1. TOPLESS mediates brassinosteroid control of shoot boundaries and root meristem development in Arabidopsis thaliana
- Author
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Ana I. Caño-Delgado, Ana Espinosa-Ruiz, Norma Fàbregas, Miguel de Lucas, Cristina Martínez, Nadja Bosch, Salomé Prat, Ministerio de Ciencia e Innovación (España), Ministerio de Economía y Competitividad (España), European Research Council, and European Commission
- Subjects
0301 basic medicine ,Cell division ,Organ boundary ,Organogenesis ,Quiescence ,03 medical and health sciences ,chemistry.chemical_compound ,TOPLESS ,Arabidopsis ,Gene expression ,Botany ,Brassinosteroid ,Molecular Biology ,Transcription factor ,biology ,Meristem ,biology.organism_classification ,Cell biology ,030104 developmental biology ,chemistry ,Quiescent center ,EAR domain ,Ectopic expression ,BES1 ,BR signaling ,Developmental Biology - Abstract
The transcription factor BRI1-EMS-SUPRESSOR 1 (BES1) is a master regulator of brassinosteroid (BR)-regulated gene expression. BES1 together with BRASSINAZOLE-RESISTANT 1 (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 shoot apical meristem and the regulation of 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 QC cell division rate to the bes1-d mutation, while bes1-d defects are suppressed by the dominant interfering protein encoded by tpl-1, with these effects respectively correlating with changes in CUC3 and BRAVO expression. Together, our data unveil a pivotal role of the co-repressor TPL in the shoot and root meristems, which relies on its interaction with BES1 and regulation of BES1 target gene expression., C.M. was initially supported by a Juan de la Cierva contract from the Spanish Ministry of Science and Innovation (Ministerio de Ciencia e Innovación). This work was supported by grants BIO2011-30546 and BIO2014-60064-R from the Spanish Ministry of Economy and Competitiveness (Ministerio de Economía y Competitividad, MINECO). The A.I.C.-D. laboratory is funded by a BIO2013-43873 grant from MINECO and by a European Research Council Consolidator Grant (ERC-2015-CoG-683163).
- Published
- 2021