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Edited by Natasha V. Raikhel, Center for Plant Cell Biology, Riverside, CA, and approved June 14, 2016 (received for review May 7, 2016)
Significance
Plant tissues are resistant to the potentially damaging UV-B radiation intrinsic to sunlight. UV-B photoreception by a UV RESISTANCE LOCUS 8 (UVR8) photoreceptor regulates gene expression in plants associated with UV-B acclimation and stress tolerance and with morphological changes. Mechanistically, UV-B photon reception by specific tryptophan residues of UVR8 homodimers results in monomerization and enhanced nuclear accumulation of UVR8. Active UVR8 monomers interact with the key signaling protein CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1). This UV-B–dependent interaction is a crucial step in signal propagation, but the link between this mechanism and UVR8 nuclear accumulation and gene expression remains ill defined. Our results emphasize the importance of nuclear-localized UVR8 and highlight a previously unknown activity of COP1 in mediating UVR8 nuclear accumulation in response to UV-B.
Abstract
The UV-B photoreceptor UV RESISTANCE LOCUS 8 (UVR8) promotes UV-B acclimation and tolerance in Arabidopsis thaliana. UVR8 localizes to both cytosol and nucleus, but its main activity is assumed to be nuclear. UV-B photoreception stimulates nuclear accumulation of UVR8 in a presently unknown manner. Here, we show that CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1) is required for UV-B–induced nuclear accumulation of UVR8, but bypassing the COP1 requirement for UVR8 nuclear accumulation did not rescue the cop1 mutant UV-B phenotype. Using a glucocorticoid receptor (GR)-based fusion protein system to conditionally localize GR-UVR8 to the nucleus, we have demonstrated that both photoactivation and nuclear localization of UVR8 are required for UV-B–induced photomorphogenic responses. In contrast, there was no UV-B response when UV-B–activated UVR8 was artificially retained in the cytosol. In agreement with a predominantly nuclear activity, constitutively active UVR8W285A accumulated in the nucleus also in the absence of UV-B. Furthermore, GR-COP1 expression lines suggested that UV-B–activated UVR8 can be coimported into the nucleus by COP1. Our data strongly support localization of UVR8 signaling in the nucleus and a dual role for COP1 in the regulation of UV-B–induced UVR8 nuclear accumulation and in UVR8-mediated UV-B signaling.
Footnotes
- ↵1To whom correspondence should be addressed. Email: roman.ulm{at}unige.ch.
Author contributions: R.Y. and R.U. designed research; R.Y., M.Y.S., and S.L. performed research; R.Y., M.Y.S., S.L., and R.U. analyzed data; and R.Y. and R.U. wrote the paper.
The authors declare no conflict of interest.
This article is a PNAS Direct Submission.
This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1607074113/-/DCSupplemental.
UVR8 nuclear accumulation requires COP1
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