Florigenic and antiflorigenic signalling in plants

The evidence that Flowering Locus T (FT) protein and its paralog Twin Sister of FT, act as the long distance floral stimulus, or at least that they are part of it in diverse plant species, has attracted much attention in recent years. Studies to understand the physiological and molecular apparatuses that integrate spatial and temporal signals to regulate developmental transition in plants have occupied countless scientists and have resulted in an unmanageably large amount of research data. Analysis of these data has helped to identify multiple systemic florigenic and antiflorigenic regulators. This study gives an overview of the recent research on gene products, phytohormones and other metabolites that have been demonstrated to have florigenic or antiflorigenic functions in plants.

💡 Research Summary

The review “Florigenic and Antiflorigenic Signalling in Plants” synthesizes the current understanding of the mobile flowering signal—commonly termed florigen—and its antagonistic counterparts, drawing together genetic, hormonal, and metabolic evidence from a broad range of species. Central to the discussion is the protein Flowering Locus T (FT) and its close paralog Twin Sister of FT (TSF). FT is produced in the photoperiod‑sensing leaves in response to environmental cues such as day length, temperature, and nutrient status. Once synthesized, FT protein (and in some cases FT mRNA) enters the phloem and travels long distances to the shoot apical meristem (SAM). At the SAM, FT interacts with the bZIP transcription factor FD, forming an FT–FD complex that recruits 14‑3‑3 proteins and activates downstream floral meristem identity genes including APETALA 1 (AP1), SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 (SOC1), and LEAFY (LFY). This cascade converts the vegetative meristem into a reproductive one, thereby initiating flowering.

The review also details the antiflorigenic side of the system. Proteins such as TERMINAL FLOWER 1 (TFL1) and Arabidopsis CENTRORADIALIS (ATC) share high sequence similarity with FT but act as functional antagonists. TFL1 binds the same 14‑3‑3/FD platform but forms a repressive complex that blocks transcription of floral identity genes, thereby maintaining indeterminate growth and delaying the transition to flowering. The balance between FT/TSF and TFL1/ATC is a key determinant of flowering time, and the two sets of proteins compete for the same interaction partners, providing a molecular switch that can be tipped by upstream signals.

Hormonal regulation is presented as a multilayered network that modulates both florigen production and its antagonists. Gibberellins (GA) and cytokinins (CK) generally promote FT expression, often by stabilizing the CONSTANS (CO) protein that directly activates FT transcription under long‑day conditions. Conversely, auxin (IAA) can suppress FT transcription, while abscisic acid (ABA) and salicylic acid (SA) are associated with stress responses that elevate TFL1 expression and inhibit FT, thus acting as antiflorigenic signals. The review emphasizes that hormonal cross‑talk integrates environmental stress cues with developmental timing, allowing plants to postpone flowering under unfavorable conditions.

Metabolic cues and non‑coding RNAs add further nuance. Lipid composition of phloem membranes influences FT mobility, and specific sugars or amino‑acid derivatives can affect FT protein stability. MicroRNAs, especially miR156 and miR172, constitute a developmental timer: high miR156 levels in juvenile stages repress SPL transcription factors that would otherwise activate FT, while the rise of miR172 in mature plants relieves this repression, facilitating FT expression. These small RNAs thus provide a post‑transcriptional layer that fine‑tunes the florigen/antiflorigen balance.

Integrating these observations, the authors propose a “spatiotemporal integration model.” External cues (photoperiod, temperature, nutrient availability) dictate the synthesis and long‑distance transport of FT/TSF, while internal hormonal and metabolic states modulate the efficiency of FT–FD complex formation at the SAM. Simultaneously, antiflorigenic proteins (TFL1, ATC) and miRNA networks act as brakes, ensuring that flowering only proceeds when conditions are optimal. This model explains how diverse plant species achieve precise control over the vegetative‑to‑reproductive transition.

The review concludes by outlining future research directions. High‑resolution structural studies of FT movement, comparative functional analyses of FT/TSF orthologs in crop species, and dynamic modeling of hormone‑gene interactions under fluctuating environmental conditions are highlighted as priorities. The authors argue that manipulating the florigenic/antiflorigenic circuitry—through gene editing of FT, TFL1, or their regulators, or through targeted hormone treatments—offers promising strategies for crop improvement, enabling breeders to tailor flowering time for different latitudes, climates, and agricultural practices.