Regulatory mechanism of flowering time by the COP10-DET1-DDB1 complex in Arabidopsis thaliana

Abstract

Most plants use day length to determine the optimal timing of flowering. Arabidopsis thaliana is a facultative long-day (LD) plant that flowers early in LD and late in short day (SD) conditions. The COP10-DET1-DDB1 (CDD) complex delays flowering and mutants of CDD components (i.e., det1-1, cop10-4, and ddb1a-2) flower early in LD, SD, or both. However, the regulatory functions of these CDD components remain unknown. Here we examine the molecular mechanisms by which the CDD complex represses flowering, using det1-1 mutants, which flower much earlier in SD. The det1-1 mutation alters the rhythm of mRNA abundance of FKF1, but not GI

this causes their peaks to overlap during daytime in SD, leading to daytime expression of CO. In addition, DET1 and COP10 interact with GI, and GI binding affinity to the FT promoter increases in det1-1 mutants, suggesting that the CDD complex restricts GI function, which directly promotes FT expression independently of CO. Moreover, we found that DET1 induces FLC expression possibly via histone modification of H3K4 and H3K27 by interaction with CUL4-CDD-MSI4/FVE. These results indicate that the CDD complex acts in both photoperiod and autonomous pathways to delay expression of floral integrators FT and SOC1. Consistent with this, the early flowering of det1-1 mutants disappears in the ft-1 soc1-2 background. Thus, we propose a model that DET1, likely in CDD form, suppresses flowering under SD by repressing daytime expression of FKF1 and GI binding activity to the FT promoter, and also by epigenetically inducing expression of FLC.