Summary• Here, the link between UV-B stimulus and the abscisic acid (ABA)-induced nitric oxide (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 (H 2 O 2 ) 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. H 2 O 2 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 H 2 O 2 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 H 2 O 2 generation, and that an NOS-like-dependent mechanism increases NO production to maintain cell homeostasis and attenuate UV-B-derived cell damage.

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 mmol m -2 s -1 UV-B. Both hydrogen peroxide (H 2 O 2 ) 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 H 2 O 2 still increased. When the uvr8-1 null mutant was exposed to UV-B, stomata remained open, irrespective of the fluence rate. Neither NO nor H 2 O 2 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 H 2 O 2 and NO generation in response to UV-B exposure.

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.

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Ultraviolet-B radiation (UV-B, 280–315 nm) is an important environmental signal that regulates growth and development in plants. Two dose-dependent UV-B response pathways were described in plants: a specific one, mediated by UVR8 (the specific UV-B receptor) and an unspecific one, activated by the oxidative damage produced by radiation. The constitutively expressed receptor appears inactive as a dimer, with the two monomers dissociating upon UV-B irradiation. The monomer then interacts with COP1, an ubiquitin ligase, hindering its ability to poly-ubiquitinate transcriptional factor HY5, thus averting its degradation and activating the photomorphogenic response. HY5 induces the synthesis of proteins RUP1 and RUP2, which interact with UVR8, releasing COP1, and inducing the re-dimerization of UVR8. This mechanism has been thoroughly characterized in Arabidopsis, where studies have demonstrated that the UVR8 receptor is key in UV-B response. Although Arabidopsis importance as a model plant many mechanisms described in this specie differ in other plants. In this paper, we review the latest information regarding UV-B response mediated by UVR8 in different species, focusing on the differences reported compared to Arabidopsis. For instance, UVR8 is not only induced by UV-B but also by other agents that are expressed differentially in diverse tissues. Also, in some of the species analyzed, proteins with low homology to RUP1 and RUP2 were detected. We also discuss how UVR8 is involved in other developmental and stress processes unrelated to UV-B. We conclude that the receptor is highly versatile, showing differences among species.

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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.

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