<i>FLOWERING LOCUS C</i> Encodes a Novel MADS Domain Protein That Acts as a Repressor of Flowering

TLDR

Late flowering in winter-annual Arabidopsis ecotypes is suppressed by vernalization and is driven by dominant alleles at FRIGIDA and FLOWERING LOCUS C. The study investigates whether FLC acts as a flowering repressor and proposes that its activity level modulates flowering time through a rheostat-like mechanism. FLC was isolated by positional cloning and encodes a novel MADS domain protein. Loss of FLC leads to early flowering, whereas overexpression delays flowering, and its expression is positively regulated by FRI and negatively by LUMINIDEPENDENS and vernalization.

Abstract

Winter-annual ecotypes of Arabidopsis are relatively late flowering, unless the flowering of these ecotypes is promoted by exposure to cold (vernalization). This vernalization-suppressible, late-flowering phenotype results from the presence of dominant, late-flowering alleles at two loci, FRIGIDA (FRI) and FLOWERING LOCUS C (FLC). In this study, we report that flc null mutations result in early flowering, demonstrating that the role of active FLC alleles is to repress flowering. FLC was isolated by positional cloning and found to encode a novel MADS domain protein. The levels of FLC mRNA are regulated positively by FRI and negatively by LUMINIDEPENDENS. FLC is also negatively regulated by vernalization. Overexpression of FLC from a heterologous promoter is sufficient to delay flowering in the absence of an active FRI allele. We propose that the level of FLC activity acts through a rheostat-like mechanism to control flowering time in Arabidopsis and that modulation of FLC expression is a component of the vernalization response.