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.