In a review in 2004 Van Baarlen noted that the formation of endogenous NO and H2O2 was recorded in distinction to the compatible interaction, i.e. during disease development of liliaceous plant and Botrytis elliptica. Another event associated with plant resistance in which NO appears to be involved is phytoalexin buildup (Able 2003). Exogenous NO stimulated the accumulation of rishitin in potato tubers. Furthermore, the outcome of this compound’s inhibited production was identified after the use of a NO scavenger (Noritake et al. 1996). Several times after NO treatment of soybean cotyledons, the production of particular phytoalexins was identified (Modolo et al. 2002). NO could also play a role in the emergence of general systemic acquired resistance (SAR). In tobacco, exogenous NO increases the accumulation of salicylic acid, which plays a key role in SAR (Durner et al. 1998). Activation of the PR-1 macromolecule, produced by NO, occurs with the participation of SA, because an identical result was not seen in transgenic plants unable to accumulate SA (NahG). Furthermore, disease spots formed by tobacco mosaic virus (TMV) on leaves pretreated with NO were dramatically decreased as compared with transgenic plants. SAR was lowered by using inhibitors specific for animal NOS or NO scavengers (Song and Goodman 2001). As a result, our findings suggest that NO plays an important role in the development of a distal signal network, resulting in increased SAR in tobacco.
NO may be transferred to plants in the form of nitrosoglutathione (GSNO), much as in mammals’ vascular systems (Durner and Klessig 1999). It is hypothesized that GSNO may act as both an intracellular and organismal NO carrier, and that it is distributed throughout the plant via vascular tissue bundles. Glutathione-dependent formaldehyde dehydrogenase (GS-FDH)/I-nitrosoglutathione reductase (GSNOR) may play an important role in turning off/on the NO or GSNO signal, as well as modifying the amount of intracellular thiols, which may cause nitrosative stress (Diaz et al. 2003). In Arabidopsis, Feechan et al. (2005) discovered that the deletion of AtGSNOR1, an S-nitrosoglutathione enzyme, resulted in an increase in cellular S-nitrosothiols, which was correlated with a decrease in resistance to microbial infection. Throughout the prevalence of avirulent microorganisms and the consequent hypersensitized response, NO demonstrates an unusually wide range of affinities to a variety of signaling chemicals. The popularity of an avirulent microbe is associated with a robust aerobic burst, during which there is a redoubled creation of ROS/RNS, primarily superoxide (O2•), peroxide (H2O2), or gas (NO), and the commencement of an avirulent microbe. In soybean cell suspension infected with avirulent P. syringae pv. glycinea, treatment with NO donor, sodium nitroprusside, significantly increased the induction of death by exogenous H2O2 or ROS (Delledonne et al. 1998). This response was significantly inhibited not solely by the NO scavenger 2-4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (CPTIO), but additionally by diphenyleneiodonium, a substance in the leukocyte NADPH enzyme that inhibits the plant oxidative burst, and by an enzyme that destroys H2O2; NO reacted synergistically, resulting in a 10-fold increase in ROI-induced death (Delledonne et al. 1998).
NO production, along with H2O2 and O2, was observed to be associated with elicitor-elicited mortality in Mexican cypress. The co-accumulation of ROS and NO, as well as the interplay between H2O2, O2, and NO, mediated the death response. The use of protein scavengers/inhibitors was used to investigate the role of NO and O2 in death. NO and H2O2 reciprocally promoted each other’s assembly, whereas NO and O2 reciprocally suppressed each other’s production. The interaction between NO and O2, but not between NO and H2O2, triggered PCD via peroxynitrite (ONOO−) (Neill et al. 2002; Zhao 2005). The stress response in bacterially triggered PCD in soybean and Arabidopsis concerned reactions to NO and H2O2, with interactions between NO and H2O2 being synergistic and additive in different ways, which is consistent with previous findings. After exposing tobacco leaves to a high intensity of stress, NO-mediated death was seen in enzyme-deficient (CAT1AS) plants but not in wild types, revealing the interaction of NO with H2O2 throughout the NO-mediated death response (Zago et al. 2006).
Plants protect themselves from microorganisms by triggering elaborate defenses. Similarly, it was recently demonstrated that NO works synergistically with ROS to prolong host mortality in soybean suspension cells, and that NOS inhibitors impair the hypersensitized resistance response in Arabidopsis and tobacco (Delledonne et al. 1998). It was discovered that the host plant has intracellular defense mechanisms to combat the oxidative stress caused by pathogens. Increased activity of the catalyst inhibitor system, total phenol content, and phenyl ammonia lyase activity slowed oxidative burst, which was presumably mediated by excessive chemical group content and hence involved gas signaling; this explained the protection against pathogen stress (Dwivedi et al. 2016). Following that, extensive studies revealed that NO could influence the expression of genes encoding a variety of plant effector and restriction proteins (Polverari et al. 2003; Huang et al. 2004; Parani et al. 2004; Zago et al. 2006). Furthermore, recent research on catalase-deficient tobacco plants discovered a small number of genes that are particularly controlled by NO or H2O2 (Zago et al. 2006). Interestingly, most of the notable genes were affected by both NO and H2O2, showing a significant overlap in these two separate chemical process signaling agents (Figure 1.2).
Figure 1.2 Schematic representation of NO signaling against biotic stress in plants.
1.3.1 Interaction of NO with Other Molecules to Confer Biotic Stress Responses in Plants
Plants defend themselves against microorganism attack by activating elaborate defenses. Similarly, it has been recently demonstrated first that NO acts synergistically with ROS to extend host death in soybean suspension cells, and second that NOS inhibitors compromise the hypersensitized resistance response in Arabidopsis and tobacco (Delledonne et al. 1998). NO and ROS induce SA synthesis, and elevated SA may subsequently result in improved NO and ROS levels. SA additionally induces expression of genes that may be NO targets/sensors (e.g. pathogen-induced oxido-reductase [PIOX]). What is more, SA may enhance the results of NO activity through interaction with many NOX-regulated enzymes (e.g. catalase and aconitase). On the other hand, SA, which is a very important antioxidant in mammals, may counter the effects of NO. As an example, NO blocks respiration via inhibition of cytochrome enzyme, while SA induces production of various NO-resistant enzymes and sensors/targets in plants (e.g. pathogen-induced oxygenase, PIOX). NO and SA have an effect on common targets (e.g. catalase, aconitase). SA counteracts NO action (e.g. NO inhibits cytochrome enzyme, whereas SA induces a different oxidase). The induction of necrobiosis and/or defense factor activation occurs via the action of NO, SA, and ROS. NO is not only thought to perform throughout the event of hypersensitive cell death but is also needed in the establishment of disease resistance. Melatonin also enhances pathogen resistance in plants by increasing the levels of SA and ethylene. Lee et al. (2015) reported that decreased level of melatonin content in Arabidopsis mutant lowers the SA content thereby reducing resistance to pathogen infection. It also stimulates elevation of endogenous NO levels and increased expression of defense-related genes, along with disease resistance against Pst DC3000 infection.
Melatonin confers plants with innate immunity via the NO- and H2O2-dependent pathway by stimulating mitogen-activated protein kinase kinase kinase 3 (MAPKKK3) and oxidative signal-inducible1 (OXI1). Melatonin stimulates accumulation of NO and SA and improved tomato TMV resistance (Zhao et al. 2019).
Interaction between NO and glutathione is an important component to the NPR1-dependent defense signaling pathway in A. thaliana (Kovacs et al. 2015). Cao et al. (2019) found that brassinosteroids aid in stimulating the susceptibility of maize to maize chlorotic mottle virus infection in a NO-dependent manner. Nitric oxide further acts as a downstream signaling molecule in brassinosteroid-mediated virus susceptibility to maize chlorotic mottle virus in maize. The brassinosteroids provide systemic resistance against viruses along with H2O2 and NO in