The flowering-time gene FLOWERING LOCUS T (FT)

FT is a strong promoter of flowering and was first identified in the classic flowering-time screens described by Koornneef (Koornneef et al., 1991) . FT is a small protein of 23KD and is homologous to phosphatidylethanolamione-binding proteins, which are also called RAF kinase inhibitor proteins (Kardailsky et al., 1999; Kobayashi et al., 1999) . FT belongs to a group of six closely related proteins, which includes TFL1 and CENTRORADIALIS (CEN) of Antirrhinum (Ratcliffe et al., 1998; Amaya et al., 1999; Ratcliffe et al., 1999) .

FT promotes flowering

The early flowering of 35S::FT plants is strongly suppressed by fd mutations (Daimon et al., 2004). This gene encodes a bzip transcription factor that interacts with FT in yeast. FD is expressed in the shoot apex, and appears to upregulate the meristem identity genes AP1 and CAL. FT mRNA is expressed in the phloem (Takada and Goto, 2003) . The suggestion that FT interacts with FD at the meristem but FT mRNA is only present in the phloem has led to the idea that FT protein may represent a long distant signal that travels from the leaves, initiating floral development either directly through FD, or through an intermediate (Daimon et al., 2004) .

TERMINAL FLOWER 2 (TFL2) an Arabidopsis homolog of heterochromatin protein1 represses the expression of FT continuously throughout development (Larsson et al., 1998; Kotake et al., 2003) . TFL2, CO and FT are all expressed in the leaf vascular tissue. Daylength independent flowering is observed in tfl2 mutants, which is a consequence of de-repression of FT expression. TFL2 is able to partially counteract the effect of CO overexpression by reducing FT mRNA levels (Takada and Goto, 2003).

Summary of Flowering time

The control of flowering is controlled by exogenous and endogenous stimuli, ensuring that flowering occurs at an optimal time for fertilisation and seed development to occur. Until recently, much of the understanding of how plants undergo the change from vegetative to reproductive growth came from classical physiological experiments performed in the early to mid 20th Century. Recent work has greatly increased our understanding of the molecular mechanisms controlling flowering by using species such as rice and Arabidopsis as models.

In particular, this has provided molecular models of how vernalisation and photoperiodism are controlled that support and extends classical models based on physiological approaches.


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