# Repression of the FT-signaling pathway mediated by organ patterning genes

Fernando Andrés, Maida Romera-Branchat, Rafael Martinez-Gallegos, Vipul

Patel, Korbinian Schneeberger, George Coupland

► To cite this version:

Fernando Andrés, Maida Romera-Branchat, Rafael Martinez-Gallegos, Vipul Patel, Korbinian Schneeberger, et al.. Repression of the FT-signaling pathway mediated by organ patterning genes. Workshop on molecular mechanisms controlling flower development, Jun 2015, Girona, Spain. 2015. hal-01607942

HAL Id: hal-01607942

https://hal.science/hal-01607942

Submitted on 2 Jun 2020

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Repression of the FT-signaling pathway mediated by organ patterning genes

Fernando Andrés, Maida Romera-Branchat, Rafael Martínez-Gallegos, Vipul Patel, Korbinian Schneeberger and George Coupland

Max Planck Institute for Plant Breeding Research, Cologne, Germany.

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). These environmental cues are integrated into flowering signaling networks by the thermosensory, vernalization/autonomous and photoperiodic genetic pathways. FLOWERING LOCUS T (FT) is a key component of the photoperiodic pathway. In *Arabidopsis thaliana*, FT mRNA is expressed specifically in the companion cells of the phloem and its protein systemically moves to the shoot apex to activate flowering. FT is unloaded into the shoot meristem, and physically interacts with a bZIP transcription factor called FD, which is expressed in the meristem. FD is required for FT function, and the FT-FD complex is believed to activate the transcription of several flowering-promoter genes. Primary transcriptional targets of FD are the floral identity genes *APETALA1* (*AP1*) and *LEAFY* (*LFY*), whose expression in lateral organ primordia confers floral fate. Therefore, FT-FD complex is predicted to be active in the incipient floral primordia in order to induce the expression of *AP1* and *LFY* and promote floral meristem identity. BEL1-like homeodomain (BELL) transcription factors play important roles in SAM function. PENNYWISE (*PNY*) is a BELL protein which is involved in lateral organ patterning and the acquisition of competence to respond to floral inductive signals. Interestingly, simultaneous mutations in *PNY* and its paralog POUND-FOOLISH (*PNF*) block the ability of FT to activate flowering. However, how organ patterning genes can affect the FT-signaling pathway remains unclear. We performed a sensitized screen for *Arabidopsis* mutants and identified a set of mutations that reduce the capacity of FT to promote early flowering. By employing Next Generation Sequencing we identified a new mutant allele of *PENNYWISE* (*PNY*) (called *pny-58*) which strongly suppresses the flowering function of *FT*. We made use of this new allele to unravel the genetic and molecular connections between the FT-signaling pathway and organ patterning genes. 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. *BOP1/2* are normally expressed in a few cells at the base of the developing leaves and
incipient leaf primordia. However, we observed that in the absence of functional *PNY*, the patterns of expression of *BOP1/2* mRNA become broader in the SAM. This indicates that an important function of *PNY* is to limit the *BOP1/2* mRNA at specific locations. Surprisingly, our genetic and molecular studies show that this broader expression of *BOP1/2* delays 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*.