A forty year journey: The generation and roles of NO in plants.

In this year there is the 40th anniversary of the first publication of plant nitric oxide (NO) emission by Lowell Klepper. In the decades since then numerous milestone discoveries have revealed that NO is a multifunctional molecule in plant cells regulating both plant development and stress responses. Apropos of the anniversary, these authors aim to review and discuss the developments of past concepts in plant NO research related to NO metabolism, NO signaling, NO's action in plant growth and in stress responses and NO's interactions with other reactive compounds. Despite the long-lasting research efforts and the accumulating experimental evidences numerous questions are still needed to be answered, thus future challenges and research directions have also been drawn up.

S-Nitrosothiol Signaling Is involved in Regulating Hydrogen Peroxide Metabolism of Zinc-Stressed Arabidopsis.

Accumulation of heavy metals such as zinc (Zn) disturbs the metabolism of reactive oxygen (e.g. hydrogen peroxide, H2O2) and nitrogen species (e.g. nitric oxide, NO; S-nitrosoglutathione, GSNO) in plant cells; however, their signal interactions are not well understood. Therefore, this study examines the interplay between H2O2 metabolism and GSNO signaling in Arabidopsis. Comparing the Zn tolerance of the wild type (WT), GSNO reductase (GSNOR) overexpressor 35S::FLAG-GSNOR1 and GSNOR-deficient gsnor1-3, we observed relative Zn tolerance of gsnor1-3, which was not accompanied by altered Zn accumulation capacity. Moreover, in gsnor1-3 plants Zn did not induce NO/S-nitrosothiol (SNO) signaling, possibly due to the enhanced activity of NADPH-dependent thioredoxin reductase. In WT and 35S::FLAG-GSNOR1, GSNOR was inactivated by Zn, and Zn-induced H2O2 is directly involved in the GSNOR activity loss. In WT seedlings, Zn resulted in a slight intensification of protein nitration detected by Western blot and protein S-nitrosation observed by resin-assisted capture of SNO proteins (RSNO-RAC). LC-MS/MS analyses indicate that Zn induces the S-nitrosation of ascorbate peroxidase 1. Our data collectively show that Zn-induced H2O2 may influence its own level, which involves GSNOR inactivation-triggered SNO signaling. These data provide new evidence for the interplay between H2O2 and SNO signaling in Arabidopsis plants affected by metal stress.

Nitric oxide and gene regulation in plants.

There is increasing evidence that nitric oxide (NO), which was first identified as a unique diffusible molecular messenger in animals, plays an important role in diverse physiological processes in plants. Recent progress that has deepened our understanding of NO signalling functions in plants, with special emphasis on defence signalling, is discussed here. Several studies, based on plants with altered NO-levels, have recently provided genetic evidence for the importance of NO in gene induction. For a general overview of which gene expression levels are altered by NO, two studies, involving large-scale transcriptional analyses of Arabidopsis thaliana using custom-made or commercial DNA-microarrays, were performed. Furthermore, a comprehensive transcript profiling by cDNA-amplification fragment length polymorphism (AFLP) revealed a number of Arabidopsis thaliana genes that are involved in signal transduction, disease resistance and stress response, photosynthesis, cellular transport, and basic metabolism. In addition, NO affects the expression of numerous genes in other plant species such as tobacco or soybean. The NO-dependent intracellular signalling pathway(s) that lead to the activation or suppression of these genes have not yet been defined. Several lines of evidence point to an interrelationship between NO and salicylic acid (SA) in plant defence. Recent evidence suggests that NO also plays a role in the wounding/jasmonic acid (JA) signalling pathway. NO donors affect both wounding-induced H2O2 synthesis and wounding- or JA-induced expression of defence genes. One of the major challenges ahead is to determine how the correct specific response is evoked, despite shared use of the NO signal and, in some cases, its downstream second messengers.