Dissection of the ADR1 protein reveals multiple, functionally redundant activation domains interspersed with inhibitory regions: evidence for a repressor binding to the ADR1c region
| Autor: | Dan Chase, Clyde L. Denis, Deborah C. Audino, W J Cook |
|---|---|
| Rok vydání: | 1994 |
| Předmět: |
Glycerol
Saccharomyces cerevisiae Proteins Recombinant Fusion Proteins Genes Fungal Molecular Sequence Data Repressor Saccharomyces cerevisiae Biology Models Biological DNA-binding protein Fungal Proteins Transactivation Transcription (biology) Gene Expression Regulation Fungal DNA Fungal Promoter Regions Genetic Molecular Biology Gene Transcription factor Sequence Deletion Zinc finger Base Sequence Alcohol Dehydrogenase Zinc Fingers Cell Biology Molecular biology Cell biology DNA-Binding Proteins Repressor Proteins Regulatory sequence Trans-Activators Transcription Factors Research Article |
| Zdroj: | Molecular and Cellular Biology. 14:629-640 |
| ISSN: | 1098-5549 |
| DOI: | 10.1128/mcb.14.1.629-640.1994 |
| Popis: | The yeast transcriptional activator ADR1 is required for expression of the glucose-repressible alcohol dehydrogenase gene (ADH2), as well as genes involved in glycerol metabolism. The N-terminal half of the ADR1 protein was shown to contain three separate transactivation domains, including one (TADI) that encompasses the zinc finger DNA-binding domain. While TADII and TADIII were shown to be functionally redundant in activating ADH2 expression, deletion of only TADIII impaired ADR1 control of glycerol metabolism genes. None of these activation domains appeared to be carbon source regulated when separated from the ADH2 promoter context. Interspersed among these activation domains were two regions which, when removed, increased ADR1 activity; one was localized to the site of ADR1c mutations (residues 227 to 239) that allow glucose-insensitive ADH2 expression. The 227-to-239 region blocked ADR1 activity independently of the TAD present on ADR1, ADR1 DNA binding, and specific ADH2 promoter sequences. In addition, this region inhibited the function of a heterologous transcriptional activator. These results are consistent with the existence of an extragenic factor that binds the ADR1c region and represses ADR1 activity and suggest that other factors are responsible for aiding ADR1 in the carbon source regulation of ADH2. |
| Databáze: | OpenAIRE |
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