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First published online August 2, 2004
doi: 10.1242/10.1242/dev.01294

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Control of Arabidopsis flowering: the chill before the bloom

Department of Cell and Developmental Biology, John Innes Centre, Colney Lane, Norwich NR4 7UH, UK

View larger version (26K): [in a new window]   Fig. 1. Pathways controlling flowering-time in Arabidopsis. The flowering-time pathways control the expression of the floral pathway integrators SUPPRESSOR OF OVEREXPRESSION OF CONSTANS1 (SOC1), FT and LEAFY (LFY). These genes encode proteins that activate the floral meristem identity (FMI) genes APETALA1 (AP1), APETALA2 (AP2), FRUITFULL (FUL), CAULIFLOWER (CAL) and LFY, which convert the vegetative meristem to a floral fate. Recent expression data has indicated that FUL may also act as a floral integrator (Schmid et al., 2004). The photoperiod, gibberellin, light-quality and ambient-temperature pathways activate floral pathway integrators. The CONSTANS (CO) transcription factor functions in the photoperiod pathway; long-day photoperiods promote flowering by circadian clock (CLOCK) dependent and independent mechanisms, which control the activity of CO. Activation of flowering is antagonised by the floral repressors encoded by (shown in green) FLOWERING LOCUS C (FLC), FLOWERING LOCUS M (FLM), TERMINAL FLOWER1 (TFL1), TERMINAL FLOWER2 (TFL2), SHORT VEGETATIVE PHASE (SVP), TARGET OF EAT1 (TOE1), TARGET OF EAT2 (TOE2), SCHNARCHZAPFEN (SNZ), SCHLAFMUTZE (SMZ) and EMBRYONIC FLOWER1/2 (EMF1, EMF2). TFL1 may also be downstream of CO, as it is induced after CO activation (Simon et al., 1996). FLC expression is controlled by a number of different pathways. The genes shown in purple, FRIGIDA (FRI), FRIGIDA-LIKE1 (FRL1), FRIGIDA-LIKE2 (FRL2), PHOTOPERIOD INSENSITIVE EARLY FLOWERING1 (PIE1), AERIAL ROSETTE1 (ART1), EARLY UNDER SHORT DAYS4 (ESD4), VERNALIZATION INDEPENDENCE3 (VIP3) and VERNALIZATION INDEPENDENCE4 (VIP4), encode proteins that promote FLC expression and delay flowering. FLC expression is downregulated in response to prolonged cold by proteins encoded by the genes (shown in blue) VERNALIZATION INSENSITIVE3 (VIN3), VERNALIZATION1 (VRN1) and VERNALIZATION2 (VRN2), and also by proteins encoded by the genes of the autonomous pathway (red): FCA, FY, LUMINIDEPENDENS (LD), FLOWERING LOCUS D (FLD), FVE, FLOWERING LOCUS K (FLK) and FPA. The distinction between potential transcriptional and post-transcriptional functions of genes of the autonomous pathway is not made here, but is shown more clearly in Fig. 3.

View larger version (17K): [in a new window]   Fig. 2. Schematic representations of Arabidopsis plants summarizing the genetic control of vernalization requirement and response. The flowering phenotype of Arabidopsis is represented as either a rapid cycler (e.g. top right), which produces a flowering inflorescence, or as a winter annual accession (e.g. top left), which continues to produce rosette leaves. Rapid-cycling accessions do not require a vernalization treatment to flower early and are commonly used as laboratory backgrounds. By contrast, the majority of Arabidopsis accessions are winter annuals, which flower late unless they have been exposed to a prior vernalization treatment. Typically, 6 weeks of growth at 4°C produces a saturated vernalization response in Arabidopsis. Growth habit is indicated either with (+VRN) or without (–VRN) a vernalization treatment. When both FRI and FLC are active, the plant is vernalization responsive, as is found in many winter annual accessions. Mutations in either fri or flc can lead to rapid cycling. A vernalization-responsive FRI FLC accession is rendered insensitive to vernalization by a vrn mutation. Finally, a rapid-cycling fri FLC genotype becomes a winter annual background in the presence of an autonomous pathway mutation such as fca.

View larger version (31K): [in a new window]   Fig. 3. Model for the regulation of the floral repressor FLC throughout the Arabidopsis life cycle. During seedling growth, a group of genes encode proteins that function as activators of FLC expression (shown in purple); these genes include FRI, FRL1, FRL2, ESD4, ART1, PIE1, VIP3 and VIP4. These proteins may maintain FLC chromatin in an active state (indicated by an open structure and the presence of active histone tail modifications shown in green). The autonomous pathway functions antagonistically to the activators to repress FLC expression. The RNA-binding proteins FCA, FPA and FLK, and the polyadenylation factor FY, may function post-transcriptionally to achieve this and are shown in red. The FVE/FLD proteins act with a putative histone deacetylase (HDAC; all shown in orange) to promote an inactive FLC chromatin state, represented by a closed structure with inactive histone tail modifications (red). FLC is also repressed by exposure to long periods of cold (vernalization). The proteins acting in the vernalization pathway are shown in pink. Prolonged cold induces VIN3 expression, which promotes an inactive FLC chromatin state. Subsequently, the VRN1 and VRN2 proteins are recruited to FLC, and are required for the methylation of FLC histones and the maintenance of silencing. These marks may promote the association of silencing factors with FLC chromatin that reinforce its repression. During meiosis, gametogenesis or early embryogenesis, FLC repression is overcome, thus resetting its expression in the next generation.