Paracrine brassinosteroid signaling at the stem cell niche controls cellular regeneration

被引:28
作者
Lozano-Elena, Fidel [1 ]
Planas-Riverola, Ainoa [1 ]
Vilarrasa-Blasi, Josep [1 ,3 ]
Schwab, Rebecca [2 ,4 ]
Cano-Delgado, Ana I. [1 ]
机构
[1] UB, UAB, IRTA, CSIC,CRAG,Dept Mol Gent, E-08193 Barcelona, Spain
[2] Cold Spring Harbor Lab, 1 Bungtown Rd, Cold Spring Harbor, NY 11724 USA
[3] Carnegie Inst Sci, Dept Plant Biol, 290 Panama St, Stanford, CA 94305 USA
[4] Max Planck Inst Dev Biol, D-72076 Tubingen, Germany
基金
欧洲研究理事会;
关键词
Brassinosteroid; Quiescent center; Cell division; Stem cell; DNA damage; Paracrine; QUIESCENT CENTER; ARTIFICIAL MICRORNAS; PLANT-GROWTH; ROOT-GROWTH; RECEPTOR; DIFFERENTIATION; DIVISION; BZR1; TRANSDUCTION; NETWORK;
D O I
10.1242/jcs.204065
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Stem cell regeneration is crucial for both cell turnover and tissue healing in multicellular organisms. In Arabidopsis roots, a reduced group of cells known as the quiescent center (QC) act as a cell reservoir for surrounding stem cells during both normal growth and in response to external damage. Although cells of the QC have a very low mitotic activity, plant hormones such as brassinosteroids (BRs) can promote QC divisions. Here, we used a tissue-specific strategy to investigate the spatial signaling requirements of BR-mediated QC divisions. We generated stem cell niche-specific receptor knockout lines by placing an artificial microRNA against BRI1 (BRASSINOSTEROID INSENSITIVE 1) under the control of the QC-specific promoterWOX5. Additionally, QC-specific knock-in lines for BRI1 and its downstream transcription factor BES1 (BRI1-EMS-SUPPRESOR1) were also created using the WOX5 promoter. By analyzing the roots of these lines, we show that BES1-mediated signaling cell-autonomously promotes QC divisions, that BRI1 is essential for sensing nearby inputs and triggering QC divisions and that DNA damage promotes BR-dependent paracrine signaling in the stem cell niche as a prerequisite to stem cell replenishment.
引用
收藏
页数:11
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