Botanical Institute and Cluster of Excellence on Plant Sciences (CEPLAS), Biocenter, University of Cologne, Zülpicher Str. 47b, 50674 Cologne, Germany.
Institut für Pflanzenbiologie, Humboldtstrasse 1, Technische Universität Braunschweig, 38106 Braunschweig, Germany.
Plant Physiol. 2018 Feb;176(2):1327-1340. doi: 10.1104/pp.17.01207. Epub 2017 Nov 29.
The ambient light environment controls many aspects of plant development throughout a plant's life cycle. Such complex control is achieved because a key repressor of light signaling, the Arabidopsis () COP1/SPA E3 ubiquitin ligase causes the degradation of multiple regulators of endogenous developmental pathways. This includes the CONSTANS (CO) transcription factor that is responsible for photoperiodic control of flowering time. There are 16 CO-like proteins whose functions are only partly understood. Here, we show that 14 CO-like (COL) proteins bind CONSTITUTIVELY PHOTOMORPHOGENIC1 (COP1) and SUPPRESSOR OF PHYTOCHROME A-105 (SPA)1 in vitro. We subsequently focused on COL12 and show that COL12 binds COP1 and SPA proteins in vivo. The COL12 protein is degraded in darkness in a COP1-dependent fashion, indicating that COL12 is a substrate of the COP1/SPA ubiquitin ligase. Overexpression of COL12 causes late flowering specifically in long day conditions by decreasing the expression of This phenotype is genetically dependent on Consistent with this finding, COL12 physically interacts with CO in vivo, suggesting that COL12 represses flowering by inhibiting CO protein function. We show that COL12 overexpression did not alter CO protein stability. It is therefore likely that COL12 represses the activity of CO rather than CO levels. Overexpression of COL12 also affects plant architecture by increasing the number of rosette branches and reducing inflorescence height. These phenotypes are independent. Hence, we suggest that COL12 affects plant development through CO-dependent and CO-independent mechanisms.
环境光线控制着植物整个生命周期中许多方面的发育。这种复杂的控制是通过拟南芥(Arabidopsis)COP1/SPA E3 泛素连接酶来实现的,它是光信号的关键抑制剂,可导致多个内源性发育途径调节剂的降解。这包括负责光周期开花时间控制的 CONSTANS(CO)转录因子。有 16 种 CO 类似蛋白,其功能仅部分了解。在这里,我们表明 14 种 CO 类似(COL)蛋白在体外与 CONSTITUTIVELY PHOTOMORPHOGENIC1(COP1)和 SUPPRESSOR OF PHYTOCHROME A-105(SPA)1 结合。随后,我们集中研究了 COL12,并表明 COL12 在体内与 COP1 和 SPA 蛋白结合。COL12 蛋白在黑暗中以 COP1 依赖的方式降解,表明 COL12 是 COP1/SPA 泛素连接酶的底物。COL12 的过表达导致长日照条件下开花时间延迟,特别是通过降低的表达。这种表型在遗传上依赖于。与这一发现一致,COL12 在体内与 CO 物理相互作用,表明 COL12 通过抑制 CO 蛋白功能来抑制开花。我们表明,COL12 过表达不会改变 CO 蛋白的稳定性。因此,COL12 很可能通过抑制 CO 蛋白的活性来抑制其功能,而不是 CO 水平。COL12 的过表达还通过增加莲座叶分枝的数量和降低花序高度来影响植物的结构。这些表型是独立的。因此,我们认为 COL12 通过 CO 依赖和 CO 独立的机制影响植物的发育。