Abstract

The UV RESISTANCE LOCUS 8 (UVR8) photoreceptor specifically mediates photomorphogenic responses to UV‐B. Photoreception induces dissociation of dimeric UVR8 into monomers to initiate responses. However, the regulation of dimer/monomer status in plants growing under photoperiodic conditions has not been examined. Here we show that UVR8 establishes a dimer/monomer photo‐equilibrium in plants growing in diurnal photoperiods in both controlled environments and natural daylight. The photo‐equilibrium is determined by the relative rates of photoreception and dark‐reversion to the dimer. Experiments with mutants in REPRESSOR OF UV‐B PHOTOMORPHOGENESIS 1 (RUP1) and RUP2 show that these proteins are crucial in regulating the photo‐equilibrium because they promote reversion to the dimer. In plants growing in daylight, the UVR8 photo‐equilibrium is most strongly correlated with low ambient fluence rates of UV‐B (up to 1.5 μmol m−2 s−1), rather than higher fluence rates or the amount of photosynthetically active radiation. In addition, the rate of reversion of monomer to dimer is reduced at lower temperatures, promoting an increase in the relative level of monomer at approximately 8–10 °C. Thus, UVR8 does not behave like a simple UV‐B switch under photoperiodic growth conditions but establishes a dimer/monomer photo‐equilibrium that is regulated by UV‐B and also influenced by temperature.

Highlights

  • Ultraviolet-B radiation (UV-B; 280–315 nm) in sunlight has the potential to damage organisms, plants growing in natural conditions rarely show signs of UV-stress because they have evolved effective systems for UV-protection and damage repair

  • In the present study Arabidopsis plants were grown for 3 weeks in a light/dark cycle under white light supplemented with narrowband UV-B at different fluence rates

  • The total amount of UV RESISTANCE LOCUS 8 (UVR8) is determined relative to the control Rubisco large subunit (rbcL) protein and the dimer/monomer status is expressed as %[UVR8dimer/UVR8total]

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Summary

Introduction

Ultraviolet-B radiation (UV-B; 280–315 nm) in sunlight has the potential to damage organisms, plants growing in natural conditions rarely show signs of UV-stress because they have evolved effective systems for UV-protection and damage repair. UV-B exposure stimulates the differential expression of hundreds of plant genes (Casati & Walbot 2004; Ulm et al 2004; Brown et al 2005; Kilian et al 2007; Favory et al 2009) In many cases these responses are initiated by activation of non-UV-Bspecific signalling pathways, involving DNA damage or increases in the levels of reactive oxygen species or defence or wound signalling molecules (Kilian et al 2007; Jenkins 2009; Gonzalez Besteiro et al 2011). UVR8 is highly conserved in the plant kingdom and mediates a variety of responses to UV-B, including UVprotective sunscreen biosynthesis, suppression of hypocotyl extension, leaf expansion, phototropism, stomatal closure and inhibition of the shade avoidance response (Wargent et al 2009; Tilbrook et al 2013; Hayes et al 2014; Jenkins 2014; Tossi et al 2014; Vandenbussche et al 2014)

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