Lee Hak-Soo, Kim Yoon, Pham Giang, Kim Ju Won, Song Ji-Hye, Lee Yew, Hwang Yong-Sic, Roux Stanley J, Kim Soo-Hwan
Division of Biological Science and Technology, Yonsei University, Wonju, 220-710, Republic of Korea.
Division of Biological Science and Technology, Yonsei University, Wonju, 220-710, Republic of Korea Department of Life Science, Hanyang University, Seoul, 133-791, Republic of Korea.
J Exp Bot. 2015 Aug;66(15):4835-49. doi: 10.1093/jxb/erv316. Epub 2015 Jul 1.
Previous publications have shown that BRI1 EMS suppressor 1 (BES1), a positive regulator of the brassinosteroid (BR) signalling pathway, enhances cell divisions in the quiescent centre (QC) and stimulates columella stem cell differentiation. Here, it is demonstrated that BZR1, a BES1 homologue, also promotes cell divisions in the QC, but it suppresses columella stem cell differentiation, opposite to the action of BES1. In addition, BR and its BZR1-mediated signalling pathway are shown to alter the expression/subcellular distribution of pin-formed (PINs), which may result in changes in auxin movement. BR promotes intense nuclear accumulation of BZR1 in the root tip area, and the binding of BZR1 to the promoters of several root development-regulating genes, modulating their expression in the root stem cell niche area. These BZR1-mediated signalling cascades may account for both the ectopic activation of QC cell divisions as well as the suppression of the columella stem cell differentiation. They could also inhibit auxin-dependent distal stem cell differentiation by antagonizing the auxin/WOX5-dependent pathway. In conclusion, BZR1-/BES1-mediated BR signalling pathways show differential effects on the maintenance of root apical meristem activities: they stimulate ectopic QC division while they show opposite effects on the differentiation of distal columella stem cells in a BR concentration- and BZR1-/BES1-dependent manner.
先前的研究表明,油菜素内酯(BR)信号通路的正向调节因子BRI1 EMS抑制因子1(BES1)可增强静止中心(QC)的细胞分裂,并刺激根冠干细胞分化。在此,研究表明,BES1的同源物BZR1也能促进QC中的细胞分裂,但与BES1的作用相反,它会抑制根冠干细胞的分化。此外,研究还表明,BR及其BZR1介导的信号通路会改变pin-formed(PINs)的表达/亚细胞分布,这可能导致生长素运输的变化。BR促进BZR1在根尖区域强烈地向细胞核积累,并且BZR1与几个调控根发育的基因的启动子结合,调节它们在根干细胞龛区域的表达。这些BZR1介导的信号级联反应可能是QC细胞分裂异位激活以及根冠干细胞分化受到抑制的原因。它们还可能通过拮抗生长素/WOX5依赖的途径来抑制生长素依赖的远端干细胞分化。总之,BZR1-/BES1介导的BR信号通路对根尖分生组织活性的维持表现出不同的影响:它们刺激异位的QC分裂,同时以BR浓度和BZR1-/BES1依赖的方式对远端根冠干细胞的分化表现出相反的作用。