关键词: Arabidopsis COP1-HY5 module PIF4 SICKLE photomorphogenesis

Mesh : Anemia, Sickle Cell / metabolism Arabidopsis / metabolism Arabidopsis Proteins / genetics metabolism Basic Helix-Loop-Helix Transcription Factors / genetics Basic-Leucine Zipper Transcription Factors / genetics metabolism Gene Expression Regulation, Plant Nuclear Proteins / genetics metabolism Seedlings Ubiquitin-Protein Ligases / genetics metabolism

来  源:   DOI:10.1111/jipb.13329

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.
摘要:
拟南芥的成分光形态发生1(COP1)和植物色素相互作用因子(PIFs)是负调节因子,而矮胖型5(HY5)是幼苗光形态发育的正调节剂。这里,我们报告SICKLE(SIC),富含脯氨酸的蛋白质,充当光形态发生的新型负调节剂。HY5直接结合SIC启动子并响应于光激活SIC表达。反过来,SIC与HY5物理相互作用并干扰其对下游靶基因的转录调节。此外,SIC与PIF4相互作用并促进PIF4激活的自身转录。有趣的是,SIC被COP1靶向用于在黑暗中26S蛋白酶体介导的降解。总的来说,我们的数据表明,光诱导的SIC起到制动作用,通过介导HY5和PIF4信号来防止过度的光响应,在黑暗中COP1的降解避免了在曝光开始时对光形态发生的强烈抑制。
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