In plants, seasonal changes in day length are perceived in leaves, which initiate long-distance signaling that induces flowering at the shoot apex. The identity of the long-distance signal has yet to be determined. In Arabidopsis , activation of FLOWERING LOCUS T ( FT ) transcription in leaf vascular tissue (phloem) induces flowering. We found that FT messenger RNA is required only transiently in the leaf. In addition, FT fusion proteins expressed specifically in phloem cells move to the apex and move long distances between grafted plants. Finally, we provide evidence that FT does not activate an intermediate messenger in leaves. We conclude that FT protein acts as a long-distance signal that induces Arabidopsis flowering.

The transition from vegetative to reproductive growth is controlled by day length in many plant species. Day length is perceived in leaves and induces a systemic signal, called florigen, that moves through the phloem to the shoot apex. At the shoot apical meristem (SAM), florigen causes changes in gene expression that reprogram the SAM to form flowers instead of leaves. Analysis of flowering of Arabidopsis thaliana placed the CONSTANS/FLOWERING LOCUS T (CO/FT ) module at the core of a pathway that promotes flowering in response to changes in day length. We describe progress in defining the molecular mechanisms that activate this module in response to changing day length and the increasing evidence that FT protein is a major component of florigen. Finally, we discuss conservation of FT function in other species and how variation in its regulation could generate different flowering behaviors.

Floral development at the Arabidopsis shoot apical meristem occurs in response to environmental cues that are perceived in different tissues. Photoperiod is detected in the vascular tissue of the leaf (phloem) and promotes production of a systemic signal that induces flowering at the meristem. Vernalization, the response to winter temperatures, overcomes a block on photoperiodic floral induction. In Arabidopsis, this block is caused by inhibitors of flowering that comprise several related MADS-box transcription factors, the most prominent of which is FLC. We show that FLC delays flowering by repressing production in the leaf of at least two systemic signals, one of which is controlled by the RAF kinase inhibitor- In Arabidopsis, reproductive development is initiated by the formation of floral primordia on the flanks of the shoot apical meristem. The time at which flowering occurs is governed by environmental cues such as day length and temperature, and is influenced by endogenous signals related to the age of the plant. Classical physiological experiments demonstrated that environmental signals that influence flowering are perceived in different tissues. For example, day length is detected in expanded leaves, and in response to exposure to day lengths that trigger flowering, a systemic signal termed the floral stimulus travels through the phloem to the shoot apical meristem, where it induces floral development (Knott 1934;Zeevaart 1976;Corbesier and Coupland 2005). Vernalization, the acquisition of competence to flower that results from exposure to extended periods of low temperatures that mimic winter conditions, typically relieves a block to the photoperiod pathway (Lang 1965).Here we describe an analysis of the tissues in which key Arabidopsis genes involved in vernalization act to control flowering and demonstrate the significance of transcriptional regulation in the phloem and the meristem for the vernalization response.Genetic analyses of the control of flowering in Arabidopsis thaliana identified four major floral promotion pathways Boss et al. 2004). Environmental responses studied genetically in Arabidopsis include photoperiodic control of flowering, induction of flowering by response to long days (LD) of spring or early summer, and vernalization, which is the promotion of flowering by extended exposures to low temperatures that mimic winter conditions. The responses to day length (or photoperiod) and vernalization are mediated by pathways that specifically control responses to

Flowering of Arabidopsis is induced by long summer days (LDs). The transcriptional regulator CONSTANS (CO) promotes flowering, and its transcription is increased under LDs. We systematically misexpressed transcription factors in companion cells and identified several DOF proteins that delay flowering by repressing CO transcription. Combining mutations in four of these, including CYCLING DOF FACTOR 2 (CDF2), caused photoperiod-insensitive early flowering by increasing CO mRNA levels. CO transcription is promoted to differing extents by GIGANTEA (GI) and the F-box protein FKF1. We show that GI stabilizes FKF1, thereby reducing CDF2 abundance and allowing transcription of CO. Despite the crucial function of GI in wild-type plants, introducing mutations in the four DOF-encoding genes into gi mutants restored the diurnal rhythm and light inducibility of CO. Thus, antagonism between GI and DOF transcription factors contributes to photoperiodic flowering by modulating an underlying diurnal rhythm in CO transcript levels.

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SummaryGenes that control ovule identity were first identified in Petunia. Co-suppression of both FLORAL BINDING PROTEIN 7 (FBP7) and FBP11, two D-lineage genes, resulted in the homeotic transformation of ovules into carpelloid structures. Later in Arabidopsis it was shown that three genes, SHATTERPROOF1 (SHP1), SHP2, and SEEDSTICK (STK), redundantly control ovule identity, because in the stk shp1 shp2 triple mutant ovules lose identity and are transformed into carpel and leaf-like structures. Of these three Arabidopsis genes STK is the only D-lineage gene, and its expression, like FBP7 and FBP11, is restricted to ovules. OsMADS13 is the rice ortholog of STK, FBP7, and FBP11. Its amino acid sequence is similar to the Arabidopsis and Petunia proteins, and its expression is also restricted to ovules. We show that the osmads13 mutant is female sterile and that ovules are converted into carpelloid structures. Furthermore, making carpels inside carpels, the osmads13 flower is indeterminate, showing that OsMADS13 also has a function in floral meristem determinacy. OsMADS21 is most likely to be a paralog of OsMADS13, although its expression is not restricted to ovules. Interestingly, the osmads21 mutant did not show any obvious phenotype. Furthermore, combining the osmads13 and the osmads21 mutants did not result in any additive ovule defect, indicating that osmads21 does not control ovule identity. These results suggest that during evolution the D-lineage gene OsMADS21 has lost its ability to determine ovule identity.

Understanding the mechanisms involved in photoperiodic flowering and comparing the regulatory networks of dicots and monocots has revealed how plants respond to environmental cues and adapt to seasonal changes. The molecular architecture of such regulation shows striking similarities across diverse species. However, integration of specific pathways on a basal scheme is essential for adaptation to different environments. Artificial manipulation of flowering time by means of natural genetic resources is essential for expanding the cultivation of cereals across different environments.

Flowering of Arabidopsis thaliana is induced by exposure to long days (LDs). During this process, the shoot apical meristem is converted to an inflorescence meristem that forms flowers, and this transition is maintained even if plants are returned to short days (SDs). We show that exposure to five LDs is sufficient to commit the meristem of SD-grown plants to flower as if they were exposed to continuous LDs. The MADS box proteins SUPPRESSOR OF OVEREXPRESSION OF CONSTANS1 (SOC1) and FRUITFULL (FUL) play essential roles in this commitment process and in the induction of flowering downstream of the transmissible FLOWERING LOCUS T (FT) signal. We exploited laser microdissection and Solexa sequencing to identify 202 genes whose transcripts increase in the meristem during floral commitment. Expression of six of these transcripts was tested in different mutants, allowing them to be assigned to FT-dependent or FT-independent pathways. Most, but not all, of those dependent on FT and its paralog TWIN SISTER OF FT (TSF) also relied on SOC1 and FUL. However, this dependency on FT and TSF or SOC1 and FUL was often bypassed in the presence of the short vegetative phase mutation. FLOR1, which encodes a leucine-rich repeat protein, was induced in the early inflorescence meristem, and flor1 mutations delayed flowering. Our data contribute to the definition of LD-dependent pathways downstream and in parallel to FT.