The floral inhibitor FLOWERING LOCUS C (FLC) is a crucial regulator of flowering time in Arabidopsis, and is positively regulated by the FRIGIDA (FRI) gene in late-flowering winter-annual accessions. In rapid-cycling accessions, FLC expression is suppressed by the autonomous floral-promotion pathway (AP); thus AP mutants contain high levels of FLC and are late flowering. Previous work has shown that the upregulation of FLC in FRI- or AP-mutant backgrounds is correlated to an increase in histone H3 lysine 4 (H3K4) trimethylation at the FLC locus. This increase in trimethylation requires a PAF1-like complex and EARLY FLOWERING IN SHORT DAYS (EFS), a putative histone H3 methyltransferase. We have identified a putative zinc-finger-containing transcription factor, SUF4, that is required for the upregulation of FLC by FRI. suf4 mutations strongly suppress the late-flowering phenotype of FRI, but only weakly suppress AP mutants. As with mutants in efs or the PAF1-like complex, suf4 mutants show reduced H3K4 trimethylation at FLC. An interesting distinction between the phenotypes of suf4 mutants and mutants in efs or the PAF1-like complex is observed in the expression of genes that are adjacent to FLC or FLC-like genes. In efs and PAF1-like-complex mutants, the expression of FLC, FLC-like genes and adjacent genes is suppressed. In suf4 mutants, however, only FLC expression is suppressed. These data are consistent with a model in which SUF4 may act to specifically recruit EFS and the PAF1-like complex to the FLC locus.