Abstract
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.
Highlights
Arabidopsis flowers early under long days (LD) and late under short days (SD)
These results indicate that DET1 acts as a strong floral repressor in SD and has a key role in maintaining the photoperiod sensitivity of the regulation of flowering time in Arabidopsis
We showed that gi-1 and ft-1 nearly completely suppressed the early flowering of det[1] mutants and that DET1 directly interacts with GI in vitro and in vivo (Fig. 4)
Summary
Arabidopsis flowers early under long days (LD) and late under short days (SD). The repressor of photomorphogenesis DE-ETIOLATED1 (DET1) delays flowering; det[1] mutants flower early, especially under SD, but the molecular mechanism of DET1 regulation remains unknown. DET1 interacts with MSI4/FVE, which epigenetically inhibits FLC expression, indicating that the lack of FLC expression in det[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. FLOWERING LOCUS C (FLC) has a central place in those two pathways and directly regulates FT and SOC1 expression by binding to their promoters[9,10,11]. This indicates that MSI4/FVE plays a significant role in FLC expression by making a complex with various chromatin remodeling factors
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