A loss-of-function mutation in the / gene enhances the late-flowering and semi-dwarf phenotypes of the clock mutant under continuous light without affecting expression.

The circadian clock plays important roles in the control of photoperiodic flowering in . Mutations in the () and () genes () accelerate flowering under short days, whereas delays flowering under continuous light (LL). The mutant also exhibits short hypocotyls and petioles under LL. However, the molecular mechanisms underlying the regulation of both flowering time and organ lengths in the LHY/CCA1-dependent pathway are not fully understood. To address these questions, we performed EMS mutagenesis of the line and screened for mutations that enhance the phenotypes under LL. In this screen, we identified a novel allele of () and named it (). A similar level of enhancement of the delay in flowering was observed in these two mutants when combined with the mutations. The and mutations did not significantly affect the expression level of the floral repressor gene under LL. Our results suggest that a defect in brassinosteroid (BR) signaling delayed flowering independent of the expression level, at least in plants with the mutation grown under LL. The / mutation did not enhance the late-flowering phenotype of plants overexpressing under LL, suggesting that SVP and BR function in a common pathway that controls flowering time. Our results suggest that the mutant exhibits delayed flowering due to both the BR signaling-dependent and -independent pathways under LL.