J Integr Plant Biol ›› 2022, Vol. 64 ›› Issue (9): 1706-1723.DOI: 10.1111/jipb.13329

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  • 收稿日期:2022-06-29 接受日期:2022-07-18 出版日期:2022-09-01 发布日期:2022-09-16

SICKLE represses photomorphogenic development of Arabidopsis seedlings via HY5- and PIF4-mediated signaling

Tao Li1†, Haojie Li1†, Hongmei Lian1, Pengyu Song2, Yulong Wang3, Jie Duan2, Zhaoqing Song4, Yan Cao2, Dongqing Xu4, Jigang Li2 and Huiyong Zhang1*   

  1. 1 College of Life Sciences, Henan Agricultural University, Zhengzhou 450002, China
    State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing 100193, China
    3 School of Life Sciences, Westlake University, Hangzhou 310024, China
    4 State Key Laboratory of Crop Genetics and Germplasm Enhancement, National Center for Soybean Improvement, College of Agriculture, Nanjing Agricultural University, Nanjing 210095, China

    These authors contributed equally to this work.
    * Correspondence: Huiyong Zhang (huiyong.zhang@henau.edu.cn)
  • Received:2022-06-29 Accepted:2022-07-18 Online:2022-09-01 Published:2022-09-16

Abstract:

Arabidopsis CONSTITUTIVELY PHOTOMORPHOGENIC1 (COP1) and PHYTOCHROME INTERACTING FACTORs (PIFs) are negative regulators, and ELONGATED HYPOCOTYL5 (HY5) is a positive regulator of seedling photomorphogenic development. Here, we report that SICKLE (SIC), a proline rich protein, acts as a novel negative regulator of photomorphogenesis. HY5 directly binds the SIC promoter and activates SIC expression in response to light. In turn, SIC physically interacts with HY5 and interferes with its transcriptional regulation of downstream target genes. Moreover, SIC interacts with PIF4 and promotes PIF4-activated transcription of itself. Interestingly, SIC is targeted by COP1 for 26S proteasome-mediated degradation in the dark. Collectively, our data demonstrate that light-induced SIC functions as a brake to prevent exaggerated light response via mediating HY5 and PIF4 signaling, and its degradation by COP1 in the dark avoid too strong inhibition on photomorphogenesis at the beginning of light exposure.

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