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Arabidopsis  flowers early under long days (LD) and late under short days (SD). The repressor of photomorphogenesis  DE-ETIOLATED1  ( DET1 ) delays flowering;  det1-1  mutants flower early, especially under SD, but the molecular mechanism of DET1 regulation remains unknown. Here we examine the regulatory function of DET1 in repression of flowering. Under SD, the  det1-1  mutation causes daytime expression of  FKF1  and  CO ; however, their altered expression has only a small effect on early flowering in  det1-1  mutants. Notably, DET1 interacts with GI and binding of GI to the  FT  promoter increases in  det1-1  mutants, suggesting that DET1 mainly restricts GI function, directly promoting  FT  expression independent of  CO  expression. Moreover, DET1 interacts with MSI4/FVE, which epigenetically inhibits  FLC  expression, indicating that the lack of  FLC  expression in  det1-1  mutants likely involves altered histone modifications at the  FLC  locus. These data demonstrate that DET1 acts in both photoperiod and autonomous pathways to inhibit expression of  FT  and  SOC1 . Consistent with this, the early flowering of  det1-1  mutants disappears completely in the  ft-1 soc1-2  double mutant background. Thus, we propose that DET1 is a strong repressor of flowering and has a pivotal role in maintaining photoperiod sensitivity in the regulation of flowering time.

Negative regulatory roles of DE-ETIOLATED1 in flowering time inArabidopsis