The Arabidopsis COP9 SIGNALOSOME INTERACTING F-BOX KELCH 1 Protein Forms an SCF Ubiquitin Ligase and Regulates Hypocotyl Elongation

被引:33
作者
Franciosini, Anna [1 ]
Lombardi, Benedetta [1 ]
Iafrate, Silvia [1 ]
Pecce, Valeria [1 ]
Mele, Giovanni [2 ]
Lupacchini, Leonardo [1 ]
Rinaldi, Gianmarco [1 ]
Kondou, Youichi [3 ]
Gusmaroli, Giuliana [4 ]
Aki, Shiori [5 ]
Tsuge, Tomohiko [5 ]
Deng, Xing-Wang [4 ]
Matsui, Minami [3 ]
Vittorioso, Paola [1 ]
Costantino, Paolo [1 ]
Serino, Giovanna [1 ,6 ]
机构
[1] Sapienza Univ Roma, Dipartimento Biol & Biotecnol, Rome, Italy
[2] CNR, Ist Biol & Biotecnol Agr, I-00185 Rome, Italy
[3] RIKEN Plant Sci Ctr, Yokohama, Kanagawa, Japan
[4] Yale Univ, Dept Mol Cellular & Dev Biol, New Haven, CT USA
[5] Kyoto Univ, Inst Chem Res, Mol Biol Lab, Kyoto 6068501, Japan
[6] New York Bot Garden, Bronx, NY 10458 USA
关键词
Arabidopsis thaliana; ubiquitin; COP9; signalosome; proteasome; F-box protein; hypocotyl elongation; seedling development; FISSION YEAST COP9/SIGNALOSOME; COMPLEX; PROTEASOME; SUBUNITS; NEDD8; GENE; DEGRADATION; PHOTOMORPHOGENESIS; SUPERFAMILY; COACTIVATOR;
D O I
10.1093/mp/sst045
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The CSN is a multiprotein complex required for proper plant development. Here, we show the isolation of a new plant-specific CSN-interacting F-box protein, denominated CFK1, that is regulated by the CSN and promotes hypocotyl elongation.The regulation of protein turnover by the ubiquitin proteasome system (UPS) is a major posttranslational mechanism in eukaryotes. One of the key components of the UPS, the COP9 signalosome (CSN), regulates cullinring E3 ubiquitin ligases. In plants, CSN participates in diverse cellular and developmental processes, ranging from light signaling to cell cycle control. In this work, we isolated a new plant-specific CSN-interacting F-box protein, which we denominated CFK1 (COP9 INTERACTING F-BOX KELCH 1). We show that, in Arabidopsis thaliana, CFK1 is a component of a functional ubiquitin ligase complex. We also show that CFK1 stability is regulated by CSN and by proteasome-dependent proteolysis, and that light induces accumulation of the CFK1 transcript in the hypocotyl. Analysis of CFK1 knockdown, mutant, and overexpressing seedlings indicates that CFK1 promotes hypocotyl elongation by increasing cell size. Reduction of CSN levels enhances the short hypocotyl phenotype of CFK1-depleted seedlings, while complete loss of CSN activity suppresses the long-hypocotyl phenotype of CFK1-overexpressing seedlings. We propose that CFK1 (and its regulation by CSN) is a novel component of the cellular mechanisms controlling hypocotyl elongation.
引用
收藏
页码:1616 / 1629
页数:14
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