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COP1 抑制子 4 通过抑制 和 在 中的表达促进幼苗光形态建成。

COP1 SUPPRESSOR 4 promotes seedling photomorphogenesis by repressing and expression in .

机构信息

Institute of Plant and Food Sciences, Department of Biology, Southern University of Science and Technology, 518055 Shenzhen, China.

State Key Laboratory of Crop Genetics and Germplasm Enhancement, College of Agriculture, Nanjing Agricultural University, 210095 Nanjing, China.

出版信息

Proc Natl Acad Sci U S A. 2018 Nov 6;115(45):11631-11636. doi: 10.1073/pnas.1813171115. Epub 2018 Oct 23.

Abstract

CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1) and DE-ETIOLATED 1 (DET1) are founding components of two central repressor complexes of photomorphogenesis that trigger the degradation of a larger number of photomorphogenic-promoting factors in darkness. Here, we identify COP1 SUPPRESSOR 4 (CSU4) as a genetic suppressor of the mutation. Mutations in largely rescued the constitutively photomorphogenic phenotype of and in darkness. Loss of CSU4 function resulted in significantly longer hypocotyl in the light. Further biochemical studies revealed that CSU4 physically interacts with CIRCADIAN CLOCK-ASSOCIATED 1 (CCA1) and negatively regulates its transcriptional repression activity toward its targets. CSU4 represses the expression of in the early morning and of () in the early evening. Our study suggests that CSU4 acts as a negative regulator of CCA1 via physically associating with CCA1, which in turn, likely serves to repress expression of and to promote photomorphogenesis.

摘要

组成型光形态建成 1 型(COP1)和去黄化 1 型(DET1)是两种中央抑制复合物的组成部分,它们在黑暗中触发大量促进光形态建成的因子的降解。在这里,我们确定 COP1 抑制因子 4(CSU4)是 突变的遗传抑制剂。突变在很大程度上挽救了 和 在黑暗中的组成型光形态建成表型。CSU4 功能丧失导致光下下胚轴明显延长。进一步的生化研究表明,CSU4 与昼夜节律时钟相关蛋白 1(CCA1)物理相互作用,并负调控其对靶标的转录抑制活性。CSU4 抑制 在清晨和 ()在傍晚表达。我们的研究表明,CSU4 通过与 CCA1 物理结合来作为 CCA1 的负调节剂,而 CCA1 可能反过来抑制 和 的表达,从而促进光形态建成。

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