Pearson Correlation ◽

Early Time ◽

Rna Seq ◽

No Donor ◽

Cis Acting ◽

Plant Stem

Plant stem cells are pluripotent cells that have diverse applications in regenerative biology and medicine. However, their roles in plant growth and disease resistance are often overlooked. Using high-throughput RNA-seq data, we identified approximately 20 stem cell-related differentially expressed genes (DEGs) that were responsive to the nitric oxide (NO) donor S-nitrosocysteine (CySNO) after six hours of infiltration. Among these DEGs, the highest number of positive correlations (R ≥ 0.8) was observed for CLAVATA3/EMBRYO SURROUNDING REGION-RELATED (CLE) 12. Gene ontology (GO) terms for molecular function showed DEGs associated with signal transduction and receptor activity. A promoter study of these DEGs showed the presence of cis-acting elements that are involved in growth as well as the regulation of abiotic and biotic stress. Phylogenetic analysis of the Arabidopsis stem cell-related genes and their common orthologs in rice, soybean, poplar, and tomato suggested that most soybean stem cell-related genes were grouped with the Arabidopsis CLE type of stem cell genes, while the rice stem cell-related genes were grouped with the Arabidopsis receptor-like proteins. The functional genomic-based characterization of the role of stem cell DEGs showed that under control conditions, the clv1 mutant showed a similar phenotype to that of the wild-type (WT) plants; however, under CySNO-mediated nitrosative stress, clv1 showed increased shoot and root length compared to WT. Furthermore, the inoculation of clv1 with virulent Pst DC3000 showed a resistant phenotype with fewer pathogens growing at early time points. The qRT-PCR validation and correlation with the RNA-seq data showed a Pearson correlation coefficient of >0.8, indicating the significantly high reliability of the RNA-seq analysis.

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