During the floral transition, the shoot apical meristem (SAM) changes its identity from vegetative, when it produces leaves and shoots, to inflorescence, when it produces flowers. According to the behaviour of the SAM, the inflorescences can be classified as indeterminate, where the inflorescence SAM grows continuously, or determinate, where the SAM forms a terminal flower. In Arabidopsis, the expression of the TERMINAL FLOWER 1 (TFL1) gene in the centre of the SAM prevents its conversion into a flower and, therefore, the determination of the inflorescence. Thus, TFL1 plays a key role in the control of plant architecture, a function that is related to its particular expression pattern.
The main aim of this work has been the identification of genes that regulate the expression of TFL1. A first step toward that aim has been to perform an EMS mutagenesis of a reporter line containing a TFL1pro::GUS transgene in which the regulatory regions of TFL1 direct the expression of the GUS gene. Because of the role of TFL1 in the control of plant architecture, we screened for plants that showed defects both in the pattern of TFL1pro::GUS expression and in inflorescence architecture. Among the selected mutants, the line 63.1, that we named moss, shows increased levels of TFL1pro::GUS expression, which is also ectopic in flowers, and a dramatic alteration in inflorescence architecture. The positional cloning of the corresponding gene showed that the moss phenotype is caused by a hypomorphic mutation in the ARGONAUTE1 (AGO1) gene. Our results suggest that TFL1 expression is regulated by small RNAs through AGO1.
In order to identify the promoter regions that are critical for the expression of TFL1, we have also analyzed the TFL1 promoter by phylogenetic footprinting, and have combined these results with those from a deletion analysis previously carried out in our lab. One of the identified regulatory regions has been used in a screening with the yeast one-hybrid system. This screening resulted in the identification of TCP7, a transcription factor for which no function has been reported so far, as a protein able to bind to the TFL1 promoter. The characterization of lines where TCP7 is over-expressed or silenced showed that they have phenotypes related to the architecture of the inflorescence. Moreover, our data indicate that TCP7 represses TFL1. Our results support the idea that TCP7 controls plant architecture through the regulation of TFL1.