Abstract
In plants, endogenous and environmental signals such as light control the timing of the transition to flowering. Two phytochrome B-interacting transcription factors, VASCULAR PLANT ONE-ZINC FINGER1 (VOZ1) and VOZ2, redundantly promote flowering in Arabidopsis (Arabidopsis thaliana). In the voz1 voz2 mutant, the expression of FLOWERING LOCUS C (FLC) was up-regulated and that of FLOWERING LOCUS T (FT) was down-regulated, which was proposed to be the cause of late flowering in voz1 voz2 However, the detailed mechanism by which the VOZ genes promote flowering is not well understood. Here, we show that neither the reduced FT expression nor the late-flowering phenotype of voz1 voz2 is suppressed in the voz1 voz2 flc triple mutant. Genetic interaction experiments between voz1 voz2 and constans-2 (co-2) mutants reveal that the VOZs and CO work in the same genetic pathway. Using in vitro pull-down, electrophoretic mobility shift, and bimolecular fluorescence complementation assays, we show that VOZ1 and VOZ2 interact with CO. The voz1 voz2 35S::CO:YFP plants show suppression of the early-flowering phenotype induced by CO overexpression, suggesting that CO requires VOZ for the induction of flowering. Determination of the VOZ consensus-binding site followed by genome-wide sequence analysis failed to identify any VOZ-binding sites near known flowering time genes. Together, these results indicate that the VOZ genes regulate flowering primarily through the photoperiod pathway, independent of FLC, and suggest that VOZs modulate CO function to promote flowering.