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Abstract

In Arabidopsis thaliana and most members of the Brassicaceae family, transformation of the vegetative clade into the floral clade involves the activation and repatterning of the side shoot into a flower. At the same time, the subtending leaf (bract) is completely inhibited. Understanding the mechanism by which bracts are inhibited in Brassicaceae may provide important insight into the evolution of inflorescence architecture as well as the regulation of leaf development, but little is known about the underlying mechanisms. To understand bract inhibition we are characterizing an activation-tagged line termed bracts-1d (brx), in which development of bracts is not inhibited. In addition to defects in bract inhibition, brx mutants also develop petiole-less leaves and, in homozygous plants, develop leafy shoots in place of flowers. Expression analysis shows BRX to be expressed in morphogenetic tissues including meristems, young leaves, and floral organs. Double mutant combination with apetala1 (ap1) dramatically enhances the brx phenotype, suggesting that BRX and AP1 act on the same pathway. Using the AP1 promoter to lower expression via RNAi in the flower results in shorter sepals and petals, while using this same promoter to drive expression of BRX results in the fusion of sepals to each other and, in strong lines, to the complete inhibition of floral organ development. These results suggest that BRX may be involved in maintaining an undifferentiated state required for morphogenesis. Thus, misregulation of BRX may lead to ectopic morphogenesis or the inhibition of differentiation itself.