HUA2 is required for the expression of floral repressors in Arabidopsis thaliana

The HUA2 gene acts as a repressor of floral transition. Lesions in hua2 were identified through a study of natural variation and through two mutant screens. An allele of HUA2 from Landsberg erecta (Ler) contains a premature stop codon and acts as an enhancer of early flowering 4 (elf4) mutants. hua2 single mutants, in the absence of the elf4 lesion, flower earlier than wild type under short days. hua2 mutations partially suppress late flowering in FRIGIDA (FRI )-containing lines, autonomous pathway mutants, and a photoperiod pathway mutant. hua2 mutations suppress late flowering by reducing the expression of several MADS genes that act as floral repressors including FLOWERING LOCUS C (FLC ) and FLOWERING LOCUS M (FLM ).     

The effect of the floral repressor FLC on the timing and progression of vegetative phase change in Arabidopsis

Plants undergo two major post-embryonic developmental transitions--the juvenile-to-adult vegetative transition (vegetative phase change) and the adult-to-reproductive transition (flowering). In woody plants, these transitions can be separated by years, but in herbaceous species they are often very close together, making it difficult to differentiate the effects of vegetative phase change and floral induction on vegetative development. To distinguish between these factors, we have compared the vegetative morphology of plants highly expressing the floral repressor FLC (FRI;FLC) with plants mutant for this gene (FRI;flc-3) under both photoinductive (long day, LD and night interruption, NI) and non-photoinductive (short day, SD) conditions. We show that the onset of abaxial trichome production is insensitive to floral induction, but the distribution and overall number of abaxial trichomes, as well as several other leaf traits associated with vegetative change, are strongly influenced by flowering. Most of the major differences in leaf morphology between FRI;FLC and FRI;flc-3 plants grown in LD can be attributed to the early flowering phenotype of FRI;flc-3, because these differences are not apparent in plants grown in SD. These include differences in leaf size, hydathode number and the distribution of abaxial trichomes along the length of the leaf. Leaf shape and the total number of abaxial trichomes are affected by FLC independently of its effect on flowering. Our results demonstrate that the onset and the progression of vegetative phase change are regulated by different combinations of endogenous and environmental factors, and reveal a role for FLC in vegetative development.     

Attenuation of brassinosteroid signaling enhances FLC expression and delays flowering

A main developmental switch in the life cycle of a flowering plant is the transition from vegetative to reproductive growth. In Arabidopsis thaliana, distinct genetic pathways regulate the timing of this transition. We report here that brassinosteroid (BR) signaling establishes an unexpected and previously unidentified genetic pathway in the floral-regulating network. We isolated two alleles of brassinosteroid-insensitive 1 (bri1) as enhancers of the late-flowering autonomous-pathway mutant luminidependens (ld). bri1 was found to predominantly function as a flowering-time enhancer. Further analyses of double mutants between bri1 and known flowering-time mutants revealed that bri1 also enhances the phenotype of the autonomous mutant fca and of the dominant FRI line. Moreover, all of these double mutants exhibited elevated expression of the potent floral repressor FLOWERING LOCUS C (FLC). This molecular response could be efficiently suppressed by vernalization, leading to accelerated flowering. Additionally, specific reduction of the expression of FLC via RNA interference accelerated flowering in bri1 ld double mutants. Importantly, combining the BR-deficient mutant cpd with ld also resulted in delayed flowering and led to elevated FLC expression. Finally, we found increased histone H3 acetylation at FLC chromatin in bri1 ld mutants, as compared with ld single mutants. In conclusion, we propose that BR signaling acts to repress FLC expression, particularly in genetic situations, with, for example, dominant FRI alleles or autonomous-pathway mutants, in which FLC is activated.     

The synergistic activation of FLOWERING LOCUS C by FRIGIDA and a new flowering gene AERIAL ROSETTE 1 underlies a novel morphology in Arabidopsis

The genetic changes underlying the diversification of plant forms represent a key question in understanding plant macroevolution. To understand the mechanisms leading to novel plant morphologies we investigated the Sy-0 ecotype of Arabidopsis that forms an enlarged basal rosette of leaves, develops aerial rosettes in the axils of cauline leaves, and exhibits inflorescence and floral reversion. Here we show that this heterochronic shift in reproductive development of all shoot meristems requires interaction between dominant alleles at AERIAL ROSETTE 1 (ART1), FRIGIDA (FRI), and FLOWERING LOCUS C (FLC) loci. ART1 is a new flowering gene that maps 14 cM proximal to FLC on chromosome V. ART1 activates FLC expression through a novel flowering pathway that is independent of FRI and independent of the autonomous and vernalization pathways. Synergistic activation of the floral repressor FLC by ART1 and FRI is required for delayed onset of reproductive development of all shoot meristems, leading to the Sy-0 phenotype. These results demonstrate that modulation in flowering-time genes is one of the mechanisms leading to morphological novelties.     

Regulation of flowering time by Arabidopsis MSI1

The transition to flowering is tightly controlled by endogenous programs and environmental signals. We found that MSI1 is a novel flowering-time gene in Arabidopsis. Both partially complemented msi1 mutants and MSI1 antisense plants were late flowering, whereas ectopic expression of MSI1 accelerated flowering. Physiological experiments revealed that MSI1 is similar to genes from the autonomous promotion of flowering pathway. Expression of most known flowering-time genes did not depend on MSI1, but the induction of SOC1 was delayed in partially complemented msi1 mutants. Delayed activation of SOC1 is often caused by increased expression of the floral repressor FLC. However, MSI1 function is independent of FLC. MSI1 is needed to establish epigenetic H3K4 di-methylation and H3K9 acetylation marks in SOC1 chromatin. The presence of these modifications correlates with the high levels of SOC1 expression that induce flowering in Arabidopsis. Together, the control of flowering time depends on epigenetic mechanisms for the correct expression of not only the floral repressor FLC, but also the floral activator SOC1.     

Interaction between the light quality and flowering time pathways in Arabidopsis

Flowering in Arabidopsis is accelerated by a reduced ratio of red light to far-red light (R/FR), which indicates the proximity of competitive vegetation. By exploiting the natural genetic variation in flowering time responses to low R/FR, we obtained further insight into the complex pathways that fine-tune the transition to flowering in Arabidopsis. The Bla-6 ecotype does not flower significantly earlier in response to low R/FR, but is still able to display other features of shade avoidance, suggesting branching of low R/FR signalling. Here we show that the muted flowering response of Bla-6 is due to high levels of the floral repressor FLOWERING LOCUS C (FLC), conferred by a combination of functional FLC and FRIGIDA ( FRI ) alleles with a 'weak' FY allele. The Bla-6 FY allele encodes a protein with a corrupted WW binding domain, and we provide evidence that this locus plays a key role in the natural variation in light quality-induced flowering in Arabidopsis. In Bla-6, FLC blocks promotion to flowering by reduced R/FR by inhibiting expression of the floral integrator FLOWERING LOCUS T ( FT ) in a dose-dependent manner. Reduction of FLC removes this obstruction, and Bla6 plants then exhibit strong induction of FT and flower early in response to a low R/FR signal. This paper illustrates the intricate interaction of environmental signals and genetic factors to regulate flowering in Arabidopsis.     

Characterization of a novel developmentally retarded mutant (drm1) associated with the autonomous flowering pathway in Arabidopsis

INTRODUCTIONThe transition from vegetative growth to reproductionis one of the most important developmental events in flow-ering plants since it is related to the competence and sur-vivability of a particular species living in a particularenvironment. The…     

FRIGIDA-independent variation in flowering time of natural Arabidopsis thaliana accessions

FRIGIDA (FRI) and FLOWERING LOCUS C (FLC) are two genes that, unless plants are vernalized, greatly delay flowering time in Arabidopsis thaliana. Natural loss-of-function mutations in FRI cause the early flowering growth habits of many A. thaliana accessions. To quantify the variation among wild accessions due to FRI, and to identify additional genetic loci in wild accessions that influence flowering time, we surveyed the flowering times of 145 accessions in long-day photoperiods, with and without a 30-day vernalization treatment, and genotyped them for two common natural lesions in FRI. FRI is disrupted in at least 84 of the accessions, accounting for only approximately 40% of the flowering-time variation in long days. During efforts to dissect the causes for variation that are independent of known dysfunctional FRI alleles, we found new loss-of-function alleles in FLC, as well as late-flowering alleles that do not map to FRI or FLC. An FLC nonsense mutation was found in the early flowering Van-0 accession, which has otherwise functional FRI. In contrast, Lz-0 flowers late because of high levels of FLC expression, even though it has a deletion in FRI. Finally, eXtreme array mapping identified genomic regions linked to the vernalization-independent, late-flowering habit of Bur-0, which has an alternatively spliced FLC allele that behaves as a null allele.     

FLOWERING LOCUS C encodes a novel MADS domain protein that acts as a repressor of flowering.

Winter-annual ecotypes of Arabidopsis are relatively late flowering, unless the flowering of these ecotypes is promoted by exposure to cold (vernalization). This vernalization-suppressible, late-flowering phenotype results from the presence of dominant, late-flowering alleles at two loci, FRIGIDA (FRI) and FLOWERING LOCUS C (FLC). In this study, we report that flc null mutations result in early flowering, demonstrating that the role of active FLC alleles is to repress flowering. FLC was isolated by positional cloning and found to encode a novel MADS domain protein. The levels of FLC mRNA are regulated positively by FRI and negatively by LUMINIDEPENDENS. FLC is also negatively regulated by vernalization. Overexpression of FLC from a heterologous promoter is sufficient to delay flowering in the absence of an active FRI allele. We propose that the level of FLC activity acts through a rheostat-like mechanism to control flowering time in Arabidopsis and that modulation of FLC expression is a component of the vernalization response.     

PIE1, an ISWI family gene,is required for FLC activation and floral repression in Arabidopsis

Proper control of the floral transition is critical for reproductive success in flowering plants. In Arabidopsis, FLOWERING LOCUS C (FLC) is a floral repressor upon which multiple floral regulatory pathways converge. Mutations in PHOTOPERIOD-INDEPENDENT EARLY FLOWERING1 (PIE1) suppress the FLC-mediated delay of flowering as a result of the presence of FRIGIDA or of mutations in autonomous pathway genes. PIE1 is required for high levels of FLC expression in the shoot apex, but it is not required for FLC expression in roots. PIE1 is similar to ATP-dependent, chromatin-remodeling proteins of the ISWI and SWI2/SNF2 family. The role of PIE1 as an activator of FLC is consistent with the general role of ISWI and SWI2/SNF2 family genes as activators of gene expression. The pie1 mutation also causes early flowering in noninductive photoperiods independently of FLC; thus, PIE1 appears to be involved in multiple flowering pathways. PIE1 also plays a role in petal development, as revealed by the suppression of petal defects of the curly leaf mutant by the pie1 mutation.     

EARLY FLOWERING 5 acts as a floral repressor in Arabidopsis

EARLY FLOWERING 5 (ELF5) is a single-copy gene involved in flowering time regulation in Arabidopsis. ELF5 encodes a nuclear-targeted protein that is related to the human nuclear protein containing a WW domain (Npw)38-binding protein (NpwBP). Lesions in ELF5 cause early flowering in both long days and short days. elf5 mutations partially suppress the late flowering of both autonomous-pathway mutants and FRIGIDA (FRI)-containing lines by reducing the expression of FLOWERING LOCUS C (FLC), a floral repressor upon which many of the flowering pathways converge. elf5 mutations also partially suppress photoperiod-pathway mutants, and this, along with the ability of elf5 mutations to cause early flowering in short days, indicates that ELF5 also affects flowering independently of FLC.