BZS1, a B-box Protein, Promotes Photomorphogenesis Downstream of Both Brassinosteroid and Light Signaling Pathways
文献类型: 外文期刊
作者: Fan, Xi-Ying 2 ; Sun, Yu 3 ; Cao, Dong-Mei 2 ; Bai, Ming-Yi 1 ; Luo, Xiao-Min 2 ; Yang, Hong-Juan 2 ; Wei, Chuang-Qi 3 ;
作者机构: 1.Carnegie Inst Sci, Dept Plant Biol, Stanford, CA 94305 USA
2.Chinese Acad Sci, Inst Bot, Beijing 100093, Peoples R China
3.Hebei Normal Univ, Coll Life Sci, Inst Mol Cell Biol, Shijiazhuang 050016, Hebei, Peoples R China
4.Shanxi Acad Agr Sci, Inst Hort, Shanxi 030031, Peoples R China
5.Chinese Acad Sci, Grad Sch, Beijing 100049, Peoples R China
关键词: photomorphogenesis;light signaling;Brassinosteroid;BZS1;Arabidopsis
期刊名称:MOLECULAR PLANT ( 影响因子:13.164; 五年影响因子:16.357 )
ISSN: 1674-2052
年卷期: 2012 年 5 卷 3 期
页码:
收录情况: SCI
摘要: Photomorphogenesis is controlled by multiple signaling pathways, including the light and brassinosteroid (BR) pathways. BR signaling activates the BZR1 transcription factor, which is required for suppressing photomorphogenesis in the dark. We identified a suppressor of the BR hypersensitive mutant bzr1-1D and named it bzr1-1D suppressor1-Dominant (bzs1-D). The bzs1-D mutation was caused by overexpression of a B-box zinc finger protein BZS1, which is transcriptionally repressed by BZR1. Overexpression of BZS1 causes de-etiolation in the dark, short hypocotyls in the light, reduced sensitivity to BR treatment, and repression of many BR-activated genes. Knockdown of BZS1 by co-suppression partly suppressed the short hypocotyl phenotypes of BR-deficient or insensitive mutants. These results support that BZS1 is a negative regulator of BR response. BZS1 overexpressors are hypersensitive to different wavelengths of light and loss of function of BZS1 reduces plant sensitivity to light and partly suppresses the constitutive photomorphogenesis 1 (cop1) mutant in the dark, suggesting a positive role in light response. BZS1 protein accumulates at an increased level after light treatment of dark-grown BZS1-OX plants and in the cop1 mutants, and BZS1 interacts with COP1 in vitro, suggesting that light regulates BZS1 through COP1-mediated ubiquitination and proteasomal degradation. These results demonstrate that BZS1 mediates the crosstalk between BR and light pathways.
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