The Continuous Flowering Regulator, RoKSN, Is Induced by Gibberellins to Modulate Flowering in Rose

The transition from vegetative growth to flowering is a key event in plant life, and is finely regulated by endogenous and environmental signals. In rose, the ability to flower continuously represents an important economical and ornamental trait. The continuous flowering (CF) phenotype is due to a mutation of a TFL1 homologue, RoKSN.  The insertion of a retrotransposon blocks the transcription of RoKSN and leads to the absence of floral repressor. In once-flowering (OF) genotypes, RoKSN is repressed in spring to induce blooming. Later its induction blocks all new flowering. CF and OF roses respond differently to gibberellins (GA). Exogenous application of GA leads to the inhibition of flowering in OF and has no effect on CF roses. In OF roses, this inhibition is correlated with an accumulation of RoKSN transcripts. Our objective is to understand the regulation of flowering by GA in rose. Using histological and molecular approaches, we showed that in OF roses, GA blocked floral initiation, and the meristems remained vegetative. This inhibition correlated with a large induction of the floral repressor, RoKSN. To further understand the inhibition of flowering by RoKSN, we demonstrated that RoKSN binds RoFD (FLOWERING LOCUS D), a transcription factor involves in flowering activation. Thus, we propose that RoKSN inhibits the formation of the activator complex RoFT (FLOWERING LOCUS T)/RoFD, to repress flowering. Our results demonstrate a new regulation of TERMINAL FLOWER 1 homologue by GA to control rose flowering.