FLOWERING LOCUS T (FT) is a conserved promoter of flowering that acts downstream of various regulatory pathways, including one that mediates photoperiodic induction through CONSTANS (CO), and is expressed in the vasculature of cotyledons and leaves. A bZIP transcription factor, FD, preferentially expressed in the shoot apex is required for FT to promote flowering. FD and FT are interdependent partners through protein interaction and act at the shoot apex to promote floral transition and to initiate floral development through transcriptional activation of a floral meristem identity gene, APETALA1 (AP1). FT may represent a long-distance signal in flowering.

SUMMARY When to form flowers is a developmental decision that profoundly impacts the fitness of flowering plants. In Arabidopsis this decision is ultimately controlled by the induction and subsequent activity of the transcription factors LEAFY (LFY), FRUITFULL (FUL) and APETALA1 (AP1). Despite their central importance, our current understanding of the regulation of LFY, FUL and AP1 expression is still incomplete. We show here that all three genes are directly activated by the microRNA targeted transcription factor SQUAMOSA PROMOTER BINDING PROTEIN-LIKE 3 (SPL3). Our findings suggest that SPL3 acts together with other microRNA-regulated SPL transcription factors to control the timing of flower formation. Moreover, the identified SPL activity defines a distinct pathway in control of this vital developmental decision.

In Arabidopsis, several genetic pathways controlling the floral transition (flowering) are integrated at the transcriptional regulation of FT, LFY and SOC1. TSF is the closest homolog of FT in Arabidopsis. TSF expression was induced rapidly upon activation of CONSTANS (CO). The mRNA levels of TSF and FT showed similar patterns of diurnal oscillation and response to photoperiods: an evening peak, higher levels in long day (LD) than in short day (SD) conditions, and immediate up-regulation upon day-length extension. These observations suggest that TSF is a direct regulatory target of CO. tsf mutation delayed flowering in SD conditions and enhanced the phenotype of ft in both LD and SD conditions. TSF and FT also shared similar modes of regulation by FLC, an integrator of autonomous and vernalization pathways, and other factors such as EBS and PHYB. Consistently, TSF overexpression caused a precocious flowering phenotype independent of photoperiods or CO, or FLC. These observations suggest that TSF is a new member of the floral pathway integrators and promotes flowering largely redundantly with FT but makes a distinct contribution in SD conditions. TSF and FT seem to act independently of each other and of LFY, and partially upstream of SOC1. Interestingly, the expression patterns of TSF and FT in seedlings did not overlap, although both were expressed in the phloem tissues. Our work revealed additional complexity and spatial aspects of the regulatory network at the pathway integration level. We propose that the phloem is the site where multiple regulatory pathways are integrated at the transcriptional regulation of FT and TSF.

The transition from vegetative growth to flower formation is critical for the survival of flowering plants. The plant-specific transcription factor LEAFY (LFY) has central, evolutionarily conserved roles in this process, both in the formation of the first flower and later in floral patterning. We performed genome-wide binding and expression studies to elucidate the molecular mechanisms by which LFY executes these roles. Our study reveals that LFY directs an elaborate regulatory network in control of floral homeotic gene expression. LFY also controls the expression of genes that regulate the response to external stimuli in Arabidopsis. Thus, our findings support a key role for LFY in the coordination of reproductive stage development and disease response programs in plants that may ensure optimal allocation of plant resources for reproductive fitness. Finally, motif analyses reveal a possible mechanism for stage-specific LFY recruitment and suggest a role for LFY in overcoming polycomb repression.

A classical role of the hormone auxin is in the formation of flowers at the periphery of the reproductive shoot apex. Mutants in regulators of polar auxin transport or in the auxin-responsive transcription factor MONOPTEROS (MP) form naked inflorescence "pins" lacking flowers. How auxin maxima and MP direct initiation of flower primordia is poorly understood. Here, we identify three genes whose expression is directly induced by auxin-activated MP that furthermore jointly regulate flower primordium initiation. These three genes encode known regulators of flower development: LEAFY (LFY), which specifies floral fate, and two AINTEGUMENTA-LIKE/PLETHORA transcription factors, key regulators of floral growth. Our study thus reveals a mechanistic link between flower primordium initiation and subsequent steps in flower morphogenesis. Finally, we uncover direct positive feedback from LFY to the auxin pathway. The auxin LFY module we describe may have been recruited during evolution to pattern other plant organ systems.