scholarly journals Novel regulators of nitric oxide signaling triggered by host perception in a plant pathogen

2019 ◽  
Author(s):  
Yi Ding ◽  
Donald M. Gardiner ◽  
Di Xiao ◽  
Kemal Kazan
Keyword(s):  
Nitric Oxide ◽  
Physical Contact ◽  
Plant Roots ◽  
Host Recognition ◽  
No Production ◽  
Soil Pathogens ◽  
Nitric Oxide Signaling ◽  
Molecular Events ◽  
Repeat Domain ◽  
Host Signals

AbstractThe rhizosphere interaction between plant roots or pathogenic microbes is initiated by mutual exchange of signals. However, how soil pathogens sense host signals is largely unknown. Here, we studied early molecular events associated with host recognition in Fusarium graminearum, an economically important fungal pathogen that can infect both roots and heads of cereal crops. We found that host-sensing prior to physical contact with plant roots radically alters the transcriptome and triggers nitric oxide (NO) production in F. graminearum. We identified an ankyrin-repeat domain containing protein (FgANK1) required for host-mediated NO production and virulence in F. graminearum. In the absence of host plant, FgANK1 resides in the cytoplasm. In response to host signals, FgANK1 translocates to the nucleus and interacts with a zinc finger transcription factor (FgZC1), also required for NO production and virulence in F. graminearum. Our results reveal new mechanistic insights into host-recognition strategies employed by soil pathogens.

scholarly journals Regulators of nitric oxide signaling triggered by host perception in a plant pathogen

2020 ◽  
Vol 117 (20) ◽  
pp. 11147-11157 ◽  
Author(s):  
Yi Ding ◽  
Donald M. Gardiner ◽  
Di Xiao ◽  
Kemal Kazan
Keyword(s):  
Nitric Oxide ◽  
Specific Binding ◽  
Physical Contact ◽  
Plant Roots ◽  
Host Recognition ◽  
No Production ◽  
Soil Pathogens ◽  
Nitric Oxide Signaling ◽  
Molecular Events ◽  
Host Signals

The rhizosphere interaction between plant roots or pathogenic microbes is initiated by mutual exchange of signals. However, how soil pathogens sense host signals is largely unknown. Here, we studied early molecular events associated with host recognition in Fusarium graminearum, an economically important fungal pathogen that can infect both roots and heads of cereal crops. We found that host sensing prior to physical contact with plant roots radically alters the transcriptome and triggers nitric oxide (NO) production in F. graminearum. We identified an ankyrin-repeat domain containing protein (FgANK1) required for host-mediated NO production and virulence in F. graminearum. In the absence of host plant, FgANK1 resides in the cytoplasm. In response to host signals, FgANK1 translocates to the nucleus and interacts with a zinc finger transcription factor (FgZC1), also required for specific binding to the nitrate reductase (NR) promoter, NO production, and virulence in F. graminearum. Our results reveal mechanistic insights into host-recognition strategies employed by soil pathogens.

scholarly journals Hydrogen sulfide, an enhancer of vascular nitric oxide signaling: mechanisms and implications

2017 ◽  
Vol 312 (1) ◽  
pp. C3-C15 ◽  
Author(s):  
Csaba Szabo
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Soluble Guanylate Cyclase ◽  
Specific Activity ◽  
Cardiovascular Effects ◽  
Biologically Active ◽  
Reduced Form ◽  
No Production ◽  
Nitric Oxide Signaling ◽  
No Signaling

Nitric oxide (NO) vascular signaling has long been considered an independent, self-sufficient pathway. However, recent data indicate that the novel gaseous mediator, hydrogen sulfide (H2S), serves as an essential enhancer of vascular NO signaling. The current article overviews the multiple levels at which this enhancement takes place. The first level of interaction relates to the formation of biologically active hybrid S/N species and the H2S-induced stimulation of NO release from its various stable “pools” (e.g., nitrite). The next interactions occur on the level of endothelial calcium mobilization and PI3K/Akt signaling, increasing the specific activity of endothelial NO synthase (eNOS). The next level of interaction occurs on eNOS itself; H2S directly interacts with the enzyme: sulfhydration of critical cysteines stabilizes it in its physiological, dimeric state, thereby optimizing eNOS-derived NO production and minimizing superoxide formation. Yet another level of interaction, further downstream, occurs at the level of soluble guanylate cyclase (sGC): H2S stabilizes sGC in its NO-responsive, physiological, reduced form. Further downstream, H2S inhibits the vascular cGMP phosphodiesterase (PDE5), thereby prolonging the biological half-life of cGMP. Finally, H2S-derived polysulfides directly activate cGMP-dependent protein kinase (PKG). Taken together, H2S emerges an essential endogenous enhancer of vascular NO signaling, contributing to vasorelaxation and angiogenesis. The functional importance of the H2S/NO cooperative interactions is highlighted by the fact that H2S loses many of its beneficial cardiovascular effects when eNOS is inactive.

scholarly journals Plant Nitric Oxide Signaling under Drought Stress

Plants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 360
Author(s):  
Su-Ee Lau ◽  
Mohd Fadhli Hamdan ◽  
Teen-Lee Pua ◽  
Noor Baity Saidi ◽  
Boon Chin Tan
Keyword(s):  
Nitric Oxide ◽  
Abiotic Stress ◽  
Drought Stress ◽  
Higher Plants ◽  
Genetic Manipulation ◽  
Growth Conditions ◽  
No Production ◽  
Stress Signaling ◽  
Nitric Oxide Signaling

Water deficit caused by drought is a significant threat to crop growth and production. Nitric oxide (NO), a water- and lipid-soluble free radical, plays an important role in cytoprotection. Apart from a few studies supporting the role of NO in drought responses, little is known about this pivotal molecular amendment in the regulation of abiotic stress signaling. In this review, we highlight the knowledge gaps in NO roles under drought stress and the technical challenges underlying NO detection and measurements, and we provide recommendations regarding potential avenues for future investigation. The modulation of NO production to alleviate abiotic stress disturbances in higher plants highlights the potential of genetic manipulation to influence NO metabolism as a tool with which plant fitness can be improved under adverse growth conditions.

scholarly journals Muscle fiber type differences in nitrate and nitrite storage and nitric oxide signaling in rats

2020 ◽  
Author(s):  
Gary M. Long ◽  
Derrick A. Gray ◽  
Ashley D. Troutman ◽  
Amanda Fisher ◽  
Mary Beth Brown ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Fiber Type ◽  
Vastus Lateralis ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Cgmp Level ◽  
No Production ◽  
Nitric Oxide Signaling ◽  
Slow Twitch ◽  
Fast Twitch

AbstractRecent studies have emphasized the importance of the nitric oxide synthase (NOS)-independent, nitrate (NO3−) → nitrite (NO2−) → nitric oxide (NO) pathway in skeletal muscle. In particular, it has been hypothesized that this pathway is especially active in type II, or fast-twitch, muscle fibers, necessitating greater NO3− and NO2− storage. We therefore measured NO3− and NO2− concentrations in the predominantly fast-twitch vastus lateralis and predominantly slow-twitch soleus muscles of rats. Contrary to the above hypothesis, we found that NO3− and NO2− concentrations were 3.4-fold and 1.8-fold higher, respectively, in the soleus. On the other hand, NO signaling (i.e., cyclic guanosine monophosphate (cGMP) level) was comparable in the two muscles. Although the physiological significance of these observations remains to be determined, we speculate that NO production via the NO3− → NO2− → NO pathway is normally higher in slow-twitch muscles, thus helping compensate for their inherently lower NOS activity.

scholarly journals High temperature inhibits cnidarian-dinoflagellate symbiosis establishment through nitric oxide signaling

2020 ◽  
Author(s):  
Lilian J. Hill ◽  
Leonardo T. Salgado ◽  
Paulo S. Salomon ◽  
Annika Guse
Keyword(s):  
Nitric Oxide ◽  
Temperature Stress ◽  
Elevated Temperatures ◽  
No Production ◽  
Molecular Signaling ◽  
No Donor ◽  
Nitric Oxide Signaling ◽  
Coral Reef Ecosystems ◽  
No Signaling ◽  
Symbiont Acquisition

AbstractCoral reef ecosystems depend on a functional symbiosis between corals and photosynthetic dinoflagellate symbionts (Symbiodiniaceae), which reside inside the coral cells. Symbionts transfer nutrients essential for the corals’ survival, and loss of symbionts (‘coral bleaching’) can result in coral death. Temperature stress is one factor that can induce bleaching and is associated with the molecule nitric oxide (NO). Likewise, symbiont acquisition by aposymbiotic hosts is sensitive to elevated temperatures, but to date the role of NO signaling in symbiosis establishment is unknown. To address this, we use symbiosis establishment assays in aposymbiotic larvae of the anemone model Exaiptasia pallida (Aiptasia). We show that elevated temperature (32°C) enhances NO production in cultured symbionts but not in aposymbiotic larvae. Additionally, we find that symbiosis establishment is impaired at 32°C, and this same impairment is observed at control temperature (26°C) in the presence of a specific NO donor (GSNO). Conversely, the specific NO scavenger (cPTIO) restores symbiosis establishment at 32°C; however, reduction in NO levels at 26°C reduces the efficiency of symbiont acquisition. Our findings indicate that explicit NO levels are crucial for symbiosis establishment, highlighting the complexity of molecular signaling between partners and the adverse implications of temperature stress on coral reefs.

scholarly journals The diatom-derived aldehyde decadienal affects life cycle transition in the ascidian Ciona intestinalis through nitric oxide/ERK signalling

Open Biology ◽  
2015 ◽  
Vol 5 (3) ◽  
pp. 140182 ◽  
Author(s):  
Immacolata Castellano ◽  
Elena Ercolesi ◽  
Giovanna Romano ◽  
Adrianna Ianora ◽  
Anna Palumbo
Keyword(s):  
Nitric Oxide ◽  
Larval Development ◽  
Target Genes ◽  
Life Stage ◽  
Ciona Intestinalis ◽  
Redox Balance ◽  
No Production ◽  
Molecular Events ◽  
Erk Phosphorylation ◽  
Polyunsaturated Aldehydes

Polyunsaturated aldehydes (PUAs) are fatty-acid-derived metabolites produced by some microalgae, including different diatom species. PUAs are mainly produced as a wound-activated defence mechanism against microalgal predators or released from senescent cells at the end of a bloom. PUAs, including 2,4- trans -decadienal (DD), induce deleterious effects on embryonic and larval development of several planktonic and benthic organisms. Here, we report on the effects of DD on larval development and metamorphosis of the ascidian Ciona intestinalis. Ciona larval development is regulated by the cross-talking of different molecular events, including nitric oxide (NO) production, ERK activation and caspase 3-dependent apoptosis. We report that treatment with DD at the competence larval stage results in a delay in metamorphosis. DD affects redox balance by reducing total glutathione and NO levels. By biochemical and quantitative gene expression analysis, we identify the NO-signalling network affected by DD, including the upregulation of ERK phosphatase mkp1 and consequent reduction of ERK phosphorylation, with final changes in the expression of downstream ERK target genes. Overall, these results give new insights into the molecular pathways induced in marine organisms after exposure to PUAs during larval development, demonstrating that this aldehyde affects key checkpoints of larval transition from the vegetative to the reproductive life stage.

Hematopoietic Stem Cell Development Is Dependent on Blood Flow and Nitric Oxide Signaling

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 728-728 ◽  
Author(s):  
Trista E. North ◽  
Wolfram Goessling ◽  
Marian Peeters ◽  
Pulin Li ◽  
Allegra M. Lord ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Stem Cells ◽  
Blood Flow ◽  
Physiological Mechanism ◽  
No Production ◽  
Hematopoietic Stem ◽  
Nitric Oxide Signaling ◽  
No Signaling ◽  
Increased Blood Flow

Abstract During vertebrate embryogenesis, definitive hematopoietic stem cells (HSC) arise in the aorta-gonads-mesonephros (AGM). Based on the functional conservation of AGM hematopoiesis from fish to man, an evolutionary advantage for the production of stem cells within the aorta must exist. The identification of the signals that induce HSCs at this developmental stage is of significant interest. Through a chemical genetic screen in zebrafish, a diverse group of compounds that regulate blood flow were found to affect the production of runx1/cmyb+ HSCs. These compounds represented modulators of the adrenergic and renin/angiotensin pathways, and Ca+, Na+ and nitric oxide (NO) signaling. In general, we determined that compounds which increased blood flow enhanced HSC number, whereas chemicals that decreased blood flow diminished runx1/cmyb expression. The conserved physiological mechanism of action of each compound on the vasculature was confirmed in vivo by confocal microscopy of transgenic fli1:GFP reporter fish. In the zebrafish, the step-wise initiation of heartbeat, establishment of vigorous circulation and onset of definitive hematopoiesis in the aorta-gonad-mesonephros region (AGM) suggests that blood flow may trigger HSC formation. silent heart (sih) embryos that lack a heartbeat and fail to establish blood circulation exhibit severely reduced numbers of runx1+ HSCs in the AGM. Blood flow modifying agents primarily exerted their effects after the onset of the heartbeat (>24 hpf), however, only compounds that increase NO production (L-Arginine, S-nitroso-N-acetyl-penicillamine (SNAP)) could induce HSC formation prior to the initiation of circulation (5 somites to 22 hpf). Furthermore, SNAP rescued HSC production in sih mutant zebrafish, whereas other drugs that increased blood flow could not. Treatment with the NO synthase (NOS) inhibitor, N-nitro-L-arginine methyl ester (L-NAME), and morpholino-oligonucleotide (MO)-knockdown of nos1 (nnos/enos) blocked HSC development. Additionally, modulation of downstream components of the NO pathway affected HSC production in the zebrafish embryo. Together these data indicate that NO signaling is the downstream effector of blood flow on AGM HSC induction. To document that NO-mediated regulation of HSC formation was conserved across vertebrate species, we examined definitive HSC production in the murine AGM. Nos3 (eNos) was found to be expressed in the AGM endothelium and aortic hematopoietic clusters. Additionally, Nos3 expression specifically marks the population of HSCs with long-term adult bone marrow repopulating activity. Intrauterine NOS inhibition with L-NAME resulted in a lack of hematopoietic clusters in the AGM and a failure to generate transplantable hematopoietic progenitors. Our work provides a direct link between the initiation of circulation and the onset of AGM hematopoiesis, and identifies NO signaling as a conserved downstream regulator of HSC development. ^TEN and WG contributed equally to this work

Skeletal muscle nitric oxide signaling and exercise: a focus on glucose metabolism

2012 ◽  
Vol 303 (3) ◽  
pp. E301-E307 ◽  
Author(s):  
Glenn K. McConell ◽  
Stephen Rattigan ◽  
Robert S. Lee-Young ◽  
Glenn D. Wadley ◽  
Troy L. Merry
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Glucose Uptake ◽  
No Production ◽  
Nitric Oxide Signaling ◽  
Beneficial Effects ◽  
Low Concentrations ◽  
High Concentrations ◽  
Cellular Components

Nitric oxide (NO) is an important vasodilator and regulator in the cardiovascular system, and this link was the subject of a Nobel prize in 1998. However, NO also plays many other regulatory roles, including thrombosis, immune function, neural activity, and gastrointestinal function. Low concentrations of NO are thought to have important signaling effects. In contrast, high concentrations of NO can interact with reactive oxygen species, causing damage to cells and cellular components. A less-recognized site of NO production is within skeletal muscle, where small increases are thought to have beneficial effects such as regulating glucose uptake and possibly blood flow, but higher levels of production are thought to lead to deleterious effects such as an association with insulin resistance. This review will discuss the role of NO in skeletal muscle during and following exercise, including in mitochondrial biogenesis, muscle efficiency, and blood flow with a particular focus on its potential role in regulating skeletal muscle glucose uptake during exercise.

scholarly journals Plant Nitric Oxide Signaling under Drought Stress

2021 ◽  
Author(s):  
Su-Ee Lau ◽  
Mohd Fadhli Hamdan ◽  
Teen-Lee Pua ◽  
Noor Baity Saidi ◽  
Boon Chin Tan
Keyword(s):  
Nitric Oxide ◽  
Abiotic Stress ◽  
Drought Stress ◽  
Higher Plants ◽  
Genetic Manipulation ◽  
Growth Conditions ◽  
No Production ◽  
Stress Signaling ◽  
Nitric Oxide Signaling

Water deficit caused by drought is a significant threat to crop growth and production. Nitric oxide (NO), a water- and lipid-soluble free radical, plays an important role in cytoprotection. Apart from a few studies supporting the role of NO in drought responses, little is known about this pivotal molecular amendment in the regulation of abiotic stress signaling. In this review, we highlight the knowledge gaps in NO roles under drought stress and the technical challenges underlying NO detection and measurements, and we provide recommendations regarding potential avenues for future investigation. The modulation of NO production to alleviate abiotic stress disturbances in higher plants highlights the potential of genetic manipulation to influence NO metabolism as a tool with which plant fitness can be improved under adverse growth conditions.

Ecdysteroid coordinates optic lobe neurogenesis via a nitric oxide signaling pathway

Development ◽  
2000 ◽  
Vol 127 (16) ◽  
pp. 3543-3551
Author(s):  
D.T. Champlin ◽  
J.W. Truman
Keyword(s):  
Nitric Oxide ◽  
Protein Synthesis ◽  
Manduca Sexta ◽  
Optic Lobe ◽  
No Synthase ◽  
No Production ◽  
Local Production ◽  
Nitric Oxide Signaling ◽  
No Signaling ◽  
Low Levels

Proliferation of neural precursors in the optic lobe of Manduca sexta is controlled by circulating steroids and by local production of nitric oxide (NO). Diaphorase staining, anti-NO synthase (NOS) immunocytochemistry and the NO-indicator, DAF-2, show that cells throughout the optic anlage contain NOS and produce NO. Signaling via NO inhibits proliferation in the anlage. When exposed to low levels of ecdysteroid, NO production is stimulated and proliferation ceases. When steroid levels are increased, NO production begins to decrease within 15 minutes independent of RNA or protein synthesis and cells rapidly resume proliferation. Resumption of proliferation is not due simply to the removal of NO repression though, but also requires an ecdysteroid stimulatory pathway. The consequence of these opposing pathways is a sharpening of the responsiveness to the steroid, thereby facilitating a tight coordination between development of the different elements of the adult visual system.

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