論文

査読有り
2015年10月

Binding of GID1 to DELLAs promotes dissociation of GAF1 from DELLA in GA dependent manner

PLANT SIGNALING & BEHAVIOR
  • Jutarou Fukazawa
  • ,
  • Takeshi Ito
  • ,
  • Yuji Kamiya
  • ,
  • Shinjiro Yamaguchi
  • ,
  • Yohsuke Takahashi

10
10
開始ページ
e1052923
終了ページ
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1080/15592324.2015.1052923
出版者・発行元
TAYLOR & FRANCIS INC

Gibberellins (GAs) are important phytohormones for plant growth and development. DELLAs are members of the plant-specific GRAS protein family and act as repressors of GA signaling. DELLAs are rapidly degraded in the presence of GAs. GA-GID1-DELLA complexes are recognized and ubiquitinated by the SCFSLY complex. The sleepy1 (sly1) F-box mutant exhibits dwarfism and low-germination phenotypes due to high accumulation of DELLAs. Overexpression of GID1 in the sly1 mutant partially rescues these phenotypes without degradation of DELLAs suggesting that proteolysis independent regulation of DELLAs exists in GA signaling. But the molecular mechanisms of non-proteolytic regulation of DELLA are largely unknown. Recently we identified a DELLA binding transcription factor, GAI-ASSOCIATED FACTOR1 (GAF1). GAF1 also interacts with co-repressor TOPLESS RELATED (TPR) in nuclei. DELLAs and TPR act as coactivator and corepressor of GAF1, respectively. GAs converts the GAF1 complex from transcriptional activator to repressor via degradation of DELLAs. The overexpression of PAM, lacking of DELLAs binding region of GAF1, partially rescue dwarf phenotypes of GA deficient or GA insensitive mutant. In this study, we investigate the relationship between non-proteolytic regulation of DELLAs and GA signaling via DELLA-GAF1 complex using modified yeast two-hybrid system.

リンク情報
DOI
https://doi.org/10.1080/15592324.2015.1052923
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/26237582
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000363704300015&DestApp=WOS_CPL
ID情報
  • DOI : 10.1080/15592324.2015.1052923
  • ISSN : 1559-2316
  • eISSN : 1559-2324
  • PubMed ID : 26237582
  • Web of Science ID : WOS:000363704300015

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