Espinosa-Ruiz Ana, Martínez Cristina, de Lucas Miguel, Fàbregas Norma, Bosch Nadja, Caño-Delgado Ana I, Prat Salomé
Department of Plant Molecular Genetics, Centro Nacional de Biotecnología-CSIC, Darwin 3, Madrid E-28049, Spain.
Department of Molecular Genetics, Centre for Research in Agricultural Genomics (CRAG) CSIC-IRTA-UAB-UB, Barcelona E-08193, Spain.
Development. 2017 May 1;144(9):1619-1628. doi: 10.1242/dev.143214. Epub 2017 Mar 20.
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 and targets and suppresses their expression. Ectopic expression of TPL leads to similar organ boundary defects and alterations in QC cell division rate to the mutation, while defects are suppressed by the dominant interfering protein encoded by , with these effects respectively correlating with changes in and 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.
转录因子BRI1-EMS-抑制因子1（BES1）是油菜素内酯（BR）调控基因表达的主要调节因子。BES1与抗油菜素唑1（BZR1）共同驱动多个基因的激活或抑制表达，并在BR合成的负调控中发挥重要作用。在此，我们报道BES1通过其ERF相关两亲性抑制（EAR）基序与TOPLESS（TPL）相互作用，对于BES1介导的茎尖分生组织中器官边界形成的控制以及根中静止中心（QC）细胞分裂的调节至关重要。我们表明TPL通过BES1与靶标的启动子结合并抑制其表达。TPL的异位表达导致与突变相似的器官边界缺陷和QC细胞分裂率改变，而的缺陷被编码的显性干扰蛋白抑制，这些效应分别与和表达的变化相关。总之，我们的数据揭示了共抑制因子TPL在茎和根分生组织中的关键作用，这依赖于其与BES1的相互作用以及对BES1靶基因表达的调节。
