TOPLESS mediates brassinosteroid control of shoot boundaries and root meristem development in Arabidopsis thaliana
Author(s) -
Ana EspinosaRuíz,
Cristina Martínez,
Miguel de Lucas,
Norma Fàbregas,
Nadja Bosch,
Ana I. CañoDelgado,
Salomé Prat
Publication year - 2017
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.143214
Subject(s) - biology , brassinosteroid , ectopic expression , meristem , transcription factor , microbiology and biotechnology , repressor , gene , mutant , regulation of gene expression , psychological repression , arabidopsis , genetics , transcription (linguistics) , gene expression , linguistics , philosophy
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 argets 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 pl-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.
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