Abstract

The winter annuals of Arabidopsis thaliana require vernalization-mediated silencing of the strong flowering repressor FLOWERING LOCUS C (FLC) for floral promotion competence. FRIGIDA (FRI) encoding a proline-rich protein with two coiled-coil domains increases transcript level of FLC , but the molecular mechanism remains elusive. The natural mutations of FRI cause an early flowering with reduced FLC expression in most of rapid life cycle ecotypes including Col-0. Forward genetic approaches using the winter annuals have identified additional early flowering frl1, fes1, suf4 and flx, similar to fri as mutants of FLC -specific activators. We showed 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 , a C2H2 type zinc finger protein 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.