First published online July 7, 2006; 10.1105/tpc.105.040097
The Plant Cell 18:1975-1990 (2006)
© 2006 American Society of Plant Biologists
CONSTITUTIVELY PHOTOMORPHOGENIC1 Is Required for the UV-B Response in Arabidopsis[W]
Attila Oravecza,b,1,
Alexander Baumanna,1,
Zoltán Mátéb,
Agnieszka Brzezinskaa,
Jean Molinierc,
Edward J. Oakeleyc,
Éva Ádámd,
Eberhard Schäfera,
Ferenc Nagyb,d and
Roman Ulma,2
a Institute of Biology II/Botany, University of Freiburg, D-79104 Freiburg, Germany
b Institute of Plant Biology, Agricultural Biotechnological Center, Szent-Györgyi A 4, H-2101 Gödöll , Hungary
c Friedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland
d Institute of Plant Biology, Biological Research Center, H-6726 Szeged, Hungary
2 To whom correspondence should be addressed. E-mail roman.ulm{at}biologie.uni-freiburg.de; fax 49-761-203-2612.
CONSTITUTIVELY PHOTOMORPHOGENIC1 (COP1) is a negative regulator of photomorphogenesis in Arabidopsis thaliana. COP1 functions as an E3 ubiquitin ligase, targeting select proteins for proteasomal degradation in plants as well as in mammals. Among its substrates is the basic domain/leucine zipper (bZIP) transcription factor ELONGATED HYPOCOTYL5 (HY5), one of the key regulators of photomorphogenesis under all light qualities, including UV-B responses required for tolerance to this environmental threat. Here, we report that, in contrast with the situation in visible light, COP1 is a critical positive regulator of responses to low levels of UV-B. We show that in the cop1-4 mutant, flavonoid accumulation and genome-wide expression changes in response to UV-B are blocked to a large extent. COP1 is required for HY5 gene activation, and both COP1 and HY5 proteins accumulate in the nucleus under supplementary UV-B. SUPPRESSOR OF PHYTOCHROME A-105 family proteins (SPA1 to SPA4) that are required for COP1 function in dark and visible light are not essential in the response to UV-B. We conclude that COP1 performs a specific and novel role in the plants' photomorphogenic response to UV-B, coordinating HY5-dependent and -independent pathways, which eventually results in UV-B tolerance.
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