The Delayed Terminal Flower Phenotype Is Caused by a Conditional Mutation in the <i>CENTRORADIALIS</i> Gene of Snapdragon

Cremer, Frédéric; Lönnig, Wolf-Ekkehard; Saedler, Heinz; Huijser, Peter

doi:10.1104/pp.126.3.1031

Cited by 27 publications

(15 citation statements)

References 37 publications

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“…This anti-TFL1 sera detected Escherichia coli-expressed TFL1, but not its Antirrhinum majus functional homolog CENTRORADIALIS (CEN), which is 69% identical ( Figure 1A) (Bradley et al, 1996;Cremer et al, 2001). A commercial anti-TFL1 serum gave only a weak signal.…”

Section: Tfl1 Is a Cytoplasmic Unmodified 20-kd Protein Of Shoot Mermentioning

confidence: 99%

TERMINAL FLOWER1 Is a Mobile Signal ControllingArabidopsisArchitecture

2007

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Shoot meristems harbor stem cells that provide key growing points in plants, maintaining themselves and generating all aboveground tissues. Cell-to-cell signaling networks maintain this population, but how are meristem and organ identities controlled? TERMINAL FLOWER1 (TFL1) controls shoot meristem identity throughout the plant life cycle, affecting the number and identity of all above-ground organs generated; tfl1 mutant shoot meristems make fewer leaves, shoots, and flowers and change identity to flowers. We find that TFL1 mRNA is broadly distributed in young axillary shoot meristems but later becomes limited to central regions, yet affects cell fates at a distance. How is this achieved? We reveal that the TFL1 protein is a mobile signal that becomes evenly distributed across the meristem. TFL1 does not enter cells arising from the flanks of the meristem, thus allowing primordia to establish their identity. Surprisingly, TFL1 movement does not appear to occur in mature shoots of leafy (lfy) mutants, which eventually stop proliferating and convert to carpel/floral-like structures. We propose that signals from LFY in floral meristems may feed back to promote TFL1 protein movement in the shoot meristem. This novel feedback signaling mechanism would ensure that shoot meristem identity is maintained and the appropriate inflorescence architecture develops.

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Section: Tfl1 Is a Cytoplasmic Unmodified 20-kd Protein Of Shoot Mermentioning

confidence: 99%

TERMINAL FLOWER1 Is a Mobile Signal ControllingArabidopsisArchitecture

2007

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“…The closest homolog of TFL1, the ATC (for Arabidopsis CENTORADIALIS), gene does not participate in the regulation of meristem activity, and its function is not clear (Mimida et al, 2001). In Antirrhinum majus, the CENTRORADIALIS (CEN) gene is expressed in the inflorescence meristem after the floral transition, and cen null mutants produce terminal flowers but the timing of flowering is not affected, suggesting a function in inflorescence meristem maintenance but not the floral transition (Bradley et al, 1996;Cremer et al, 2001). In pea (Pisum sativum), two genes, LATE FLOWERING and DETER-MINATE, maintain the indeterminacy of the SAM during vegetative growth and the inflorescence meristem during reproductive growth, respectively (Foucher et al, 2003).…”

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Concerted Modification of Flowering Time and Inflorescence Architecture by Ectopic Expression ofTFL1-Like Genes in Maize

2010

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TERMINAL FLOWER1 (TFL1)-like genes are highly conserved in plants and are thought to function in the maintenance of meristem indeterminacy. Recently, we described six maize (Zea mays) TFL1-related genes, named ZEA CENTRORADIALIS1 (ZCN1) to ZCN6. To gain insight into their functions, we generated transgenic maize plants overexpressing their respective cDNAs driven by a constitutive promoter. Overall, ectopic expression of the maize TFL1-like genes produced similar phenotypes, including delayed flowering and altered inflorescence architecture. We observed an apparent relationship between the magnitude of the transgenic phenotypes and the degree of homology between the ZCN proteins. ZCN2, -4, and -5 form a monophylogenetic clade, and their overexpression produced the strongest phenotypes. Along with very late flowering, these transgenic plants produced a "bushy" tassel with increased lateral branching and spikelet density compared with nontransgenic siblings. On the other hand, ZCN1, -3, and -6 produced milder effects. Among them, ZCN1 showed moderate effects on flowering time and tassel morphology, whereas ZCN3 and ZCN6 did not change flowering time but still showed effects on tassel morphology. In situ hybridizations of tissue from nontransgenic plants revealed that the expression of all ZCN genes was associated with vascular bundles, but each gene had a specific spatial and temporal pattern. Expression of four ZCN genes localized to the protoxylem, whereas ZCN5 was expressed in the protophloem. Collectively, our findings suggest that ectopic expression of the TFL1-like genes in maize modifies flowering time and inflorescence architecture through maintenance of the indeterminacy of the vegetative and inflorescence meristems.

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“…Flowering plant species arose Ͼ 100 million years ago, and FT and TFL1 have been conserved in diverse species, including monocots and eudicots (10)(11)(12)(13)(14)(15). Both TFL1 and FT are key controllers of flowering and plant architecture but act in an opposite manner.…”

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A single amino acid converts a repressor to an activator of flowering

Hanzawa

Money

Bradley

2005

Proc. Natl. Acad. Sci. U.S.A.

445

428

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Homologous proteins occurring through gene duplication may give rise to novel functions through mutations affecting protein sequence or expression. Comparison of such homologues allows insight into how morphological traits evolve. However, it is often unclear which changes are key to determining new functions. To address these ideas, we have studied a system where two homologues have evolved clear and opposite functions in controlling a major developmental switch. In plants, flowering is a major developmental transition that is critical to reproductive success. Arabidopsis phosphatidylethanolamine-binding protein homologues TERMINAL FLOWER 1 (TFL1) and FLOWERING LOCUS T (FT) are key controllers of flowering, determining when and where flowers are made, but as opposing functions: TFL1 is a repressor, FT is an activator. We have uncovered a striking molecular basis for how these homologous proteins have diverged. Although <60% identical, we have shown that swapping a single amino acid is sufficient to convert TFL1 to FT function and vice versa. Therefore, these key residues may have strongly contributed to the selection of these important functions over plant evolution. Further, our results suggest that TFL1 and FT are highly conserved in biochemical function and that they act as repressors or activators of flowering through discrimination of structurally related interactors by a single residue. FLOWERING LOCUS T ͉ phosphatidylethanolamine-binding protein ͉Raf-kinase inhibitor protein ͉ TERMINAL FLOWER 1 N ovel morphologies arise through the evolution of new protein functions. Duplicated genes are a key source of new functions, acquiring mutations that affect expression and͞or protein sequence (1, 2). Studies of large gene families show that different members diverge and participate in different developmental pathways, for example, homeobox and MADS box genes in various species (3-5). However, it is often unclear and difficult to determine which changes in homologues are critical to establish a novel function.The Arabidopsis homologues TERMINAL FLOWER 1 (TFL1) and FLOWERING LOCUS T (FT) provide an excellent model to address this question (6-9). Flowering plant species arose Ͼ 100 million years ago, and FT and TFL1 have been conserved in diverse species, including monocots and eudicots (10-15). Both TFL1 and FT are key controllers of flowering and plant architecture but act in an opposite manner. TFL1 is a repressor, and FT is an activator. Further, gain-of-function studies gave clear and opposite phenotypes in vivo, showing that protein sequence, rather than expression pattern, largely determines the different functions of TFL1 and FT (8,9,16).TFL1 is expressed in the shoot apical meristem (SAM) and represses the transition to flowering; tfl1 mutants flower early (6,7,17,18). TFL1 also maintains indeterminate growth of the SAM by repressing floral meristem identity genes; tfl1 mutants have their SAMs converted into terminal flowers. TFL1 therefore controls plant architecture by determining where flowers are made a...

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The Delayed Terminal Flower Phenotype Is Caused by a Conditional Mutation in the CENTRORADIALIS Gene of Snapdragon

Cited by 27 publications

References 37 publications

TERMINAL FLOWER1 Is a Mobile Signal ControllingArabidopsisArchitecture

TERMINAL FLOWER1 Is a Mobile Signal ControllingArabidopsisArchitecture

Concerted Modification of Flowering Time and Inflorescence Architecture by Ectopic Expression ofTFL1-Like Genes in Maize

A single amino acid converts a repressor to an activator of flowering

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