植物一氧化氮(NO)研究进展

一氧化氮(NO)是植物的重要生物活性分子,它参与植物生长发育的许多过程,如种子萌发、下胚轴伸长、叶扩展、根生长、侧根形成、细胞凋亡以及植物抗逆反应等。大量的证据表明,植物可以通过与动物NO合酶类似的酶产生NO。此外,植物还可通过硝酸还原酶产生NO。NO在植物中的信号传递途径仍不十分清楚,植物有可能采用与动物相类似的机制。由于植物的大多数生长发育现象都受到植物激素的调节和控制,NO与植物激素之间的关系也受到越来越多的关注。通过激素起作用可能是植物内源NO作用的机理之一。     

植物一氧化氮(NO)研究进展

一氧化氮（NO）是植物的重要生物活性分子,它参与植物生长发育的许多过程,如种子萌发、下胚轴伸长、叶扩展、根生长、侧根形成、细胞凋亡以及植物抗逆反应等。大量的证据表明,植物可以通过与动物NO合酶类似的酶产生NO。此外,植物还可通过硝酸还原酶产生NO。NO在植物中的信号传递途径仍不十分清楚,植物有可能采用与动物相类似的机制。由于植物的大多数生长发育现象都受到植物激素的调节和控制,NO与植物激素之间的关系也受到越来越多的关注。通过激素起作用可能是植物内源NO作用的机理之一。     

Nitric oxide and reactive nitrogen species in airway epithelial signaling and inflammation

Nitric oxide (NO(.-)) is produced by many diverse cell types as a cellular or intracellular signaling molecule, by the activation of nitric oxide synthases (NOSs). All three known NOS isoforms are expressed within the respiratory tract and mediate various airway functional properties such as airway smooth muscle tone, ciliary function, epithelial electrolyte transport, and innate host defense. The respiratory epithelium is a major source of NO(.-), in which it regulates normal epithelial cell function and signaling as well as signaling pathways involved in airway inflammation. In addition to its normal physiological properties, increased airway NO(.-) production in inflammatory respiratory tract diseases such as asthma may activate additional signaling mechanisms to regulate inflammatory-immune pathways, and epithelial barrier (dys)function or repair. The biological actions of NO(.-) are controlled at various levels, including mechanisms that regulate NOS localization and activation, and variable oxidative metabolism of NO(.-), resulting in generation of bioactive reactive nitrogen species (RNS). Moreover, in addition to altered production of NO(.-) or RNS, the presence of various target enzymes and/or metabolic regulators of NO(.-)/RNS can be dramatically altered during airway inflammatory conditions, and contribute to alterations in NO(.-)-mediated signaling pathways in disease. This review summarizes current knowledge regarding NO(.-)-mediated epithelial signaling, as well as disease-related changes in airway NOS biology and target enzymes that affect NO(.-)/RNS signaling mechanisms. A detailed understanding of these various changes and their impact on NO(.-) signaling pathways are needed to fully appreciate the contributions of NO(.-)/RNS to airway inflammation and to develop suitable therapeutic approaches based on regulating NO(.-) function.     

To NO or not to NO: 'where?' is the question

Nitric oxide (NO) is a gaseous radical with unique biological functions essential for the cardiovascular system, host defense and neuro-transmission. For two decades it was thought that NO was able to diffuse freely across relatively long distances and to traverse major parts of the cell, if not multiple cell layers. However, NO has been proven to be extremely reactive: it reacts with other reactive oxygen species, heavy metals, as well as with cysteine and tyrosine residues in proteins. In accordance, it is now widely accepted that once NO is generated, it is very short-lived and diffuses only over a short distance. This urges for the local production of NO and the localization of NO synthases in the proximity of their downstream targets. This review discusses the highly organized localization of NO synthases, with the endothelial isoform (eNOS) as its main focus, since from this synthase most is known about its subcellular localization and regulation.     

Formation and possible roles of nitric oxide in plant roots

Nitric oxide has been reported to act as a signalling molecule in different plant tissues and to participate in a variety of physiological processes. It is produced by different enzymes and sources. The root-specific plasma membrane-bound enzymes forming NO from the substrates nitrate and nitrite are of particular interest because roots serve as interfaces between plants and the soil. The co-ordinated activity of the root-specific plasma membrane-bound nitrate reductase (PM-NR) and nitrite:NO reductase (NI-NOR) suggests that NO might also be involved in root signalling and development. The rate of enzymatic production of this NO depends largely on the environmental conditions, mainly the availability of nitrate and oxygen and it is proposed that this NO plays a role during anoxia as an indicator of the external nitrate availability and in regulating symbiotic interactions at the root surface.     

Mechanisms for nitric oxide synthesis in plants

The discovery that nitric oxide (NO) acts as a signal fundamentally shifted our understanding of free radicals from toxic by-products of oxidative metabolism to key regulators of cellular functions. This discovery has led to intense investigation into the synthesis of NO in both animals and plants. Nitric oxide synthases (NOS) are the primary sources of NO in animals and are complex, highly regulated enzymes that oxidize arginine to NO and citrulline. Plant NO synthesis, however, appears more complex and includes both nitrite and arginine-dependent mechanisms. The components of the arginine pathway have been elusive as no known orthologues of animal NOS exist in plants. An Arabidopsis gene (AtNOS1) has been identified that is needed for NO synthesis in vivo and has biochemical properties similar to animal cNOS, yet it has no sequence similarity to any known animal NOS. An Atnos1 insertion mutant has been useful for genetic studies of NO regulation and for uncovering new roles for NO signalling. The elucidation of plant NO synthesis promises to yield novel mechanisms that may be applicable to animal systems.     

Cortical microtubule as a sensor and target of nitric oxide signal during the defence responses to Verticillium dahliae toxins in Arabidopsis

The molecular mechanisms of signal transduction of plants in response to Verticillium dahliae (VD) are not known. Here, we show that Arabidopsis reacts to VD-toxins with a rapid burst of nitric oxide (NO) and cortical microtubule destabilization. VD-toxins treatment triggered a disruption of cortical microtubules network. This disruption can be influenced by NO production. However, cortical microtubule disruptions were not involved in regulating the NO production. The results indicated that NO may act as an upstream signalling molecule to trigger the depolymerization of cortical microtubule. Cortical microtubules may act as a target of NO signal and as a sensor to mediate the activation of PR-1 gene expression. These results suggested that NO production and cortical microtubule dynamics appeared to be parts of the important signalling system and are involved in the defence mechanisms to VD-toxins in Arabidopsis .     

Disclosing JAK/STAT links to cell adhesion and cell polarity

The components of many signalling pathways are localised in specific cellular compartments in polarised cells. This is particularly clear in the case of the receptors that localise to the apical or basal membrane in the epithelial cells. In many cases this subcellular localisation is important for the activation of the signalling pathways. In this review we analyse recent developments uncovering an interesting interplay between JAK/STAT signalling and components regulating cell polarity and adhesion during development. Not only the JAK/STAT signalling components are polarised in epithelial cells but many genes controlling cell polarity and adhesion are targets of STAT and in some cases these components act as pathway activators. The fact that in most morphogenetic processes cell adhesion and polarity proteins are regulated downstream of the pathway, hints at a possible unifying mechanistic explanation for the diverse morphogenetic processes controlled by JAK/STAT during development.     

NO-cGMP Signaling and Regenerative Medicine Involving Stem Cells

Nitric oxide (NO) is a short lived diatomic free radical species synthesized by nitric oxide synthases (NOS). The physiological roles of NO depend on its local concentrations as well as availability and the nature of downstream target molecules. At low nanomolar concentrations, activation of soluble guanylyl cyclase (sGC) is the major event initiated by NO. The resulting elevation in the intracellular cyclic GMP (cGMP) levels serves as signals for regulating diverse cellular and physiological processes. The participation of NO and cGMP in diverse physiological processes is made possible through cell type specific spatio-temporal regulation of NO and cGMP synthesis and signal diversity downstream of cGMP achieved through specific target selection. Thus cyclic GMP directly regulates the activities of its downstream effectors such as Protein Kinase G (PKG), Cyclic Nucleotide Gated channels (CNG) and Cyclic nucleotide phosphodiesterases, which in turn regulate the activities of a number of proteins that are involved in regulating diverse cellular and physiological processes. Localization and activity of the NO-cGMP signaling pathway components are regulated by G-protein coupled receptors, receptor and non receptor tyrosine kinases, phosphatases and other signaling molecules. NO also serves as a powerful paracrine factor. At micromolar concentrations, NO reacts with superoxide anion to form reactive peroxinitrite, thereby leading to the oxidation of important cellular proteins. Extensive research efforts over the past two decades have shown that NO is an important modulator of axon outgrowth and guidance, synaptic plasticity, neural precursor proliferation as well as neuronal survival. Excessive NO production as that evoked by inflammatory signals has been identified as one of the major causative reasons for the pathogenesis of a number of neurodegenerative diseases such as ALS, Alzheimers and Parkinson diseases. Regenerative therapies involving transplantation of embryonic stem cells (ES cells) and ES cell derived lineage committed neural precursor cells have recently shown promising results in animal models of Parkinson disease (PD). Recent studies from our laboratory have shown that a functional NO-cGMP signaling system is operative early during the differentiation of embryonic stem cells. The cell type specific, spatio-temporally regulated NO-cGMP signaling pathways are well suited for inductive signals to use them for important cell fate decision making and lineage commitment processes. We believe that manipulating the NO-cGMP signaling system will be an important tool for large scale generation of lineage committed precursor cells to be used for regenerative therapies. Special issue dedicated to John P. Blass.     

Nitric oxide function and signalling in plant disease resistance

Nitric oxide (NO) is one of only a handful of gaseous signalling molecules. Its discovery as the endothelium-derived relaxing factor (EDRF) by Ignarro revolutionized how NO and cognate reactive nitrogen intermediates, which were previously considered to be toxic molecules, are viewed. NO is now emerging as a key signalling molecule in plants, where it orchestrates a plethora of cellular activities associated with growth, development, and environmental interactions. Prominent among these is its function in plant hypersensitive cell death and disease resistance. While a number of sources for NO biosynthesis have been proposed, robust and biologically relevant routes for NO production largely remain to be defined. To elaborate cell death during an incompatible plant-pathogen interaction NO functions in combination with reactive oxygen intermediates. Furthermore, NO has been shown to regulate the activity of metacaspases, evolutionary conserved proteases that may be intimately associated with pathogen-triggered cell death. NO is also thought to function in multiple modes of plant disease resistance by regulating, through S-nitrosylation, multiple nodes of the salicylic acid (SA) signalling pathway. These findings underscore the key role of NO in plant-pathogen interactions.     

Nitric oxide function in plant abiotic stress

Abiotic stress is one of the main threats affecting crop growth and production. An understanding of the molecular mechanisms that underpin plant responses against environmental insults will be crucial to help guide the rational design of crop plants to counter these challenges. A key feature during abiotic stress is the production of nitric oxide (NO), an important concentration dependent, redox‐related signalling molecule. NO can directly or indirectly interact with a wide range of targets leading to the modulation of protein function and the reprogramming of gene expression. The transfer of NO bioactivity can occur through a variety of potential mechanisms but chief among these is S‐nitrosylation, a prototypic, redox‐based, post‐translational modification. However, little is known about this pivotal molecular amendment in the regulation of abiotic stress signalling. Here, we describe the emerging knowledge concerning the function of NO and S‐nitrosylation during plant responses to abiotic stress.