The Transcription Factor COL12 Is a Substrate of the COP1/SPA E3 Ligase and Regulates Flowering Time and Plant Architecture

• Published in: Plant physiology (Bethesda) 2018-02, Vol.176 (2), p.1327-1340
• Main Authors: Ordoñez-Herrera, Natalia, Trimborn, Laura, Menje, Melanie, Henschel, Monique, Robers, Lennart, Kaufholdt, David, Hänsch, Robert, Adrian, Jessika, Ponnu, Jathish, Hoecker, Ute
• Format: Article
• Language: English
• Subjects: Arabidopsis - physiology; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Cell Cycle Proteins - genetics; Cell Cycle Proteins - metabolism; Darkness; DNA-Binding Proteins - genetics; DNA-Binding Proteins - metabolism; Flowers - genetics; Flowers - physiology; Gene Expression Regulation, Plant; Plants, Genetically Modified; Protein Interaction Domains and Motifs; SIGNALING AND RESPONSE; Time Factors; Transcription Factors - genetics; Transcription Factors - metabolism; Ubiquitin-Protein Ligases - genetics; Ubiquitin-Protein Ligases - metabolism
• ISSN: 0032-0889; 1532-2548
• DOI: 10.1104/pp.17.01207

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 (Arabidopsis thaliana) 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 FLOWERING LOCUS T. This phenotype is genetically dependent on CO. 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 CO independent. Hence, we suggest that COL12 affects plant development through CO-dependent and CO-independent mechanisms.