Abstract

UV-B photon reception by the Arabidopsis thaliana homodimeric UV RESISTANCE LOCUS8 (UVR8) photoreceptor leads to its monomerization and a crucial interaction with CONSTITUTIVELY PHOTOMORPHOGENIC1 (COP1). Relay of the subsequent signal regulates UV-B-induced photomorphogenesis and stress acclimation. Here, we report that two separate domains of UVR8 interact with COP1: the β-propeller domain of UVR8 mediates UV-B-dependent interaction with the WD40 repeats-based predicted β-propeller domain of COP1, whereas COP1 activity is regulated by interaction through the UVR8 C-terminal C27 domain. We show not only that the C27 domain is required for UVR8 activity but also that chemically induced expression of the C27 domain is sufficient to mimic UV-B signaling. We further show, in contrast with COP1, that the WD40 repeat proteins REPRESSOR OF UV-B PHOTOMORPHOGENESIS1 (RUP1) and RUP2 interact only with the UVR8 C27 domain. This coincides with their facilitation of UVR8 reversion to the ground state by redimerization and their potential to interact with UVR8 in a UV-B-independent manner. Collectively, our results provide insight into a key mechanism of photoreceptor-mediated signaling and its negative feedback regulation.

Highlights

  • The unavoidable exposure of plants to UV-B radiation (280 to 315 nm) is mitigated by effective toleration mechanisms

  • Given that UV RESISTANCE LOCUS8 (UVR8)-CONSTITUTIVELY PHOTOMORPHOGENIC1 (COP1) interaction is critical for UV-B signaling, we tested the interaction of UVR8N396 and UVR8C44 with COP1 in a yeast two-hybrid assay

  • UV-B-dependent interaction of the UV-B photoreceptor UVR8 with COP1 is a key event in UV-B signaling that induces photomorphogenic responses and acclimation to UV-B (Heijde and Ulm, 2012; Li et al, 2013; Jenkins, 2014)

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Summary

Introduction

The unavoidable exposure of plants to UV-B radiation (280 to 315 nm) is mitigated by effective toleration mechanisms. In contrast with a number of UV-B light-induced genes, auxin-responsive genes are widely and rapidly repressed in response to UV-B light, and this response is dependent on UVR8 (Favory et al, 2009; Hayes et al, 2014; Vandenbussche et al, 2014) 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). C27 was found to interact constitutively with COP1 in a yeast two-hybrid assay (Cloix et al, 2012) It was not known whether the C27 domain is sufficient to activate UV-B-related responses in vivo

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