Arabidopsis COP10 forms a complex with DDB1 and DET1 in vivo and enhances the activity of ubiquitin conjugating enzymes

  1. Yuki Yanagawa1,6,
  2. James A. Sullivan1,6,
  3. Setsuko Komatsu2,
  4. Giuliana Gusmaroli1,
  5. Genki Suzuki1,5,
  6. Jianning Yin3,
  7. Toyotaka Ishibashi4,
  8. Yusuke Saijo1,
  9. Vicente Rubio1,
  10. Seisuke Kimura4,
  11. Jian Wang3, and
  12. Xing Wang Deng1,7
  1. 1Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, Connecticut 06520-8104, USA; 2National Institute of Agrobiological Sciences, Kannondai, Tsukuba, Ibaraki 305-8602, Japan; 3Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 101300, China; 4Department of Applied Biological Science, Faculty of Science and Technology, Tokyo University of Science, Yamazaki, Noda, Chiba 278-8510, Japan

Abstract

COP10 is a ubiquitin-conjugating enzyme variant (UEV), which is thought to act together with COP1, DET1, and the COP9 signalosome (CSN) in Arabidopsis to repress photomorphogenesis. Here, we demonstrate that COP10 interacts with ubiquitin-conjugating enzymes (E2s) in vivo, and can enhance their activity in vitro, an activity distinct from previous characterized UEVs such as MMS2 and UEV1. Furthermore, we show that COP10 forms a complex with UV-damaged DNA-binding protein 1a (DDB1a) and de-etiolated 1 (DET1), and physically interacts with COP1 and the CSN. Purified CDD (COP10, DDB1, DET1) complex also shows enhancement of E2 activity (UEA) similar to that observed with COP10 itself. Our data suggests that COP10, along with COP1 and the CSN, promotes the degradation of positive regulators of photomorphogenesis, such as the transcription factor HY5, via the ubiquitin/26S proteasome system. Thus, the CDD complex may act as a ubiquitylation-promoting factor to regulate photomorphogenesis.

Keywords

Footnotes

  • Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.1229504.

  • ↵6 These authors contributed equally to this work.

  • ↵5 Present address: RIKEN Yokohama Institute, Tsurumi, Yokohama, Kanagawa 230-0045, Japan.

  • ↵7 Corresponding author. E-MAIL xingwang.deng{at}yale.edu; FAX (203) 432-5726.

    • Accepted July 8, 2004.
    • Received June 7, 2004.
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  1. doi: 10.1101/gad.1229504 Genes & Dev. 18: 2172-2181 Cold Spring Harbor Laboratory Press

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