Dorsoventral asymmetry in flowers is thought to have evolved many times from a radially symmetrical ancestral condition. The first gene controlling floral asymmetry, cycloidea in Antirrhinum, has been isolated. The cycloidea gene is expressed at a very early stage in dorsal regions of floral meristems, where it affects growth rate and primordium initiation. Expression continues through to later stages in dorsal primordia to affect the asymmetry, size and cell types of petals and stamens.

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.

Although curvature of biological surfaces has been considered from mathematical and biophysical perspectives, its molecular and developmental basis is unclear. We have studied the cin mutant of Antirrhinum , which has crinkly rather than flat leaves. Leaves of cin display excess growth in marginal regions, resulting in a gradual introduction of negative curvature during development. This reflects a change in the shape and the progression of a cell-cycle arrest front moving from the leaf tip toward the base. CIN encodes a TCP protein and is expressed downstream of the arrest front. We propose that CIN promotes zero curvature (flatness) by making cells more sensitive to an arrest signal, particularly in marginal regions.

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Flowering plants exhibit two types of inflorescence architecture: determinate and indeterminate. The centroradialis mutation causes the normally indeterminate inflorescence of Antirrhinum to terminate in a flower. We show that centroradialis is expressed in the inflorescence apex a few days after floral induction, and interacts with the floral-meristem-identity gene floricaula to regulate flower position and morphology. The protein CEN is similar to animal proteins that associate with lipids and GTP-binding proteins. We propose a model for how different inflorescence structures may arise through the action and evolution of centroradialis.

To understand how genes control floral asymmetry, we have isolated and analyzed the role of the RADIALIS (RAD) gene in Antirrhinum. We show that the RAD gene encodes a small MYB-like protein that is specifically expressed in the dorsal region of developing flowers. RAD has a single MYB-like domain that is closely related to one of the two MYB-like domains of DIV, a protein that has an antagonistic effect to RAD on floral development. Interactions between RAD and other genes indicate that floral asymmetry depends on the interplay between two pairs of transcription factors. First, a pair of TCP proteins is expressed in dorsal regions of the floral meristem, leading to the activation of RAD in the dorsal domain. The RAD MYB-like protein then antagonizes the related DIV MYB-like protein, preventing DIV activity in dorsal regions. In addition to its role in dorsal regions, RAD acts nonautonomously on lateral regions either directly, through RAD protein movement, or indirectly, through a signaling molecule.F loral asymmetry is thought to have evolved many times independently as a specialized mechanism for pollinator interaction (1-3). In a few cases, most notably in Antirrhinum majus, the molecular genetic basis of floral asymmetry has begun to be understood. Four key genes have been shown to control dorsoventral asymmetry in Antirrhinum: CYCLOIDEA (CYC), DICHOTOMA (DICH), RADIALIS (RAD), and DIVARICATA (DIV) (4-8). Two of these genes, CYC and DICH, promote dorsal identity and encode proteins belonging to the TCP family of transcription factors. DIV promotes ventral identity and encodes a protein belonging to the MYB family of transcription factors, carrying two MYB-like domains. However, the mechanism by which CYC, DICH, and DIV interact remains unclear. To address this question, we have isolated and characterized RAD, the fourth member of this group of genes, and explored how it acts in combination with the other genes to establish floral asymmetry.Flowers of wild-type Antirrhinum are zygomorphic, having a single plane of symmetry (bilateral symmetry), in contrast to actinomorphic flowers, which have multiple planes of symmetry (radial symmetry) (3). The zygomorphy of Antirrhinum flowers reflects morphological distinctions between the upper (dorsal) and lower (lateral and ventral) organs of whorls two and three. In whorl two, each flower has two dorsal petals, two lateral petals, and one ventral petal, whereas whorl three comprises a single arrested dorsal stamen (staminode), two lateral stamens, and two ventral stamens (Fig. 1 a and b).The CYC and DICH genes are required for dorsoventral asymmetry in Antirrhinum and are expressed from an early stage in the dorsal domain of the floral meristem (5, 7, 9). At later stages, CYC expression persists throughout most of the dorsal domain, whereas DICH becomes restricted to the most dorsal half of the dorsal domain. Inactivation of both CYC and DICH results in peloric (radially symmetrical) flowers, in which all petals have ventral identity (Fig. 1h). In cyc or dich single ...

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