Flowering plants exhibit one of two types of inflorescence architecture: indeterminate, in which the inflorescence grows indefinitely, or determinate, in which a terminal flower is produced. The indeterminate condition is thought to have evolved from the determinate many times, independently. In two mutants in distantly related species, terminal flower 1 in Arabidopsis and centroradialis in Antirrhinum, inflorescences that are normally indeterminate are converted to a determinate architecture. The Antirrhinum gene CENTRORADIALIS (CEN) and the Arabidopsis gene TERMINAL FLOWER 1 (TFL1) were shown to be homologous, which suggests that a common mechanism underlies indeterminacy in these plants. However, unlike CEN, TFL1 is also expressed during the vegetative phase, where it delays the commitment to inflorescence development and thus affects the timing of the formation of the inflorescence meristem as well as its identity.

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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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