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Ultraviolet-B (UV-B) is present in sunlight (280-315 nm) and has diverse effects on living organisms. Low fluence rate of exposure induces a specific photomorphogenic response regulated by the UV-B response locus 8 (UVR8) receptor. UVR8 was first described in Arabidopsis thaliana. In the absence of stimuli it is located in the cytoplasm as a homodimer. However, upon UV-B irradiation, it switches to a monomer and interacts with the ubiquitin ligase E3 COP1 via the UVR8 β-propeller domain and the VP core. This induces the expression of the transcription factor HY5 leading to changes in the expression of genes associated with UV-B acclimation and stress tolerance. UVR8 senses UV-B through tryptophan residues being Trp233 and 285 the most important. Based on the comparison and analysis of UVR8 functionally important motifs, we report a comprehensive phylogeny of UVR8, trying to identify UVR8 homologs and the ancestral organism where this gene could be originated. Results obtained showed that Chlorophytes are the first organisms from the Viridiplantae group where UVR8 appears. UVR8 is present in green algae, bryophytes, lycophytes, and angiosperms. All the sequences identified contain tryptophans 233 and 285, arginines involved in homodimerization and the VP domain suggesting they are true UVR8 photoreceptors. We also determined that some species from bryophytes and angiosperms contain more than one UVR8 gene copy posing the question if UVR8 could constitute a gene family in these species. In conclusion, we described the functional conservation among UVR8 proteins from green algae to higher plants.

UV RESISTANCE LOCUS8 (UVR8) signaling involves CONSTITUTIVELY PHOTOMORPHOGENIC1, the ELONGATED HYPOCOTYL5 (HY5) transcription factor, and the closely related HY5 HOMOLOG. Some UV-B responses mediated by UVR8 are also regulated by nitric oxide (NO), a bioactive molecule that orchestrates a wide range of processes in plants. In this study, we investigated the participation of the UVR8 pathway and its interaction with NO in UV-B-induced stomatal movements in Arabidopsis (Arabidopsis thaliana). Stomata in abaxial epidermal strips of Arabidopsis ecotype Landsberg erecta closed in response to increasing UV-B fluence rates, with maximal closure after 3-h exposure to 5.46 μmol m⁻² s⁻¹ UV-B. Both hydrogen peroxide (H₂O₂) and NO increased in response to UV-B, and stomatal closure was maintained by NO up to 24 h after the beginning of exposure. Stomata of plants expressing bacterial NO dioxygenase, which prevents NO accumulation, did not close in response to UV-B, although H₂O₂ still increased. When the uvr8-1 null mutant was exposed to UV-B, stomata remained open, irrespective of the fluence rate. Neither NO nor H₂O₂ increased in stomata of the uvr8-1 mutant. However, the NO donor S-nitrosoglutathione induced closure of uvr8-1 stomata to the same extent as in the wild type. Experiments with mutants in UVR8 signaling components implicated CONSTITUTIVELY PHOTOMORPHOGENIC1, HY5, and HY5 HOMOLOG in UV-B-induced stomatal closure. This research provides evidence that the UVR8 pathway regulates stomatal closure by a mechanism involving both H₂O₂ and NO generation in response to UV-B exposure.

Nitric oxide (NO) is a signaling molecule that mediates many plant responses to biotic and abiotic stresses, including salt stress. Interestingly, salinity increases NO production selectively in mesophyll cells of sorghum leaves, where photosynthetic C₄ phosphoenolpyruvate carboxylase (C₄ PEPCase) is located. PEPCase is regulated by a phosphoenolpyruvate carboxylase-kinase (PEPCase-k), which levels are greatly enhanced by salinity in sorghum. This work investigated whether NO is involved in this effect. NO donors (SNP, SNAP), the inhibitor of NO synthesis NNA, and the NO scavenger cPTIO were used for long- and short-term treatments. Long-term treatments had multifaceted consequences on both PPCK gene expression and PEPCase-k activity, and they also decreased photosynthetic gas-exchange parameters and plant growth. Nonetheless, it could be observed that SNP increased PEPCase-k activity, resembling salinity effect. Short-term treatments with NO donors, which did not change photosynthetic gas-exchange parameters and PPCK gene expression, increased PEPCase-k activity both in illuminated leaves and in leaves kept at dark. At least in part, these effects were independent on protein synthesis. PEPCase-k activity was not decreased by short-term treatment with cycloheximide in NaCl-treated plants; on the contrary, it was decreased by cPTIO. In summary, NO donors mimicked salt effect on PEPCase-k activity, and scavenging of NO abolished it. Collectively, these results indicate that NO is involved in the complex control of PEPCase-k activity, and it may mediate some of the plant responses to salinity.

Brassinosteroids (BRs) regulate various physiological processes, such as tolerance to stresses and root growth. Recently, a connection was reported between BRs and nitric oxide (NO) in plant responses to abiotic stress. Here we present evidence supporting NO functions in BR signaling during root growth process. Arabidopsis seedlings treated with BR 24-epibrassinolide (BL) show increased lateral roots (LR) density, inhibition of primary root (PR) elongation and NO accumulation. Similar effects were observed adding the NO donor GSNO to BR-receptor mutant bri1-1. Furthermore, BL-induced responses in the root were abolished by the specific NO scavenger c-PTIO. The activities of nitrate reductase (NR) and nitric oxide synthase (NOS)-like, two NO generating enzymes were involved in BR signaling. These results demonstrate that BR increases the NO concentration in root cells, which is required for BR-induced changes in root architecture.

Abscisic acid (ABA) signaling pathways have been widely characterized in plants, whereas the function of ABA in animals is less well understood. However, recent advances show ABA production by a wide range of lower animals and higher mammals. This enables a new evaluation of ABA signaling pathways in different organisms in response to common environmental stress, such as ultraviolet (UV)-B. In this opinion article, we propose that the induction of common signaling components, such as ABA, nitric oxide (NO) and Ca(2+), in plant and animal cells in response to high doses of UV-B, suggests that the evolution of a general mechanism activated by UV-B is conserved in divergent multicellular organisms challenged by a changing common environment., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of Cristina Lombardo, Lorenzo Lamattina, Raul Cassia. Several figures in the article by Tossi et al appear to have been intentionally manipulated and, therefore, representing results that are not accurate. The specific concerns are 1) the NO/-UVB panel in Fig. 1B is an apparent duplication of the Fig. 4 NO/PC panel; 2) the Flavonoid/UVB panel in Fig. 1B is an apparent duplication of the Fig. 4 Flavonoid/U panel; and 3), many of the RT-PCR bands in Fig. 5 are apparently identical. The apparent duplications of the panels in Fig. 1B and Fig. 4 appears to have been done intentionally. The brightness of the published Fig. 1B NO/-UVB panel was decreased and rotated 180 degrees relative to the NO/PC panel in Fig. 4. The two images are identical when the brightness of Fig. 1B is enhanced and the Fig. 4 panel rotated 180 degrees as shown in the attachment. Likewise, Fig. 1B Flavonoid/UVB panel was manipulated to disguise it from the Flavonoid/U panel in Fig. 4. We thank Dr Elisabeth Bik for drawing the irregularities to the authors' attention., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

UV-B is an abiotic environmental stress in both plants and animals. Abscisic acid (ABA) is a phytohormone regulating fundamental physiological functions in plants, including response to abiotic stress. We previously demonstrated that ABA is an endogenous stress hormone also in animal cells. Here, we investigated whether autocrine ABA regulates the response to UV-B of human granulocytes and keratinocytes, the cells involved in UV-triggered skin inflammation. The intracellular ABA concentration increased in UV-B-exposed granulocytes and keratinocytes and ABA was released into the supernatant. The UV-B-induced production of NO and of reactive oxygen species (ROS), phagocytosis, and cell migration were strongly inhibited in granulocytes irradiated in the presence of a monoclonal antibody against ABA. Moreover, presence of the same antibody strongly inhibited release of NO, prostaglandin E2 (PGE(2)), and tumor necrosis factor-α (TNF-α) by UV-B irradiated keratinocytes. Lanthionine synthetase C-like protein 2 (LANCL2) is required for the activation of the ABA signaling pathway in human granulocytes. Silencing of LANCL2 in human keratinocytes by siRNA was accompanied by abrogation of the UV-B-triggered release of PGE(2), TNF-α, and NO and ROS production. These results indicate that UV-B irradiation induces ABA release from human granulocytes and keratinocytes and that autocrine ABA stimulates cell functions involved in skin inflammation., (Copyright © 2011 Wiley Periodicals, Inc.)

The link between ultraviolet (UV)-B, nitric oxide (NO) and phenylpropanoid biosynthetic pathway (PPBP) was studied in maize and Arabidopsis. The transcription factor (TF) ZmP regulates PPBP in maize. A genetic approach using P-rr (ZmP+) and P-ww (ZmP⁻) maize lines demonstrate that: (1) NO protects P-rr leaves but not P-ww from UV-B-induced reactive oxygen species (ROS) and cell damage; (2) NO increases flavonoid and anthocyanin content and prevents chlorophyll loss in P-rr but not in P-ww and (3) the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) blocks the UV-B-induced expression of ZmP and their targets CHS and CHI suggesting that NO plays a key role in the UV-B-regulated PPBP. Involvement of endogenous NO was studied in Arabidopsis nitric oxide dioxygenase (NOD) plants that express a NO dioxygenase gene under the control of a dexamethasone (DEX)-inducible promoter. Expression of HY5 and MYB12, TFs involved in PPBP regulation, was induced by UV-B, reduced by DEX in NOD plants and recovered by subsequent NO treatment. C4H regulates synapate esters synthesis and is UV-B-induced in a NO-independent pathway. Data indicate that UV-B perception increases NO concentration, which protects plant against UV-B by two ways: (1) scavenging ROS; and (2) up-regulating the expression of HY5, MYB12 and ZmP, resulting in the PPBP activation., (© 2011 Blackwell Publishing Ltd.)

Nitric oxide (NO) is a small, ubiquitous bioactive molecule, postulated as a broad spectrum anti-stress compound. The NADPH oxidase inhibitor apocynin induces the accumulation of endogenous NO in leaves of maize seedlings through a nitric oxide synthase (NOS)-like activity, and confers an augmented tolerance to UV-B-induced oxidative damage. Here we propose a mechanism for the apocynin-induced NO increase in plants. NOS catalyzes the oxidation of arginine to citrulline and NO. It is suggested that apocynin inhibits arginase, the enzyme that hydrolyzes L-arginine to urea and L-ornithine, increasing the arginine availability for arginine-dependent NO synthesis. Superoxide (O(2)(-)) is a strong NO scavenger due to its high reactivity with NO to give peroxynitrite (ONOO(-)). Superoxide is mainly produced by plant NADPH oxidase (pNOX). Inhibition of pNOX by apocynin at relatively high NO concentration, could reduces the formation of O(2)(-) and ONOO(-), increasing the availability of a huge amount of NO. We consider apocynin as a very attractive compound for studying NO-regulated processes in plants since it can replace the use of NO donors and overcome the subsequent technical problems.

The effect of apocynin on nitric oxide (NO) synthesis and oxidative stress was studied in corn (Zea mays) seedlings. After treatment with 100 microM apocynin, strongly increased amounts of NO were detected in the leaves. This NO production was reduced by more than 70% by N(G)-nitro-l-arginine methyl ester (L-NAME), a NO synthase (NOS) inhibitor, but there was no reduction in NO production when apocynin was applied in combination with diphenylene iodonium (a plant NOX inhibitor). When maize seedlings were UV-B-irradiated, cellular damage occurred and reactive oxygen species (ROS) were found widely distributed in chloroplasts and mesophyll cells. Pre-treatment with apocynin and coinciding NO accumulation prevented this damage. However, the protective effect was averted by L-NAME application. Leaf discs placed in 1M H(2)O(2) for 24h showed a reduction in chlorophyll content that could also be avoided by apocynin treatment. Our results show that apocynin induces the accumulation of NO in leaves of maize seedlings through a NOS-like activity, a mechanism alternative to NOX inhibition, and confers an augmented tolerance to different types of abiotic oxidative stress. Indeed, we propose the use of apocynin as an alternative approach to study NO functionality in plants.

Here, the link between UV-B stimulus and the abscisic acid (ABA)-induced nitricoxide (NO) synthesis pathway was studied in leaves of maize (Zea mays).The ABA concentration increased by 100% in UV-B irradiated leaves. Leaves of viviparous 14 (vp14), a mutant defective in ABA synthesis, were more sensitive to UV-B-induced damage than those of the wild type (wt). ABA supplementation attenuated UV-B-induced damage in both the wt and vp14. The hydrogen peroxide(H2O2) concentration increased in the irradiated wt, but changed only slightly in vp14. This increase was prevented by diphenylene iodonium (DPI), an inhibitor of NADPH oxidase (pNOX).NO was detected using the fluorophore 4,5-diamino-fluorescein diacetate(DAF-2DA). DAF-2DA fluorescence increased twofold in UV-B-irradiated wt leaves but not in vp14 leaves. H2O2 and NO production was restored in vp14 plants supplied with 100 μM ABA. Catalase, DPI and the NO synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) partially blocked UV-B-induced NO accumulation, suggesting that H2O2 as well as NOS-like activity is required for a full plant response to UV-B. NO protects against UV-B-induced cell damage.Our results suggest that UV-B perception triggers an increase in ABA concentration,which activates pNOX and H2O2 generation, and that an NOS-like-dependent mechanism increases NO production to maintain cell homeostasis and attenuate UV-B-derived cell damage.