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The COP9 SIGNALOSOME Is Required for Postembryonic Meristem Maintenance in Arabidopsis thaliana

Molecular Plant 2015年第11期8卷 1623-1634页

作者： anna franciosini Laila Moubayidin Kaiqi Du Nahill H. Matari Alessandra Boccaccini Simone Butera Paola Vittorioso Sabrina Sabatini Pablo D. Jenik Paolo Costantino Giovanna Serino Dipartimento di Biologia e Biotecnologie 'C. Darwin' Sapienza Universita di Roma Piazzale Aldo Moro 5 00185 Rome Italy Department of Biology Franklin & Marshall College Lancaster PA 17604-3003 USA Istituto Pasteur - Fondazione Cenci Bolognetti Dipartimento di Biologia e Biotecnologie 'C. Darwin' Sapienza Universita di Roma Piazzale Aldo Moro 500185 Rome Italy Institute of Agricultural Biology and Biotechnology National Research Council of Italy (CNR) via Salaria km 29300 00015 Monterotondo Scalo Rome Italy

Cullin-RING E3 ligases （CRLs） regulate different aspects of plant development and are activated by modification of their cullin subunit with the ubiquitin-like protein NEDD8 （NEural precursor cell expressed Developmentally Down-regulated 8）（neddylation） and deactivated by NEDD8 removal （deneddylation）. The CONSTITUTIVELY PHOTOMORPHOGENIC9 （COP9） signalosome （CSN） acts as a molecular switch of CRLs activity by reverting their neddylation status, but its contribution to embryonic and early seedling development remains poorly characterized. Here, we analyzed the phenotypic defects of csn mutants and monitored the cullin deneddylation/neddylation ratio during embryonic and early seedling development. We show that while csn mutants can complete embryogenesis （albeit at a slower pace than wildtype） and are able to germinate （albeit at a reduced rate）, they progressively lose meristem activity upon germination until they become unable to sustain growth. We also show that the majority of cullin proteins are progressively neddylated during the late stages of seed maturation and become deneddylated upon seed germination. This developmentally regulated shift in the cullin neddylation status is absent in csn mutants. We conclude that the CSN and its cullin deneddylation activity are required to sustain postembryonic meristem function in Arabidopsis.

关键词： Arabidopsis thaliana cullin-Ring ubiquitin ligase COP9 signalosome embryo development seed maturation meristem

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

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Molecular Plant 2013年第5期6卷 1616-1629页

作者： anna franciosini Benedetta Lombardi Silvia lafrate Valeria.Pecce Giovanni Mele Leonardo Lupacchini Gianmarco Rinaldi Youichi Kondou Giuliana Gusmaroli Shiori Aki Tomohiko Tsuge Xing-Wang Deng Minami Matsui Paola Vittorioso Paolo Costantin Giovanna Serino Dipartimento di Biologia e Biotecnologie Sapienza Universita di Roma Italy Istituto di Biologia e Biotecnologia Agraria Consiglio Nazionale delle Ricerche Italy RIKEN Plant Science Center Yokohama Japan Department of Molecular Cellular and Development Biology Yale University New Haven CT USA Present address: Department of Biology University of South Carolina Beaufort Bluff'ton AC USA Molecular Biology Laboratory Institute for Chemical Research Kyoto University Japan The New York Botanical Garden Bronx NY USA

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 ＇cullin-ring＇ 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 proteoly- sis, 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 CFKl-depleted seedlings, while complete loss of CSN activity sup- presses the Iong-hypocotyl phenotype of CFKl-overexpressing seedlings. We propose that CFK1 （and its regulation by CSN） is a novel component of the cellular mechanisms controlling hypocotyl elongation.

关键词： Arabidopsis thaliana ubiquitin COP9 signalosome proteasome F-box protein hypocotyl elongation seed-ling development.

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