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Genomic Evidence for COP1 as a Repressor of Light-Regulated Gene Expression and Development in Arabidopsis

Microarray gene expression profiling was used to examine the role of COP1 in the light control of Arabidopsis genome expression. Qualitatively similar gene expression profiles were observed between wild-type seedlings grown in white light and multiple cop1 mutant alleles grown in the dark. Furthermo...

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Bibliographic Details
Published in:The Plant cell 2002-10, Vol.14 (10), p.2383-2398
Main Authors: Ma, Ligeng, Gao, Ying, Qu, Lijia, Chen, Zhangliang, Li, Jinming, Zhao, Hongyu, Deng, Xing Wang
Format: Article
Language:English
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Summary:Microarray gene expression profiling was used to examine the role of COP1 in the light control of Arabidopsis genome expression. Qualitatively similar gene expression profiles were observed between wild-type seedlings grown in white light and multiple cop1 mutant alleles grown in the dark. Furthermore, overexpression of the dominant-negative-acting N terminus of COP1 (N282) in darkness produced a genome expression profile similar to those produced by white light and the cop1 mutations. Different cop1 mutant alleles, N282, and light treatment also resulted in distinct expression profiles in a small fraction of the genes examined. In the light, the genome expression of cop1 mutations displayed an exaggerated light response. COP1-regulated genes in the dark were estimated to account for >20% of the genome. Analysis of these COP1-regulated genes revealed that >28 cellular pathways are coordinately but antagonistically regulated by light and COP1. Interestingly, the gene expression regulation attributable to HY5 in the light is included largely within those genes regulated by COP1 in the dark. Thus, this genomic study supports the hypothesis that COP1 acts as a repressor of photomorphogenesis, possibly by controlling the degradation of transcription factors and their target gene expression. The majority of light-controlled genome expression could be accounted for by the negative regulation of COP1 activity.
ISSN:1040-4651
1532-298X
1532-298X
DOI:10.1105/tpc.004416