Journal
PLANT CELL
Volume 24, Issue 11, Pages 4590-4606Publisher
AMER SOC PLANT BIOLOGISTS
DOI: 10.1105/tpc.112.103994
Keywords
-
Funding
- National Institutes of Health [GM47850]
- Ministry of Science and Technology of China [2012CB910900]
- State Key Laboratory of Protein and Plant Gene Research at Peking University
- China Postdoctoral Science Foundation [2012M510266]
- Postdoctoral Fellowship at Center for Life Sciences
- Direct For Biological Sciences
- Div Of Molecular and Cellular Bioscience [0929100] Funding Source: National Science Foundation
Ask authors/readers for more resources
As sessile organisms, higher plants have evolved the capacity to sense and interpret diverse light signals to modulate their development. In Arabidopsis thaliana, low-intensity and long-wavelength UV-B light is perceived as an informational signal to mediate UV-B-induced photomorphogenesis. Here, we report that the multifunctional E3 ubiquitin ligase, CONSTITUTIVE PHOTOMORPHOGENESIS1 (COP1), a known key player in UV-B photomorphogenic responses, is also a UV-B-inducible gene. Two transcription factors, FAR-RED ELONGATED HYPOCOTYL3 (FHY3) and ELONGATED HYPOCOTYL5 (HY5), directly bind to distinct regulatory elements within the COP1 promoter, which are essential for the induction of the COP1 gene mediated by photomorphogenic UV-B signaling. Absence of FHY3 results in impaired UV-B-induced hypocotyl growth and reduced tolerance against damaging UV-B. Thus, FHY3 positively regulates UV-B-induced photomorphogenesis by directly activating COP1 transcription, while HY5 promotes COP1 expression via a positive feedback loop. Furthermore, FHY3 and HY5 physically interact with each other, and this interaction is diminished by UV-B. Together, our findings reveal that COP1 gene expression in response to photomorphogenic UV-B is controlled by a combinatorial regulation of FHY3 and HY5, and this UV-B-specific working mode of FHY3 and HY5 is distinct from that in far-red light and circadian conditions.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available