Plants in the genus
Arabidopsis are facultative LD plants that flower much earlier under LD conditions than SD regimens, with the photoperiod (or LD) pathway contributing to floral acceleration.
LHY and
CCA1 genes, among other factors, have central roles in the circadian clock of
Arabidopsis, which plays a key role in measuring day length.
GI gene mediates the circadian clock and floral activator genes,
CO and
FT, to control photoperiodic flowering.
GI is required to set the peak phase of
CO expression at the end of the light period under LD conditions, so that the
CO protein is stabilized and activated by light to increase
FT expression. However, recent studies have demonstrated that the role of SDs is not solely to switch off CO activity. For example, GI interacts with SPY, a negative regulator of the GA signal. The flowering times of
gi mutants were still significantly later under SD conditions than LD regimes, which suggests that
GI has a potential role in accelerating the start of flowering, even under SDs. Over-expression of either
FT or
TSF genes caused early flowering, and the acceleration of flowering was enhanced under SDs, suggesting that SDs have an additional role to that in the
LHY/
CCA1-
GI-
CO-
FT pathway. In this short review, we discuss the hidden roles of SDs in controlling flowering based on recent studies of the molecular genetics of flowering time in
Arabidopsis.
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