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The floral transition occurs at the shoot apical meristem (SAM) in response to favourable external and internal signals. Among these signals, variations in daylength (photoperiod) act as robust seasonal cues to activate flowering. In Arabidopsis, long-day photoperiods stimulate production in the leaf vasculature of a systemic florigenic signal that is translocated to the SAM. According to the current model, FLOWERING LOCUS T (FT), the main Arabidopsis florigen, causes transcriptional reprogramming at the SAM, so that lateral primordia eventually acquire floral identity. FT functions as a transcriptional coregulator with the bZIP transcription factor FD, which binds DNA at specific promoters. FD can also interact with TERMINAL FLOWER 1 (TFL1), a protein related to FT that acts as a floral repressor. Thus, the balance between FT-TFL1 at the SAM influences the expression levels of floral genes targeted by FD. Here, we show that the FD-related bZIP transcription factor AREB3, which was previously studied in the context of phytohormone abscisic acid signalling, is expressed at the SAM in a spatio-temporal pattern that strongly overlaps with FD and contributes to FT signalling. Mutant analyses demonstrate that AREB3 relays FT signals redundantly with FD, and the presence of a conserved carboxy-terminal SAP motif is required for downstream signalling. AREB3 shows unique and common patterns of expression with FD, and AREB3 expression levels are negatively regulated by FD thus forming a compensatory feedback loop. Mutations in another bZIP, FDP, further aggravate the late flowering phenotypes of fd areb3 mutants. Therefore, multiple florigen-interacting bZIP transcription factors have redundant functions in flowering at the SAM. Author summary: In this research, we studied how plants regulate the time to flower. This process is highly sensitive to the environment, including seasonal changes in day length. In Arabidopsis thaliana long day conditions, typical of spring and summer, stimulate the production of a specialised protein signal called florigen in leaves to initiate flowering at the shoot (the growing tip of the plant). Florigen proteins move long distance to the shoot where they interact with another set of proteins, the best known of which is FD, belonging to group A bZIPs. Here, we discovered that all group A bZIP proteins can also bind to the florigen. We also found that the bZIP AREB3, present at the shoot like FD, when mutated together with FD caused an aggravated delay in flowering compared with single mutant plants. Mutations in a third bZIP, FDP, resulted in an even later flowering compared with double mutants, showing that the effect of these mutations is cumulative. It appears that the more of this family of regulatory proteins we remove, the later the plant flowers. In conclusion, we discovered that many more bZIPs than previously thought can interact with florigens to regulate flowering time. [ABSTRACT FROM AUTHOR]