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Abstract
Regulation of the homeodomain transcription factor WUSCHEL concentration is critical for stem cell homeostasis in Arabidopsis shoot apical meristems. WUSCHEL regulates the transcription of CLAVATA3 through a concentration-dependent activation-repression switch. CLAVATA3, a secreted peptide, activates receptor kinase signaling to repress WUSCHEL transcription. Considering the revised regulation, CLAVATA3 mediated repression of WUSCHEL transcription alone will lead to an unstable system. Here we show that CLAVATA3 signaling regulates nuclear-cytoplasmic partitioning of WUSCHEL to control nuclear levels and its diffusion into adjacent cells. Our work also reveals that WUSCHEL directly interacts with EXPORTINS via EAR-like domain which is also required for destabilizing WUSCHEL in the cytoplasm. We develop a combined experimental and computational modeling approach that integrates CLAVATA3-mediated transcriptional repression of WUSCHEL and post-translational control of nuclear levels with the WUSCHEL concentration-dependent regulation of CLAVATA3. We show that the dual control by the same signal forms a seamless connection between de novo WUSCHEL synthesis and sub-cellular partitioning in providing robustness to the WUSCHEL gradient.
Highlights
Regulation of the homeodomain transcription factor WUSCHEL concentration is critical for stem cell homeostasis in Arabidopsis shoot apical meristems
To determine the further explore the role of CLV3-signaling in regulating the nuclear export of WUS, we tested whether WUS interacts with EXPORTIN proteins
Using Bimolecular Fluorescence Complementation (BiFC), we found a physical interaction between WUS with XPO1A and XPO1B in N. benthamiana leaf pavement cells (Supplementary Fig. 5)
Summary
Regulation of the homeodomain transcription factor WUSCHEL concentration is critical for stem cell homeostasis in Arabidopsis shoot apical meristems. Our model predictions and the experimental analysis reveal that the simultaneous control of WUS synthesis and subcellular partitioning by the CLV3 regulates nuclear WUS concentration which, in turn, regulates CLV3 levels, forming a dynamic feedback mechanism in the robust maintenance of the WUS protein gradient. The observed reduction of WUS protein levels in the L3 layers of wild type and clv[] SAMs upon MCLV3 treatment is likely due to reduced WUS protein synthesis caused by the repression of WUS transcription (Fig. 1i–k). Even after prolonged MCLV3 treatments extending up to 72 hr, WUS protein continued to accumulate in SAMs despite a severe downregulation of WUS transcript levels (Fig. 2i, j) These results suggested a new role for CLV3-signaling in regulating the nuclear levels and stability of the WUS protein
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