Floral size is an ecologically important trait related to pollination success and genetic fitness. Independently of the sexual reproduction strategy, in many plants, floral size seems to be controlled by several genetic programs that are to some extent independent of vegetative growth. Flower size seems to be governed by at least two independent mechanisms, one controlling floral architecture that affects organ number and a second one controlling floral organ size. Different organ-dependent growth control may account for the final proportions of a flower as a whole. Genes controlling floral organ identity, floral symmetry and organ polarity as well as auxin and gibberellin response, also play a role in establishing the final size and architecture of the flower. The final size of an organ seems to be controlled by a systemic signal that might in some cases overcome transgenic modifications of cell division and expansion. Nevertheless, modification of basic processes like cell wall deposition might produce important changes in the floral organs. The coordination of the direction of cell division and expansion by unknown mechanisms poses a challenge for future research. KEY WORDS: floral meristem, cell cycle, systemic signal, floral patterning, floral architectureThe final shape and body size of multicellular organisms is the result of a genetic program and the influence of environmental conditions. In animals and plants the intrinsic growth rate is modulated by nutrient availability that determines the final size of the organism. In animals, both body size and longevity are to some extent controlled by the insulin pathway that is in itself dependent on nutrient conditions (Nijhout, 2003). But one important difference between plants and animals is that in plants, the formation of the different organs happens after embryonic development, thus not only organ or body size is influenced by environmental clues but also the types of organs produced. Our understanding of the way final plant size is achieved has been obtained using two different approaches: physiologists have tried to understand the roles of the so called plant growth regulators and environmental signals on plant development whereas geneticists have concentrated their efforts in finding mutants, genes or natural variation affecting growth in any of its forms. Although these two research lines appear separate, the reality is that they have been linked by an enormous amount of work done by plant breeders studying gene and environment interactions on agricultural traits that are related to growth, like yield, fruit size, biomass production etc. The efforts done in the model system Arabidopsis have helped to bring together the more basic approaches since mutations affected in plant growth regulator synthesis, degradation and Int. J. Dev. Biol. 49: 513-525 (2005) Which are the mechanisms that control the final size of an organism is a question without a clear answer yet. There are two basic processes that could contribute to its control: cell divis...

Control of organ size is the product of coordinated cell division and expansion. In plants where one of these pathways is perturbed, organ size is often unaffected as compensation mechanisms are brought into play. The number of founder cells in organ primordia, dividing cells, and the period of cell proliferation determine cell number in lateral organs. We have identified the Antirrhinum FORMOSA (FO) gene as a specific regulator of floral size. Analysis of cell size and number in the fo mutant, which has increased flower size, indicates that FO is an organ-specific inhibitor of cell division and activator of cell expansion. Increased cell number in fo floral organs correlated with upregulation of genes involved in the cell cycle. In Arabidopsis the AINTEGUMENTA (ANT) gene promotes cell division. In the fo mutant increased cell number also correlates with upregulation of an Antirrhinum ANT-like gene (Am-ANT) in inflorescences that is very closely related to ANT and shares a similar expression pattern, suggesting that they may be functional equivalents. Increased cell proliferation is thought to be compensated for by reduced cell expansion to maintain organ size. In Arabidopsis petal cell expansion is inhibited by the BIGPETAL (BPE) gene, and in the fo mutant reduced cell size corresponded to upregulation of an Antirrhinum BPE-like gene (Am-BPE). Our data suggest that FO inhibits cell proliferation by negatively regulating Am-ANT, and acts upstream of Am-BPE to coordinate floral organ size. This demonstrates that organ size is modulated by the organ-specific control of both general and local gene networks.

Summary The transcriptional network topology of B function in Antirrhinum, required for petal and stamen development, is thought to rely on initial activation of transcription of DEFICIENS (DEF) and GLOBOSA (GLO), followed by a positive autoregulatory loop maintaining gene expression levels. Here, we show that the mutant compacta (co), whose vegetative growth and petal size are affected, plays a role in B function. Late events in petal morphogenesis such as development of conical cell area and scent emissions were reduced in co and def nicotianoides (def nic), and absent in co def nic double mutants, suggesting a role for CO in petal identity. Expression of DEF was down‐regulated in co but surprisingly GLO was not affected. We investigated the levels of DEF and GLO at late stages of petal development in the co, def nic and glo‐1 mutants, and established a reliable transformation protocol that yielded RNAi‐DEF lines. We show that the threshold levels of DEF or GLO required to obtain petal tissue are approximately 11% of wild‐type. The relationship between DEF and GLO transcripts is not equal or constant and changes during development. Furthermore, down‐regulation of DEF or GLO does not cause parallel down‐regulation of the partner. Our results demonstrate that, at late stages of petal development, the B function transcriptional network topology is not based on positive autoregulation, and has additional components of transcriptional maintenance. Our results suggest changes in network topology that may allow changes in protein complexes that would explain the fact that not all petal traits appear early in development.

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