Dataset from: A bistable SOC1/FUL-AP2 network prevents inflorescence reversion and maintains reproductive identity in Arabidopsis

In annual plants such as Arabidopsis thaliana, the transition from vegetative growth to flowering is typically irreversible, and inflorescence development is robust to environmental fluctuations. The mechanisms underlying this irreversibility and robustness remain unclear. The late-flowering suppressor of overexpression of constans 1 fruitfull (soc1 ful) double mutant provides a tractable system to study these questions, because it undergoes inflorescence reversion, forming leaves after initiating flowers.

Here, we identify the transcription factor APETALA2 (AP2) as both necessary and sufficient to induce inflorescence reversion. During floral transition, SOC1 and FUL repress AP2 transcription to promote inflorescence development. Introducing an ap2 mutation into soc1 ful suppresses the reversion phenotype, demonstrating that sustained AP2 repression is critical for developmental stability of the inflorescence.

Conversely, inducible expression of an AP2 transgene resistant to repression by SOC1, FUL, and to microRNA172 triggers rapid reversion in the inflorescence meristem by down-regulating multiple flowering genes across distinct pathways. This effect is accompanied by restoration of a meristem morphology characteristic of early floral transition, including remodeling of the WUSCHEL expression domain and an increased number of incipient primordia.

Mathematical modeling indicates that the SOC1–FUL–AP2 network functions as a bistable system exhibiting hysteresis, thereby impeding reversal of the floral transition. These findings define a gene regulatory circuit that confers robustness and irreversibility to plant reproductive development.