COP1 and ELF3 control circadian function and photoperiodic flowering by regulating GI stability.
COP1 and ELF3 control circadian function and photoperiodic flowering by regulating GI stability.
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DOI：
10.1016/j.molcel.2008.09.026
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发表时间：
2008-12-05
期刊：
影响因子：
16
通讯作者：
Deng, Xing Wang
中科院分区：
文献类型：
--
作者：
Yu, Jae-Woong;Rubio, Vicente;Lee, Na-Yeoun;Bai, Sulan;Lee, Sun-Young;Kim, Sang-Sook;Liu, Lijing;Zhang, Yiyue;Irigoyen, Maria Luisa;Sullivan, James A.;Zhang, Yu;Lee, Ilha;Xie, Qi;Paek, Nam-Chon;Deng, Xing Wang
日照长度的季节性变化被植物光感受器感知并传递到生物钟以调节发育反应，例如开花时间。蓝光感应隐花色素、E3泛素连接酶COP 1和时钟相关蛋白ELF 3和GI调节这一过程，尽管它们之间的调节联系尚不清楚。在这里，我们目前的数据表明，COP 1与ELF 3的行为，以介导的光周期开花途径内的光长信号从GST2到GI。我们发现COP1和ELF3在体内相互作用，并表明ELF3允许COP1在体内与GI相互作用，导致GI在植物中降解。因此，COP 1或ELF 3的突变扰乱了GI循环积累的模式。我们提出了一个模型，其中ELF3作为底物适配器，使COP 1通过有针对性的GI不稳定来调制光输入信号到昼夜节律钟。
Seasonal changes in day length are perceived by plant photoreceptors and transmitted to the circadian clock to modulate developmental responses, such as flowering time. Blue light-sensing cryptochromes, the E3 ubiquitin-ligase COP1, and clock-associated proteins ELF3 and GI, regulate this process, although the regulatory link between them is unclear. Here, we present data showing that COP1 acts with ELF3 to mediate day length signaling from CRY2 to GI within the photoperiod flowering pathway. We found that COP1 and ELF3 interact in vivo and show that ELF3 allows COP1 to interact with GI in vivo, leading to GI degradation in planta. Accordingly, mutation of COP1 or ELF3 disturbs the pattern of GI cyclic accumulation. We propose a model in which ELF3 acts as a substrate adaptor, enabling COP1 to modulate light input signal to the circadian clock through targeted destabilization of GI.
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