Abstract

In plants subjected to UV-B radiation, responses are activated that minimize damage caused by UV-B. The bZIP transcription factor ELONGATED HYPOCOTYL5 (HY5) acts downstream of the UV-B photoreceptor UV RESISTANCE LOCUS8 (UVR8) and promotes UV-B-induced photomorphogenesis and acclimation. Expression of HY5 is induced by UV-B; however, the transcription factor(s) that regulate HY5 transcription in response to UV-B and the impact of UV-B on the association of HY5 with its target promoters are currently unclear. Here, we show that HY5 binding to the promoters of UV-B-responsive genes is enhanced by UV-B in a UVR8-dependent manner in Arabidopsis thaliana. In agreement, overexpression of REPRESSOR OF UV-B PHOTOMORPHOGENESIS2, a negative regulator of UVR8 function, blocks UV-B-responsive HY5 enrichment at target promoters. Moreover, we have identified a T/G-box in the HY5 promoter that is required for its UV-B responsiveness. We show that HY5 and its homolog HYH bind to the T/G(HY5)-box cis-acting element and that they act redundantly in the induction of HY5 expression upon UV-B exposure. Therefore, HY5 is enriched at target promoters in response to UV-B in a UVR8 photoreceptor-dependent manner, and HY5 and HYH interact directly with a T/G-box cis-acting element of the HY5 promoter, mediating the transcriptional activation of HY5 in response to UV-B.

Highlights

  • UV-B radiation (UV-B; 280 to 315 nm) is a critical regulatory signal that induces photomorphogenic responses in plants (Heijde and Ulm, 2012; Li et al, 2013; Jenkins, 2014)

  • Photoactivated UV RESISTANCE LOCUS8 (UVR8) interacts with the E3 ubiquitin ligase CONSTITUTIVELY PHOTOMORPHOGENIC1 (COP1) (Favory et al, 2009; Rizzini et al, 2011; Cloix et al, 2012; Huang et al, 2014), which is a well-known repressor of photomorphogenesis (Lau and Deng, 2012) and plays an important role in UV-B signaling (Oravecz et al, 2006)

  • chromatin immunoprecipitation (ChIP)-Quantitative PCR (qPCR) was performed for the MYB12 and CHS promoters and an intergenic region between the At4g26900 and At4g26910 genes using 10-d-old wild-type plants (Col) or hy5-215 null mutants grown in white light

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Summary

Introduction

UV-B radiation (UV-B; 280 to 315 nm) is a critical regulatory signal that induces photomorphogenic responses in plants (Heijde and Ulm, 2012; Li et al, 2013; Jenkins, 2014). The acclimation response helps to prevent or repair UV-B damage, and uvr mutants are hypersensitive to chronic levels of UV-B (Kliebenstein et al, 2002; Brown et al., 2005; Favory et al, 2009). Such uvr mutants are impaired in UV-B acclimation and not in the response to acute UV-B stress (González Besteiro et al, 2011). The UVR8-interacting and negative feedback regulators REPRESSOR OF UV-B PHOTOMORPHOGENESIS1 (RUP1) and RUP2 (Gruber et al, 2010) facilitate UVR8 redimerization in planta that disrupts the UVR8-COP1 interaction and halts signaling (Heijde and Ulm, 2013)

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