Current Biology 21, R374–R378, May 10, 2011 ª2011 Elsevier Ltd All rights reserved
038
FT, A Mobile Developmental Signal
in Plants
Philip A. Wigge
Plants synchronise their flowering with the seasons to
maximise reproductive fitness. While plants sense envi-
ronmental conditions largely through the leaves, the devel-
opmental decision to flower occurs in the shoot apex,
requiring the transmission of flowering information, some-
times over quite long distances. Interestingly, despite the
enormous diversity of reproductive strategies and life-
styles of higher plants, a key component of this mobile
flowering signal, or florigen, is contributed by a highly
conserved gene: FLOWERING LOCUS T (FT ). The FT
gene encodes a small globular protein that is able to trans-
locate from the leaves to the shoot apex through the
phloem. Plants have evolved a variety of regulatory
networks that control FT expression in response to diverse
environmental signals, enabling flowering and other devel-
opmental responses to be seasonally timed. As well as
playing a key role in flowering, recent discoveries indicate
FT is also involved in other developmental processes in the
plant, including dormancy and bud burst.
The force that through the green fuse drives the flower
Drives my green age; that blasts the roots of trees
Dylan Thomas
Since plants are sessile, they must adjust their develop-
ment to their environment. In contrast to animals, in which
the developmental blueprint is usually hardwired in the
embryo, plant development is plastic and continues
throughout the life of the organism, allowing adaptation to
the external environment and climate. Additionally, while
plants lack a central nervous system, they must coordinate
events throughout their body plan, which in the case of
redwoods can span as much as 100 meters. A key develop-
mental transition in plants is the floral transition. The timing
of the floral transition must be coordinated with a host of
environmental factors, including the seasons, climate, other
plants and sometimes pollinators, to ensure reproductive
success. Higher plants are among the most successful
organisms on Earth, and have evolved a remarkable diversity
of lifestyle strategies to colonise almost every space avail-
able. Detailed investigation of the molecular mechanisms
underlying the floral transition are revealing conserved as
well as divergent regulatory mechanisms. Interestingly, while
many of the transcription factors regulating flowering have
diverged, the mobile protein signal that triggers flowering
appears to be conserved in most if not all higher plants.
This Minireview summarises recent advances in under-
standing how FT functions in different plants, and the signif-
icance of these findings.
John Innes Centre, Colney Lane, Norwich NR4 7UH, UK.
E-mail: philip.wigge@bbsrc.ac.uk
DOI 10.1016/j.cub.2011.03.
Minireview
What is Florigen? Early Studies
Many plants show a strong acceleration in flowering when
grown under a particular photoperiod (i.e., daylength). Clas-
sical experiments were performed in the 1920s by Garner
and Allard on a late flowering tobacco strain, Maryland
Mammoth. By reducing the photoperiod experienced by
tobacco plants, it was possible to greatly accelerate flower-
ing [1]. Early experiments using controlled shading of either
leaves or the plant apex revealed that leaves are the site of
signal perception. Paradoxically, however, the effects of
floral induction occur at the growing tip of the plant, the
shoot apex, meaning that a signal must somehow be trans-
mitted from the leaves to the shoot apex for flowering to be
controlled. This led to the ‘florigen’ hypothesis, florigen
being a chemical generated by the leaves under inductive
conditions that is transported to the shoot apex to induce
flowering. Extensive grafting experiments among many
different species strongly supported this hypothesis, since
often a single induced leaf, grafted onto a non-induced plant,
would be sufficient to induce flowering [2]. Despite this
promising start, and many heroic experiments, identification
of the molecular nature of the mobile signal had to wait for
the advent of molecular genetics.
FT, a Key Florigen in Tomato, Rice and Arabidopsis
While the challenges of biochemically isolating florigen
proved to be insurmountable, the power of molecular
genetics in the model plant Arabidopsis thaliana led to the
identification of a key regulator, FLOWERING LOCUS T
(FT ). Mutations in FT caused a considerable delay in flower-
ing [3], while overexpression of FT caused precocious flow-
ering, indicating that FT is necessary and sufficient for the
acceleration of the floral transition [4,5]. Intriguingly, FT
was found to encode a small globular protein for which no
clear molecular function was apparent. Furthermore, while
most of the floral meristem genes known were specifically
expressed at the apex, FT was distinctive in being expressed
in the leaves [6]. Indeed, a major FT activator, CONSTANS
(CO), is specifically expressed in the phloem, and overex-
pressing CO in the phloem to drive high levels of FT expres-
sion in the vasculature was sufficient to trigger early flower-
ing [7], suggesting that FT, or a downstream factor, is able to
travel from the vasculature to the shoot apex.
Elegant experiments with an FT homolog from tomato,
SINGLE-FLOWER TRUSS (SFT ), revealed that branches
overexpressing SFT, when grafted onto tomato and
tobacco, are able to induce flowering. Control experiments
showed that it was impossible to detect movement of the
RNA, indicating that SFT protein, or a downstream target,
was acting as a mobile signal in the plant to trigger flowering
[8]. Subsequent experiments using FT fused to a gene en-
coding green fluorescent protein (GFP) in Arabidopsis [9]
and rice [10] also revealed the ability of FT:GFP protein to
travel from the vasculature to the shoot apex. Although
GFP itself is able to traffic from the vasculature to the
apex, there is evidence that FT is also mobile and this activity
is required for floral induction. While expression of FT specif-
ically in the phloem causes precocious flowering [7], this can
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R375

Figure 1. The FLOWERING LOCUS T (FT) sig-

nalling system in plants.
FT is expressed in the leaves under conditions
that are favourable for flowering, for example in
response to the appropriate photoperiod as
well as environmental cues such as tempera- AP1
ture. FT protein enters the phloem and is trans- FD FD
located to the shoot apical meristem (SAM). At
the SAM, FT interacts with the bZIP transcrip-
tion factor FD, enabling the activation of floral
meristem identity genes such as APETALA1
(AP1) in the domain where FD is expressed. FD
AP1

Temperature Vernalization
Day length Light quality
be prevented by expressing active but Shoot apical meristem
non-mobile forms of FT in the vascula- (SAM)
ture [11,12]. Finally, grafting experi-
ments in cucurbits demonstrated the
ability of FT protein to move in the
phloem sap and trigger flowering [13].
Taken together, these experiments environmental
Environmental
confirmed the role of FT protein as signals
signals
a mobile inducer of flowering. Since
FT
then, FT has been shown to be sufficient FT
to trigger flowering in a wide range of
plants, indicating remarkable conserva-
tion across the plant kingdom.

How Does FT Signal?

Given that FT is able to travel from the FT

Leaf FT

vasculature to the apex and induce flow- FT

ering, a key question is how it activates FT

the floral programme, since it has no

obvious signalling domain. Protein–
protein interaction studies revealed the
ability of Arabidopsis FT to bind the
basic leucine zipper (bZIP) transcription
factor FD [14,15]. Furthermore, it was
shown that FD is tightly expressed in
the shoot apex in the spatial domain
where floral meristem identity genes
are upregulated, and it was possible to
show that FD directly activates some of
these in the presence of FT [14,15].
Thus, FT protein is able to translocate
from the leaves to the apex and activate
the FD transcription factor to convert
meristems from a leaf to a floral fate
(Figure 1). Interestingly, FT is closely related to the floral
repressor, TERMINAL FLOWER1 (TFL1). Indeed, by
changing just one amino acid on FT it is possible to convert
it into a TFL1-like molecule [16]. Subsequent structural
biology studies revealed that key residues that confer FT or
TFL1-like behaviour exist on an exposed loop of these
proteins [17]. These studies suggest that FT and TFL1, given
their similarities, act through a common mechanism. A
complete understanding of the mechanism of FT signalling
awaits the crystal structure of the FT–FD complex, preferably
bound to DNA.
Floral Pathway Signal Integration
A key feature of the floral transition in plants is that it is
responsive to both environmental signals (e.g., temperature,
light quality and photoperiod) as well as endogenous signals
FT
FT FT FT
FT
FT FT
Phloem
FT transport
FT
FT
FT
Phloem
Current Biology
(e.g., hormones and age). In addition to signals that trigger
flowering, plants often have a requirement for a prolonged
period of cold (vernalization) in order to be competent to
respond to floral signals. A vernalization requirement
provides a mechanism to prevent the plant from initiating
flowering in the autumn or winter, when frost may kill the
buds. Additionally, the ability of plants to flower is often
dependent on age, and even in relatively emphemeral plants
like Arabidopsis, a pathway that measures developmental
age — signalling via microRNAs — has been shown to act
to increase floral competence in the plant with age [18].
The major pathways that affect flowering in Arabidopsis
identified by genetics are the photoperiod, gibberellin,
vernalization and autonomous pathways. This raises the
question of how these overlapping or potentially conflicting
signals are assessed and integrated to provide a single
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developmental decision. While hundreds of genes may influ-
ence the floral transition, the decision of when to flower
largely depends on the final level of FT expression. FT, along
with two other key genes, LEAFY (LFY ) and SUPPRESSOR
OF OVEREXPRESSION OF CONSTANS (SOC1), have there-
fore been termed floral pathway integrator (FPI) genes to
account for this essential role in integrating flowering infor-
mation [19].
The Major Floral Pathways
A detailed summary of the major flowering pathways is
beyond the scope of this review, but the reader is pointed
to excellent recent reviews on the photoperiod [20], gibber-
ellin [21] and vernalization pathways [22]. The photoperiod
pathway accelerates flowering under inductive conditions.
In Arabidopsis, these are long days, that is, days of about
16 hours light. The mechanism by which plants are able to
accelerate flowering in response to long days represents
a variation on the external coincidence model, first proposed
by Bunning more than 70 years ago [23]. The gene CO is an
output of the circadian clock and has a diurnal expression
pattern that peaks about 16 hours after dawn. While CO
protein is stable in the light, it is rapidly degraded in the
dark. Thus, plants growing under short days will not accumu-
late CO protein, while plants in long days will [24]. CO is a zinc
finger protein that is able to bind directly to the FT promoter
and activate its expression [25,26]. Since CO levels are also
influenced by light quality, this provides a mechanism by
which light quality could influence flowering time [27].
Gibberellin (GA) mutants are late flowering in long days,
and do not flower at all in short days [28], indicating that
GA plays a key role in controlling the floral transition. The
importance of GA in both long and short days suggests
several roles, both FT-dependent and -independent. The
FPIs LFY and SOC1 have been shown to be induced by GA
[29,30], suggesting key nodes at which GA may be acting
in the floral transition. Vernalization is one of the most heavily
studied and well understood floral regulation pathways. In
Arabidopsis, the key regulator of the vernalisation response
is the MADS box transcription factor FLOWERING LOCUS C
(FLC). In vernalization-requiring plants, FLC levels are very
high before vernalization, but stably repressed through
epigenetic marks after several weeks in the cold [31,32].
FLC has been shown to directly repress many key compo-
nents of the floral pathway, including FT, FD and SOC1
[33], accounting for how the overexpression of FLC causes
such a late flowering phenotype. The regulation of FLC
silencing is complex, and serves as a paradigm for the
activity of non-coding RNAs and post-translational histone
modifications in controlling gene expression. The vernaliza-
tion pathway also interacts with the so-called autonomous
pathway, mutations in which perturb FLC levels. It is likely,
however, that many of these genes are actually involved in
separate cellular processes, and may not function in a linear
pathway.
As well as these classical pathways controlling flowering,
a number of other factors play a role in influencing flower-
ing. Ambient temperature has a strong effect on flowering,
and indeed, high temperatures are able to accelerate flow-
ering in short photoperiods almost as much as long photo-
periods [34]. This process is FT-dependent, and mutations
in genes that perturb FT levels also often disrupt the
thermal acceleration of flowering [35,36]. The mechanism
by which warm temperature accelerates flowering,
however, is not known but is likely to involve chromatin
structure [37,38]. As well as accelerating flowering,
a number of genes function as floral repressors. These
allow a number of environmental and endogenous signals,
such as age and low temperature, to influence the floral
transition. Of particular interest, the microRNA miR156
has been shown to be a potent inhibitor of flowering, acting
by repressing a class of transcription factors, the SQUA-
MOSA PROMOTER BINDING PROTEIN-LIKE (SPL) genes,
which activate flowering targets. miR156 declines with the
age of the plant, providing a competence to respond to
floral signals [18]. Another microRNA, miR172, also plays
a key role in repressing floral repressors, in this case AP2
transcription factors of the TOE and SMZ/SNZ classes,
which have been shown to directly repress FT expression
[39]. In the leaf, TEMPRANILLO1 and TEMPRANILLO2
have also been shown to repress FT and are proposed to
balance CO activity [40].
Variations on a Theme: Learning from Other Plant
Systems
While FT was discovered in Arabidopsis, FT homologs have
been described in rice and shown to be essential inducers of
flowering. Indeed, when two FT homologs are inactivated in
rice, the plants never flower [41]. Paradoxically, however,
rice exhibits the opposite lifestyle strategy to Arabidopsis,
requiring short days for flowering to be accelerated, and
this correlates with the expression of a rice FT, Hd3a, which
is weakly expressed in long days but strongly expressed in
short days. Since it has been shown that a similar module
to the CO–FT signalling module exists in rice, this raises
the question as to how an opposite developmental outcome
can be achieved from a seemingly conserved signalling
pathway. Interestingly, the rice equivalent of CO, Hd1, plays
a critical role in mediating the photoperiod signal. While Hd1
activates FT expression in rice in short days, in long days
Hd1 is converted into a transcriptional repressor [42]. Strik-
ingly, flowering in Poplar is also regulated by FT. Poplar
trees have a prolonged immature period spanning many
years, and FT levels rise very gradually, year by year. The
mechanism by which gene expression can be increased
gradually over such a long period is not clear, but it is likely
to involve chromatin structure [43]. This is an elegant
example of how the pathways by which FT is activated can
be altered to provide an alternative outcome in response
to photoperiod. As well as modulating FT expression in
response to different environmental factors, many plants
have multiple FT-related genes. In pea, it appears that there
are at least two FT genes that are expressed in the leaf and
which interact with each other to control the floral transition
[44]. Such a pathway, whereby different FT-related genes
can interact to control the floral transition, is strikingly illus-
trated by elegant work in beet. In this case, it has been
shown that there are two key FT paralogs, BvFT1 and
BvFT2. While BvFT2 is essential for flowering, BvFT1 is
a potent repressor of flowering, counteracting the activity
of BvFT2 [45]. BvFT1 expression is down-regulated upon
vernalization, providing a novel mechanism by which plants
can overwinter. These examples highlight the remarkable
flexibility of networks using FT signalling. The FT signalling
system therefore provides a seemingly endless arrangement
of possibilities for modulating the timing of flowering
through different pathways of FT regulation as well as
paralog divergence.
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Not Just Flowering
While FT research has understandably been focussed on its
role in influencing the floral transition, there are clear
indications that FT signalling plays a wider role in plant growth
and development. As well as triggering flowering in tomato,
the FT homolog SFT also influences a number of develop-
mental responses, such as leaf maturation, stem growth and
the formation of abscission zones [46]. In addition to flowering,
there are a number of other major seasonally dependent devel-
opmental responses. Particularly important in trees is bud-set
and bud-burst, allowing deciduous trees to overwinter and
survive prolonged periods of cold. The timing of bud set and
bud break is critical for maximising fitness. In poplar, the onset
of bud dormancy is triggered by shorter days and lower
temperatures, and this is dependent on a concomitant
down-regulation in FT expression; indeed, FT-overexpressing
poplars do not set buds, indicating that the CO–FT regulatory
module plays a key role in this process [43]. Following winter,
the buds must open in the spring. Interestingly, FT may also be
involved in this process. It has been shown that prolonged
chilling of dormant poplar buds, a treatment that simulates
winter, causes both massive upregulation of FT expression
in the embryonic leaves within the bud as well as the induction
of enzymes that open the channels, or plasmodesmata (PD),
between plant cells [47]. Closing of the PD is important for
bud formation, but upon bud-burst it is proposed that opening
of the PD facilitates the transfer of growth signals, possibly
including FT, to stimulate bud growth [47].
Major Questions
The last 10 years have witnessed a dramatic advance in our
understanding of key events in the plant life cycle, including
flowering and bud formation. To a remarkable extent, several
problems that had seemed to be of almost intractable
complexity have been shown to have a common regulator,
FT. Major questions for the future will be to understand just
how FT levels are able to be controlled by so many different
environmental and endogenous signals. Particularly inter-
esting is how the level of FT expression can be so precisely
modulated, and how expression can be controlled to such
a high degree over prolonged periods, many years, for
example, in the case of trees. It is likely that such cellular
memory mechanisms involve modulating chromatin struc-
ture. While temperature has been shown to have a very
strong effect on flowering time, the mechanism by which
warm temperature accelerates flowering is still not
described. The tremendous advances in deep sequencing
now make it feasible to obtain detailed transcription factor
networks for regulatory factors and to map these changes
in transcription factors and chromatin state over time in
a tissue-specific manner genome-wide [48]. This provides
us with an unprecedented opportunity to understand the
molecular mechanisms underlying plant lifecycle decisions
[49]. The complexity of the regulatory networks involved
suggests that a whole area of mathematical modelling
approaches may need to be developed if we are to be able
to understand and test the systems under investigation.
A predictive knowledge of how FT influences so many
aspects of plant growth and development holds great
promise for breeding better crop varieties [50].
Acknowledgements
I apologise to colleagues whose work I have been unable to cite owing
to space constraints. I thank members of the lab for insightful
discussions. I am very grateful to two anonymous reviewers who
considerably improved this review with their suggestions. My
laboratory is funded by the JIC, the BBSRC and the ERC.
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