The Arabidopsis COP9 SIGNALOSOME INTERACTING F-BOX KELCH 1 Protein Forms an SCF Ubiquitin Ligase and Regulates Hypocotyl Elongation
The Arabidopsis COP9 SIGNALOSOME INTERACTING F-BOX KELCH 1 Protein Forms an SCF Ubiquitin Ligase and Regulates Hypocotyl Elongation
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DOI：
10.1093/mp/sst045
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发表时间：
2013-09-01
期刊：
影响因子：
27.5
通讯作者：
Serino, Giovanna
中科院分区：
文献类型：
--
作者：
Franciosini, Anna;Lombardi, Benedetta;Serino, Giovanna
CSN是植物正常发育所需的多蛋白复合物。在这里，我们展示了一种新的植物特异性CSN相互作用的F盒蛋白，命名为CFK 1，这是由CSN调节，促进下胚轴elongation.The泛素蛋白酶体系统（UPS）的蛋白质周转的调节是一个主要的翻译后机制在真核生物。UPS的关键成分之一，COP 9信号体（CSN），调节cullining E3泛素连接酶。在植物中，CSN参与多种细胞和发育过程，从光信号到细胞周期控制。在这项工作中，我们分离了一种新的植物特异性CSN相互作用的F-box蛋白，我们命名为CFK 1（COP 9 INTERACTING F-BOX KELCH 1）。我们表明，在拟南芥中，CFK 1是一个功能性的泛素连接酶复合物的组成部分。我们还表明，CFK 1的稳定性是由CSN和蛋白酶体依赖的蛋白水解，光诱导积累的CFK 1转录下胚轴。对CFK 1敲低、突变体和过表达幼苗的分析表明，CFK 1通过增加细胞大小促进下胚轴伸长。CSN水平的降低增强了CFK 1耗尽幼苗的短下胚轴表型，而CSN活性的完全丧失抑制了CFK 1过表达幼苗的长下胚轴表型。我们建议，CFK 1（和它的调节CSN）是一个新的组成部分的细胞机制控制下胚轴伸长。
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.