The transcription factor bri1-EMS-SUPRESSOR1 (BES1) is a master regulator of brassinosteroid (BR)-regulated gene expression. BES1 together with BRASSINAZOLE-RESISTANT1 (BZR1) drive activated or repressed expression of several genes, and have a prominent role in negative regulation of BR synthesis. Here, we report that BES1 interaction with TOPLESS (TPL), via its ERF-associated amphiphilic repression EAR motif, is essential for BES1-mediated control of organ boundary formation in the SAM and the regulation of the quiescent center (QC) cell division in roots. We show that TPL binds via BES1 to the promoters of the CUC3 and BRAVO targets and suppresses their expression. Ectopic expression of TPL leads to similar organ boundary defects and alterations in the QC cell division rate as the bes1-d mutation, while bes1-d defects are suppressed by the dominant interfering tpl-1 protein, with these effects respectively correlating with changes in CUC3 and BRAVO expression. Together, our data unveil a pivotal role of the co-repressor TOPLESS in the shoot and root meristems, which relies on its interaction with BES1 and regulation of BES1 target gene expression.
- Received August 3, 2016.
- Accepted February 27, 2017.