Repression of FT signaling pathway by BOP1/2. Repression of FT signaling

Floral organs are produced in response to environmental and endogenous cues from populations of cells that are allocated on the flanks of the shoot apical meristem (SAM). In Arabidopsis thaliana, this process is strongly controlled through the photoperiod pathway in which FLOWERING LOCUS T (FT) is a key component. FT protein moves from the leaves to the shoot meristem where it is believed to interact with the bZIP transcription factor FD. The FT-FD complex activates APETALA1 (AP1) and LEAFY (LFY) gene expression and promotes floral meristem identity. The ability of FT-FD to promote flowering is impaired by the loss-of-function of PENNYWISE (PNY), a BEL1-like homeodomain transcription factor involved in inflorescence patterning. However, how organ patterning genes can affect the FT-signaling pathway remains unclear. We identified a new mutant allele of PNY (pny-58) which strongly suppresses the flowering function of FT. Remarkably, we found that PNY binds to the promoter and regulates the expression of BLADE-ON-PETIOLE1 (BOP1) and BOP2 genes, two BTB-ankryin transcriptional co-activators. Our genetic and molecular studies show that BOP1/2 genes delay flowering by repressing the expression of FD in the SAM. In addition, we show that FD expression is reduced at the flanks of the SAM in the pny-58 mutant as a consequence of the ectopic expression of BOP1/2 genes. Therefore, AP1 and LFY cannot be properly activated by the FT-FD module and the floral transition is delayed. These results together shed light on the interaction between organ patterning genes and the FT-signaling pathway during flowering in Arabidopsis.