UV-B perception and signal transduction

Jenkins, Gareth I.; Fuglevand, Geeta; Christie, John M.

doi:10.1017/cbo9780511752346.009

Cited by 46 publications

(58 citation statements)

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“…This suggests that failure to repair UV photoproducts induced by lowfluence, short-wavelength UV-B radiation from the incubator lamps led to an accumulation of DNA damage over the 26 d of pretreatment growth that activated resistance in the mutants deficient in both photoreactivation and NER. In wild-type plants, UV-B-induced expression of genes characteristic of stress responses is associated with high fluence rates, whereas low fluence rates are linked to metabolic and developmental changes (Frohnmeyer and Staiger, 2003;Stratmann, 2003;Suesslin and Frohnmeyer, 2003;Ulm and Nagy, 2005;Jenkins and Brown, 2007). Although fluence rate plays a substantial role in determining UV-B responses, our results suggest the capacity of the plant to repair DNA damage may be an important factor in determining the type(s) of response elicited by different fluence rates.…”

Section: Discussionmentioning

confidence: 73%

UV-Induced DNA Damage Promotes Resistance to the Biotrophic Pathogen Hyaloperonospora parasitica in Arabidopsis

et al. 2008

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Plant innate immunity to pathogenic microorganisms is activated in response to recognition of extracellular or intracellular pathogen molecules by transmembrane receptors or resistance proteins, respectively. The defense signaling pathways share components with those involved in plant responses to UV radiation, which can induce expression of plant genes important for pathogen resistance. Such intriguing links suggest that UV treatment might activate resistance to pathogens in normally susceptible host plants. Here, we demonstrate that pre-inoculative UV (254 nm) irradiation of Arabidopsis (Arabidopsis thaliana) susceptible to infection by the biotrophic oomycete Hyaloperonospora parasitica, the causative agent of downy mildew, induces dose-and timedependent resistance to the pathogen detectable up to 7 d after UVexposure. Limiting repair of UV photoproducts by postirradiation incubation in the dark, or mutational inactivation of cyclobutane pyrimidine dimer photolyase, (6-4) photoproduct photolyase, or nucleotide excision repair increased the magnitude of UV-induced pathogen resistance. In the absence of treatment with 254-nm UV, plant nucleotide excision repair mutants also defective for cyclobutane pyrimidine dimer or (6-4) photoproduct photolyase displayed resistance to H. parasitica, partially attributable to short wavelength UV-B (280-320 nm) radiation emitted by incubator lights. These results indicate UV irradiation can initiate the development of resistance to H. parasitica in plants normally susceptible to the pathogen and point to a key role for UV-induced DNA damage. They also suggest UV treatment can circumvent the requirement for recognition of H. parasitica molecules by Arabidopsis proteins to activate an immune response.

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Section: Discussionmentioning

confidence: 73%

UV-Induced DNA Damage Promotes Resistance to the Biotrophic Pathogen Hyaloperonospora parasitica in Arabidopsis

et al. 2008

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“…Speculations ranged from the existence of distinct UV-B perception linked to a regulatory molecular signaling pathway to that no UV-B-dedicated photosensory mechanism existed at all and UV-B-induced changes in secondary metabolism lead to the observed UV-B photomorphogenesis (Björn 1999, Jansen 2002, Frohnmeyer and Staiger 2003, Ulm and Nagy 2005, Ulm 2006, Jenkins and Brown 2007. With identification of UVR8 as the UV-B photoreceptor, a new era has begun regarding our understanding of plant UV-B responses, and the relationship of UV-B to plant photomorphogenesis in general.…”

Section: Perception Of Uv-bmentioning

confidence: 99%

The UVR8 UV-B Photoreceptor: Perception, Signaling and Response

Tilbrook

Arongaus

Binkert

et al. 2013

The Arabidopsis Book

224

187

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Ultraviolet-B radiation (UV-B)is an intrinsic part of sunlight that is accompanied by significant biological effects. Plants are able to perceive UV-B using the UV-B photoreceptor UVR8 which is linked to a specific molecular signaling pathway and leads to UV-B acclimation. Herein we review the biological process in plants from initial UV-B perception and signal transduction through to the known UV-B responses that promote survival in sunlight. The UVR8 UV-B photoreceptor exists as a homodimer that instantly monomerises upon UV-B absorption via specific intrinsic tryptophans which act as UV-B chromophores. The UVR8 monomer interacts with COP1, an E3 ubiquitin ligase, initiating a molecular signaling pathway that leads to gene expression changes. This signaling output leads to UVR8-dependent responses including UV-B-induced photomorphogenesis and the accumulation of UV-B-absorbing flavonols. Negative feedback regulation of the pathway is provided by the WD40-repeat proteins RUP1 and RUP2, which facilitate UVR8 redimerization, disrupting the UVR8-COP1 interaction. Despite rapid advancements in the field of recent years, further components of UVR8 UV-B signaling are constantly emerging, and the precise interplay of these and the established players UVR8, COP1, RUP1, RUP2 and HY5 needs to be defined. UVR8 UV-B signaling represents our further understanding of how plants are able to sense their light environment and adjust their growth accordingly.

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“…Low levels of UV-B radiation cause certain photomorphogenic responses, including inhibition of hypocotyl elongation and root growth [2]. These UV-B photomorphogenic responses are mechanistically different from UV-B damage responses and are believed to be mediated by a UV-B-specific photoreceptor [3,4]. Recently, a UV-B photoreceptor has been identified in Arabidopsis, i.e., the β-propeller protein UV RESISTANCE LOCUS8 (UVR8) signaling through a pathway that involves the basic zipper (bZIP) transcription factor ELONGATED HYPOCOTYL5 (HY5) and the E3 ubiquitin ligase CONSTITUTIVELY PHOTO-MORPHOGENIC 1 (COP1) [5].…”

Section: Introductionmentioning

confidence: 99%

Arabidopsis STO/BBX24 negatively regulates UV-B signaling by interacting with COP1 and repressing HY5 transcriptional activity

et al. 2012

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UV-B (280-315 nm)is an integral part of solar radiation and can act either as a stress inducer or as a developmental signal. In recent years, increasing attention has been paid to the low-fluence UV-B-induced photomorphogenic response and several key players in this response have been identified, which include UVR8 (a UV-B-specific photoreceptor), COP1 (a WD40-repeat-containing RING finger protein), HY5 (a basic zipper transcription factor), and RUP1/2 (two UVR8-interacting proteins). Here we report that Arabidopsis SALT TOLERANCE (STO/BBX24), a known regulator for light signaling in plants, defines a new signaling component in UV-B-mediated photomorphogenesis. The bbx24 mutant is hypersensitive to UV-B radiation and becomes extremely dwarfed under UV-B treatment. By contrast, BBX24 overexpression transgenic lines respond much more weakly to UV-B than the bbx24 and wild-type plants. BBX24 expression is UV-B-inducible and its accumulation under UV-B requires COP1. Co-immunoprecipitation experiments indicate that BBX24 interacts with COP1

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UV-B perception and signal transduction

Cited by 46 publications

References 0 publications

UV-Induced DNA Damage Promotes Resistance to the Biotrophic Pathogen Hyaloperonospora parasitica in Arabidopsis

UV-Induced DNA Damage Promotes Resistance to the Biotrophic Pathogen Hyaloperonospora parasitica in Arabidopsis

The UVR8 UV-B Photoreceptor: Perception, Signaling and Response

Arabidopsis STO/BBX24 negatively regulates UV-B signaling by interacting with COP1 and repressing HY5 transcriptional activity

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