Ultraviolet-B-Induced Stomatal Closure in Arabidopsis Is Regulated by the UV RESISTANCE LOCUS8 Photoreceptor in a Nitric Oxide-Dependent Mechanism    

Abstract

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.

COP1 is required for UV-B–induced nuclear accumulation of the UVR8 photoreceptor

“…However, we cannot exclude that some untested (e.g., stomatal closure; ref. 45) or as yet unknown physiological response to UV-B is activated by cytosolic UVR8. The uvr8/Pro 35S :GR-UVR8 described here will allow further investigation of possible cytosolic UVR8 activity.…”

Two Distinct Domains of the UVR8 Photoreceptor Interact with COP1 to Initiate UV-B Signaling in Arabidopsis

“…This may be the basis of photomorphogenic responses to UV-B such as hypocotyl growth inhibition (Ballare et al, 1995;Kim et al, 1998;Favory et al, 2009;Hayes et al, 2014;Huang et al, 2014;Vandenbussche et al, 2014). In addition to UV-B stress acclimation and hypocotyl growth inhibition, UVR8 also has been implicated in UV-B entrainment of the circadian clock, stomatal closure, phototropic bending, inhibition of shade avoidance, leaf development, and defense responses (Wargent et al, 2009;Fehér et al, 2011;Demkura and Ballaré, 2012;Hayes et al, 2014;Tossi et al, 2014;Vandenbussche et al, 2014). The UVR8 signaling pathway includes CONSTITUTIVELY PHOTOMORPHOGENIC1 (COP1) and ELONGATED HYPOCOTYL5 (HY5) (Ulm et al, 2004;Brown et al, 2005;Oravecz et al, 2006;Stracke et al, 2010;Huang et al, 2012;Binkert et al, 2014) and the negative feedback regulators REPRESSOR OF UV-B PHOTOMORPHOGENESIS1 (RUP1) and RUP2 .…”

UV-B-Responsive Association of the Arabidopsis bZIP Transcription Factor ELONGATED HYPOCOTYL5 with Target Genes, Including Its Own Promoter

“…These UV-B-induced responses are mediated by the photoreceptor UV RESISTANCE LOCUS8 (UVR8) in Arabidopsis thaliana (Rizzini et al, 2011) and include hypocotyl growth inhibition (Ballare et al, 1995;Kim et al, 1998;Favory et al, 2009), altered leaf morphogenesis (Hectors et al, 2007;Wargent et al, 2009), stomatal closure (Tossi et al, 2014), and the biosynthesis of UV light-absorbing "sunscreen" compounds (Beggs and Wellmann, 1994;Kliebenstein et al, 2002;Stracke et al, 2010). Thus, UVR8 regulates the expression of a broad panel of genes that underlie UV-B-dependent photomorphogenic responses and acclimation (Brown et al, 2005;Favory et al, 2009).…”