Kyuha Choia,1,2, Juhyun Kima,2, Hyun-Ju Hwanga,2, Sanghee Kimb, Chulmin Parka, Sang Yeol Kima and Ilha Leea,c,3
a National Research Laboratory of Plant Developmental Genetics, School of Biological Sciences, Seoul National University, Seoul, 151-742, Korea
b Korea Polar Research Institute, Korea Ocean Research and Development Institute, Incheon 406-840, Korea
c Global Research Laboratory for Flowering at Seoul National University and University of Wisconsin, Seoul 151-742, Korea
1 Current address: Department of Plant Sciences, Downing Street, Cambridge CB2 3EA, United Kingdom.
2 These authors contributed equally to this work.
3 Address correspondence to Ilha Lee
The flowering of Arabidopsis thaliana winter annuals is delayed until the subsequent spring by the strong floral repressor FLOWERING LOCUS C (FLC). FRIGIDA (FRI) activates the transcription of FLC, but the molecular mechanism remains elusive. The fri mutation causes early flowering with reduced FLC expression similar to frl1, fes1, suf4, and flx, which are mutants of FLC-specific regulators. Here, we report that FRI acts as a scaffold protein interacting with FRL1, FES1, SUF4, and FLX to form a transcription activator complex (FRI-C). Each component of FRI-C has a specialized function. SUF4 binds to a cis-element of the FLC promoter, FLX and FES1 have transcriptional activation potential, and FRL1 and FES1 stabilize the complex. FRI-C recruits a general transcription factor, a TAF14 homolog, and chromatin modification factors, the SWR1 complex and SET2 homolog. Complex formation was confirmed by the immunoprecipitation of FRI-associated proteins followed by mass spectrometric analysis. Our results provide insight into how a specific transcription activator recruits chromatin modifiers to regulate a key flowering gene.