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

作　　者：Tao Li Haojie Li Hongmei Lian Pengyu Song Yulong Wang Jie Duan Zhaoqing Song Yan Cao Dongqing Xu Jigang Li Huiyong Zhang 

机构地区：[1]College of Life Sciences,Henan Agricultural University,Zhengzhou,450002 China [2]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

出　　处：《Journal of Integrative Plant Biology》2022年第9期1706-1723,共18页植物学报（英文版）

基　　金：supported by grants from National Natural Science Foundation of China(31670288);the Talent Support Program of Henan Agricultural University(to H.Z)。

摘　　要：Arabidopsis CONSTITUTIVELY PHOTOMORPHO GENIC1(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 proteasomemediated 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.

关 键 词：ARABIDOPSIS COP1-HY5 module PIF4 PHOTOMORPHOGENESIS SICKLE 

分 类 号：Q945[生物学—植物学]