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Transcriptional regulation of the Drosophila catalase gene by the DRE/DREF system
Reactive oxygen species (ROS) cause oxidative stress and aging. The catalase gene is a key component of the cellular antioxidant defense network. However, the molecular mechanisms that regulate catalase gene expression are poorly understood. In this study, we have identified a DNA replication‐relate...
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Published in: | Nucleic acids research 2004, Vol.32 (4), p.1318-1324 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | Reactive oxygen species (ROS) cause oxidative stress and aging. The catalase gene is a key component of the cellular antioxidant defense network. However, the molecular mechanisms that regulate catalase gene expression are poorly understood. In this study, we have identified a DNA replication‐related element (DRE; 5′‐TATCGATA) in the 5′‐flanking region of the Drosophila catalase gene. Gel mobility shift assays revealed that a previously identified factor called DREF (DRE‐ binding factor) binds to the DRE sequence in the Drosophila catalase gene. We used site‐directed mutagenesis and in vitro transient transfection assays to establish that expression of the catalase gene is regulated by DREF through the DRE site. To explore the role of DRE/DREF in vivo, we established transgenic flies carrying a catalase–lacZ fusion gene with or without mutation in the DRE. The β‐galactosidase expression patterns of these reporter transgenic lines demonstrated that the catalase gene is upregulated by DREF through the DRE sequence. In addition, we observed suppression of the ectopic DREF‐induced rough eye phenotype by a catalase amorphic Catn1 allele, indicating that DREF activity is modulated by the intracellular redox state. These results indicate that the DRE/DREF system is a key regulator of catalase gene expression and provide evidence of cross‐talk between the DRE/DREF system and the antioxidant defense system. |
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ISSN: | 0305-1048 1362-4962 1362-4962 |
DOI: | 10.1093/nar/gkh302 |