Evidences for a role of nitric oxide in iron homeostasis in plants

2020 ◽  
Author(s):  
Rajesh Kumar Tewari ◽  
Nele Horemans ◽  
Masami Watanabe
Keyword(s):  
Nitric Oxide ◽  
Iron Homeostasis ◽  
Air Pollutant ◽  
Target Cells ◽  
Antioxidant Defence ◽  
Metabolic Functions ◽  
Essential Nutrient ◽  
Fe Homeostasis ◽  
Cellular Compartments

Abstract Nitric oxide (NO) once regarded as a poisonous air pollutant, is now appreciated as a regulatory molecule essential for several biological functions in plants. In this review we not only summarize NO generation in different plant organs and cellular compartments, we also discuss the role of NO in Fe homeostasis particularly in Fe-deficient plants. Fe is one of the most limiting essential nutrient element for plants. Plants often exhibit Fe deficiency symptoms despite of sufficient tissue Fe concentration. NO appears to be not only upregulating Fe uptake mechanisms but it also makes it more bioavailable for metabolic functions. NO forms complexes with Fe which can then be delivered into target cells/ tissues. NO generated in plants can alleviate oxidative stress by regulating antioxidant defence processes probably by improving functional Fe status and by inducing post-translational modifications in the enzymes/proteins involved in the antioxidant defence responses. It is hypothesized that NO acts in cooperation with transcription factors such as bHLH, FIT and IRO (Iron-transcription factor) to regulate expression of enzymes and proteins essential for Fe homeostasis. However, further investigations are needed to unentangle the interaction of NO with the intracellular target molecules which lead to an enhanced internal Fe availability in plants.

scholarly journals Gli1 regulates the postnatal acquisition of peripheral nerve architecture

2021 ◽  
Author(s):  
Brendan Zotter ◽  
Or Dagan ◽  
Jacob Brady ◽  
Hasna Baloui ◽  
Jayshree Samanta ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Peripheral Nerves ◽  
Hedgehog Signaling ◽  
Target Cells ◽  
Gli1 Expression ◽  
Desert Hedgehog ◽  
Matrix Production ◽  
Endoneurial Cells ◽  
Cellular Compartments

ABSTRACTPeripheral nerves are organized into discrete cellular compartments. Axons, Schwann cells (SCs), and endoneurial fibroblasts (EFs) reside within the endoneurium and are surrounded by the perineurium - a cellular sheath comprised of layers of perineurial glia (PNG). SC secretion of Desert Hedgehog (Dhh) regulates this organization. In Dhh nulls, the perineurium is deficient and the endoneurium is subdivided into small compartments termed minifascicles. Human Dhh mutations cause a peripheral neuropathy with similar defects. Here we examine the role of Gli1, a canonical transcriptional effector of hedgehog signaling, in regulating peripheral nerve organization. We identify PNG, EFs, and pericytes as Gli1-expressing cells by genetic fate mapping. Although expression of Dhh by SCs and Gli1 in target cells is coordinately regulated with myelination, Gli1 expression unexpectedly persists in Dhh null EFs. Thus, Gli1 is expressed in EFs non-canonically i.e., independent of hedgehog signaling. Gli1 and Dhh also have non-redundant activities. In contrast to Dhh nulls, Gli1 nulls have a normal perineurium. Like Dhh nulls, Gli1 nulls form minifascicles, which we show likely arise from EFs. Thus, Dhh and Gli1 are independent signals: Gli1 is dispensable for perineurial development but functions cooperatively with Dhh to drive normal endoneurial development. During development, Gli1 also regulates endoneurial extracellular matrix production, nerve vascular organization, and has modest, non-autonomous effects on SC sorting and myelination of axons. Finally, in adult nerves, induced deletion of Gli1 is sufficient to drive minifascicle formation. Thus, Gli1 regulates the development and is required to maintain the endoneurial architecture of peripheral nerves.SIGNIFICANCE STATEMENTPeripheral nerves are organized into distinct cellular/ECM compartments: the epineurium, perineurium and endoneurium. This organization, with its associated cellular constituents, are critical for the structural and metabolic support of nerves and their response to injury. Here, we show Gli1 - a transcription factor normally expressed downstream of hedgehog signaling - is required for the proper organization of the endoneurium but not the perineurium. Unexpectedly, Gli1 expression by endoneurial cells is independent of, and functions non-redundantly with, Schwann Cell-derived Desert Hedgehog in regulating peripheral nerve architecture. These results further delineate how peripheral nerves acquire their distinctive organization during normal development and highlight mechanisms that may regulate their reorganization in pathologic settings including peripheral neuropathies and nerve injury.

scholarly journals Glutathione regulates subcellular iron homeostasis via transcriptional activation of iron responsive genes in Arabidopsis

2021 ◽  
Author(s):  
Ranjana Shee ◽  
Soumi Ghosh ◽  
Pinki Khan ◽  
Salman Sahid ◽  
Chandan Roy ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Transcriptional Activation ◽  
Iron Homeostasis ◽  
Fe Deficiency ◽  
Fe Content ◽  
Increased Sensitivity ◽  
Fe Homeostasis ◽  
Bhlh Transcription Factors ◽  
Dependent Pathway

Glutathione (GSH) is a ubiquitous molecule known to regulate various physiological and developmental phenomena in plants. Recently, its involvement in regulating iron (Fe) deficiency response was established in Arabidopsis. However, the role of GSH in modulating subcellular Fe homeostasis remained elusive. In this study, we dissected the role of GSH in regulating Fe homeostasis in Arabidopsis shoots under Fe limited conditions. The two GSH depleted mutants, cad2-1 and pad2-1 displayed increased sensitivity to Fe deficiency with smaller rosette diameter and higher chlorosis level compared with the Col-0 plants. Interestingly, the expression of the vacuolar Fe exporters, AtNRAMP3 and AtNRAMP4, chloroplast Fe importer, AtPIC1, along with AtFer1 and AtIRT1 were significantly down-regulated in these mutants. The expression of these genes were up-regulated in response to exogenous GSH treatment while treatment with BSO, a GSH inhibitor, down-regulated their expression. Moreover, the mutants accumulated higher Fe content in the vacuole and lower in the chloroplast compared with Col-0 under Fe limited condition suggesting a role of GSH in modulating subcellular Fe homeostasis. This regulation was, further, found to involve a GSNO-dependent pathway. Promoter analysis revealed that GSH induced the transcription of these genes presumably via S-nitrosylation of different Fe responsive bHLH transcription factors.

scholarly journals Nitric Oxide–Mediated Induction of Ferritin Synthesis in J774 Macrophages by Inflammatory Cytokines: Role of Selective Iron Regulatory Protein-2 Downregulation

Blood ◽  
1998 ◽  
Vol 91 (3) ◽  
pp. 1059-1066 ◽  
Author(s):  
Stefania Recalcati ◽  
Donatella Taramelli ◽  
Dario Conte ◽  
Gaetano Cairo
Keyword(s):  
Nitric Oxide ◽  
Posttranscriptional Regulation ◽  
Iron Homeostasis ◽  
Regulatory Protein ◽  
Intracellular Iron ◽  
Iron Regulatory Proteins ◽  
Ferritin Synthesis ◽  
Direct Demonstration ◽  
J774 Cells

Cytokine-treated macrophages represent a useful model to unravel the molecular basis of reticuloendothelial (RE) iron retention in inflammatory conditions. In the present study, we showed that stimulation of murine macrophage J774 cells with interferon (IFN)-γ/lipopolysaccharide (LPS) resulted in a nitric oxide-dependent modulation of the activity of iron regulatory proteins (IRP)-1 and 2, cytoplasmic proteins which, binding to RNA motifs called iron responsive elements (IRE), control ferritin translation. Stimulation with cytokines caused a small increase of IRP-1 activity and a strong reduction of IRP-2 activity accompanied by increased ferritin synthesis and accumulation. Cytokines induced only a minor increase of H chain ferritin mRNA, thus indicating that IRP-2–mediated posttranscriptional regulation plays a major role in the control of ferritin expression. This was confirmed by direct demonstration that the translational repression function of IRP was impaired in stimulated cells. In fact, translation in cell-free extracts of a reporter transcript under the control of an IRE sequence was repressed less efficiently by IRP-containing lysates from cytokine-treated cells than by lysates from control cells. Our findings throw light on the role of IRP-2 showing that: (1) this protein responds to a stimulus in opposite fashion to IRP-1; (2) when abundantly expressed, as in J774 cells, IRP-2 is sufficient to regulate intracellular iron metabolism in living cells; and (3) by allowing increased ferritin synthesis, IRP-2 may play a role in the regulation of iron homeostasis in RE cells during inflammation.

From Nitrate to Nitric Oxide

2016 ◽  
Vol 95 (13) ◽  
pp. 1452-1456 ◽  
Author(s):  
X.M. Qu ◽  
Z.F. Wu ◽  
B.X. Pang ◽  
L.Y. Jin ◽  
L.Z. Qin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Salivary Glands ◽  
Bacterial Species ◽  
Posterior Part ◽  
Oral Bacteria ◽  
Metabolic Functions ◽  
Final Electron ◽  
Nitrate And Nitrite ◽  
Messenger Molecule

The salivary glands and oral bacteria play an essential role in the conversion process from nitrate (NO3-) and nitrite (NO2-) to nitric oxide (NO) in the human body. NO is, at present, recognized as a multifarious messenger molecule with important vascular and metabolic functions. Besides the endogenous L-arginine pathway, which is catalyzed by complex NO synthases, nitrate in food contributes to the main extrinsic generation of NO through a series of sequential steps (NO3--NO2--NO pathway). Up to 25% of nitrate in circulation is actively taken up by the salivary glands, and as a result, its concentration in saliva can increase 10- to 20-fold. However, the mechanism has not been clearly illustrated until recently, when sialin was identified as an electrogenic 2NO3-/H+ transporter in the plasma membrane of salivary acinar cells. Subsequently, the oral bacterial species located at the posterior part of the tongue reduce nitrate to nitrite, as catalyzed by nitrate reductase enzymes. These bacteria use nitrate and nitrite as final electron acceptors in their respiration and meanwhile help the host to convert nitrate to NO as the first step. This review describes the role of salivary glands and oral bacteria in the metabolism of nitrate and in the maintenance of NO homeostasis. The potential therapeutic applications of oral inorganic nitrate and nitrite are also discussed.

Nitric oxide signaling, metabolism and toxicity in nitrogen-fixing symbiosis

2019 ◽  
Vol 70 (17) ◽  
pp. 4505-4520 ◽  
Author(s):  
Antoine Berger ◽  
Alexandre Boscari ◽  
Pierre Frendo ◽  
Renaud Brouquisse
Keyword(s):  
Nitric Oxide ◽  
Potent Inhibitor ◽  
Nodule Development ◽  
Atmospheric Nitrogen ◽  
Nitric Oxide Signaling ◽  
Metabolic Functions ◽  
Hypoxic Environment ◽  
Nodule Senescence ◽  
Key Questions

AbstractInteractions between legumes and rhizobia lead to the establishment of a symbiotic relationship characterized by the formation of a new organ, the nodule, which facilitates the fixation of atmospheric nitrogen (N2) by nitrogenase through the creation of a hypoxic environment. Significant amounts of nitric oxide (NO) accumulate at different stages of nodule development, suggesting that NO performs specific signaling and/or metabolic functions during symbiosis. NO, which regulates nodule gene expression, accumulates to high levels in hypoxic nodules. NO accumulation is considered to assist energy metabolism within the hypoxic environment of the nodule via a phytoglobin–NO-mediated respiration process. NO is a potent inhibitor of the activity of nitrogenase and other plant and bacterial enzymes, acting as a developmental signal in the induction of nodule senescence. Hence, key questions concern the relative importance of the signaling and metabolic functions of NO versus its toxic action and how NO levels are regulated to be compatible with nitrogen fixation functions. This review analyses these paradoxical roles of NO at various stages of symbiosis, and highlights the role of plant phytoglobins and bacterial hemoproteins in the control of NO accumulation.

scholarly journals Reductive Iron Assimilation and Intracellular Siderophores Assist Extracellular Siderophore-Driven Iron Homeostasis and Virulence

2014 ◽  
Vol 27 (8) ◽  
pp. 793-808 ◽  
Author(s):  
Bradford J. Condon ◽  
Shinichi Oide ◽  
Donna M. Gibson ◽  
Stuart B. Krasnoff ◽  
B. Gillian Turgeon
Keyword(s):  
Iron Homeostasis ◽  
Iron Acquisition ◽  
Wild Type ◽  
Peptide Synthetases ◽  
Asexual Sporulation ◽  
High Affinity ◽  
Iron Assimilation ◽  
Genes Encoding ◽  
Essential Nutrient

Iron is an essential nutrient and prudent iron acquisition and management are key traits of a successful pathogen. Fungi use nonribosomally synthesized secreted iron chelators (siderophores) or reductive iron assimilation (RIA) mechanisms to acquire iron in a high affinity manner. Previous studies with the maize pathogen Cochliobolus heterostrophus identified two genes, NPS2 and NPS6, encoding different nonribosomal peptide synthetases responsible for biosynthesis of intra- and extracellular siderophores, respectively. Deletion of NPS6 results in loss of extracellular siderophore biosynthesis, attenuated virulence, hypersensitivity to oxidative and iron-depletion stress, and reduced asexual sporulation, while nps2 mutants are phenotypically wild type in all of these traits but defective in sexual spore development when NPS2 is missing from both mating partners. Here, it is reported that nps2nps6 mutants have more severe phenotypes than both nps2 and nps6 single mutants. In contrast, mutants lacking the FTR1 or FET3 genes encoding the permease and ferroxidase components, respectively, of the alternate RIA system, are like wild type in all of the above phenotypes. However, without supplemental iron, combinatorial nps6ftr1 and nps2nps6ftr1 mutants are less virulent, are reduced in growth, and are less able to combat oxidative stress and to sporulate asexually, compared with nps6 mutants alone. These findings demonstrate that, while the role of RIA in metabolism and virulence is overshadowed by that of extracellular siderophores as a high-affinity iron acquisition mechanism in C. heterostrophus, it functions as a critical backup for the fungus.

scholarly journals Role of Iron Metabolism-Related Genes in Prenatal Development: Insights from Mouse Transgenic Models

Genes ◽  
2021 ◽  
Vol 12 (9) ◽  
pp. 1382
Author(s):  
Zuzanna Kopeć ◽  
Rafał R. Starzyński ◽  
Aneta Jończy ◽  
Rafał Mazgaj ◽  
Paweł Lipiński
Keyword(s):  
Iron Metabolism ◽  
Iron Homeostasis ◽  
Current Knowledge ◽  
Prenatal Development ◽  
Postnatal Life ◽  
Mammalian Development ◽  
Knock Out ◽  
Stage Of Development ◽  
Essential Nutrient

Iron is an essential nutrient during all stages of mammalian development. Studies carried out over the last 20 years have provided important insights into cellular and systemic iron metabolism in adult organisms and led to the deciphering of many molecular details of its regulation. However, our knowledge of iron handling in prenatal development has remained remarkably under-appreciated, even though it is critical for the health of both the embryo/fetus and its mother, and has a far-reaching impact in postnatal life. Prenatal development requires a continuous, albeit quantitatively matched with the stage of development, supply of iron to support rapid cell division during embryogenesis in order to meet iron needs for erythropoiesis and to build up hepatic iron stores, (which are the major source of this microelement for the neonate). Here, we provide a concise overview of current knowledge of the role of iron metabolism-related genes in the maintenance of iron homeostasis in pre- and post-implantation development based on studies on transgenic (mainly knock-out) mouse models. Most studies on mice with globally deleted genes do not conclude whether underlying in utero iron disorders or lethality is due to defective placental iron transport or iron misregulation in the embryo/fetus proper (or due to both). Therefore, there is a need of animal models with tissue specific targeted deletion of genes to advance the understanding of prenatal iron metabolism.

scholarly journals Nitric Oxide–Mediated Induction of Ferritin Synthesis in J774 Macrophages by Inflammatory Cytokines: Role of Selective Iron Regulatory Protein-2 Downregulation

Blood ◽  
1998 ◽  
Vol 91 (3) ◽  
pp. 1059-1066 ◽  
Author(s):  
Stefania Recalcati ◽  
Donatella Taramelli ◽  
Dario Conte ◽  
Gaetano Cairo
Keyword(s):  
Nitric Oxide ◽  
Posttranscriptional Regulation ◽  
Iron Homeostasis ◽  
Regulatory Protein ◽  
Intracellular Iron ◽  
Iron Regulatory Proteins ◽  
Ferritin Synthesis ◽  
Direct Demonstration ◽  
J774 Cells

Abstract Cytokine-treated macrophages represent a useful model to unravel the molecular basis of reticuloendothelial (RE) iron retention in inflammatory conditions. In the present study, we showed that stimulation of murine macrophage J774 cells with interferon (IFN)-γ/lipopolysaccharide (LPS) resulted in a nitric oxide-dependent modulation of the activity of iron regulatory proteins (IRP)-1 and 2, cytoplasmic proteins which, binding to RNA motifs called iron responsive elements (IRE), control ferritin translation. Stimulation with cytokines caused a small increase of IRP-1 activity and a strong reduction of IRP-2 activity accompanied by increased ferritin synthesis and accumulation. Cytokines induced only a minor increase of H chain ferritin mRNA, thus indicating that IRP-2–mediated posttranscriptional regulation plays a major role in the control of ferritin expression. This was confirmed by direct demonstration that the translational repression function of IRP was impaired in stimulated cells. In fact, translation in cell-free extracts of a reporter transcript under the control of an IRE sequence was repressed less efficiently by IRP-containing lysates from cytokine-treated cells than by lysates from control cells. Our findings throw light on the role of IRP-2 showing that: (1) this protein responds to a stimulus in opposite fashion to IRP-1; (2) when abundantly expressed, as in J774 cells, IRP-2 is sufficient to regulate intracellular iron metabolism in living cells; and (3) by allowing increased ferritin synthesis, IRP-2 may play a role in the regulation of iron homeostasis in RE cells during inflammation.

scholarly journals Nitric Oxide as a Unique Bioactive Signaling Messenger in Physiology and Pathophysiology

2004 ◽  
Vol 2004 (4) ◽  
pp. 227-237 ◽  
Author(s):  
Narendra Tuteja ◽  
Mahesh Chandra ◽  
Renu Tuteja ◽  
Mithilesh K. Misra
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular System ◽  
Posttranslational Modification ◽  
Penile Erection ◽  
Defense Mechanism ◽  
Target Cells ◽  
No Production ◽  
Response Modulation ◽  
Physiological Processes

Nitric oxide (NO) is an intra- and extracellular messenger that mediates diverse signaling pathways in target cells and is known to play an important role in many physiological processes including neuronal signaling, immune response, inflammatory response, modulation of ion channels, phagocytic defense mechanism, penile erection, and cardiovascular homeostasis and its decompensation in atherogenesis. Recent studies have also revealed a role for NO as signaling molecule in plant, as it activates various defense genes and acts as developmental regulator. In plants, NO can also be produced by nitrate reductase. NO can operate through posttranslational modification of proteins (nitrosylation). NO is also a causative agent in various pathophysiological abnormalities. One of the very important systems, the cardiovascular system, is affected by NO production, as this bioactive molecule is involved in the regulation of cardiovascular motor tone, modulation of myocardial contractivity, control of cell proliferation, and inhibition of platelet activation, aggregation, and adhesion. The prime source of NO in the cardiovascular system is endothelial NO synthase, which is tightly regulated with respect to activity and localization. The inhibition of chronic NO synthesis leads to neurogenic and arterial hypertensions, which later contribute to development of myocardial fibrosis. Overall, the modulation of NO synthesis is associated with hypertension. This review briefly describes the physiology of NO, its synthesis, catabolism, and targeting, the mechanism of NO action, and the pharmacological role of NO with special reference to its essential role in hypertension.

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