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EBP1 nuclear accumulation negatively feeds back on FERONIA-mediated RALF1 signaling

文献类型： 外文期刊

作者： Li, Chiyu 1 ; Liu, Xuanming 1 ; Qiang, Xiaonan 1 ; Li, Xiaoyan 1 ; Li, Xiushan 1 ; Zhu, Sirui 1 ; Wang, Long 1 ; Wang, Yu 1 ;

作者机构： 1.Hunan Univ, Coll Biol, State Key Lab Chemo Biosensing & Chemometr, Hunan Prov Key Lab Plant Funct Genom & Dev Regula, Changsha, Hunan, Peoples R China

2.Univ Calif Berkeley, Dept Plant & Microbial Biol, Berkeley, CA 94720 USA

3.Hunan Hybrid Rice Res Ctr, State Key Lab Hybrid Rice, Changsha, Hunan, Peoples R China

期刊名称：PLOS BIOLOGY （ 影响因子：8.029； 五年影响因子：9.57 ）

ISSN： 1545-7885

年卷期： 2018 年 16 卷 10 期

页码：

收录情况： SCI

摘要： FERONIA (FER), a plasma membrane receptor-like kinase, is a central regulator of cell growth that integrates environmental and endogenous signals. A peptide ligand rapid alkalinization factor 1 (RALF1) binds to FER and triggers a series of downstream events, including inhibition of Arabidopsis H+-ATPase 2 activity at the cell surface and regulation of gene expression in the nucleus. We report here that, upon RALF1 binding, FER first promotes ErbB3-binding protein 1 (EBP1) mRNA translation and then interacts with and phosphorylates the EBP1 protein, leading to EBP1 accumulation in the nucleus. There, EBP1 associates with the promoters of previously identified RALF1-regulated genes, such as CML38, and regulates gene transcription in response to RALF1 signaling. EBP1 appears to inhibit the RALF1 peptide response, thus forming a transcription-translation feedback loop (TTFL) similar to that found in circadian rhythm control. The plant RALF1-FER-EBP1 axis is reminiscent of animal epidermal growth factor receptor (EGFR) signaling, in which EGF peptide induces EGFR to interact with and phosphorylate EBP1, promoting EBP1 nuclear accumulation to control cell growth. Thus, we suggest that in response to peptide signals, plant FER and animal EGFR use the conserved key regulator EBP1 to control cell growth in the nucleus.

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