Functional Role of CREB-Binding Protein in the Circadian Clock System of Drosophila melanogaster
| Autor: | Eunjin Doh, Joonho Choe, Changtaek Choi, Juwon Kim, Jongbin Lee, Chunghun Lim |
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| Rok vydání: | 2007 |
| Předmět: |
Transcription
Genetic Timeless Circadian clock Genes Insect Motor Activity Biology Biological Clocks Coactivator Basic Helix-Loop-Helix Transcription Factors Locomotor rhythm Animals Drosophila Proteins CREB-binding protein Molecular Biology Neurons Behavior Animal ARNTL Transcription Factors Articles Cell Biology Histone acetyltransferase CREB-Binding Protein Molecular biology Circadian Rhythm CLOCK Drosophila melanogaster Mutagenesis Larva Mutation biology.protein Histone deacetylase activity Protein Binding |
| Zdroj: | Molecular and Cellular Biology. 27:4876-4890 |
| ISSN: | 1098-5549 |
| DOI: | 10.1128/mcb.02155-06 |
| Popis: | Rhythmic histone acetylation underlies the oscillating expression of clock genes in the mammalian circadian clock system. Cellular factors that contain histone acetyltransferase and histone deacetylase activity have been implicated in these processes by direct interactions with clock genes, but their functional relevance remains to be assessed by use of appropriate animal models. Here, using transgenic fly models, we show that CREB-binding protein (CBP) participates in the transcriptional regulation of the Drosophila CLOCK/CYCLE (dCLK/CYC) heterodimer. CBP knockdown in pigment dispersing factor-expressing cells lengthens the period of adult locomotor rhythm with the prolonged expression of period and timeless genes, while CBP overexpression in timeless-expressing cells causes arrhythmic circadian behaviors with the impaired expression of these dCLK/CYC-induced clock genes. In contrast to the mammalian circadian clock system, CBP overexpression attenuates the transcriptional activity of the dCLK/CYC heterodimer in cultured cells, possibly by targeting the PER-ARNT-SIM domain of dCLK. Our data suggest that the Drosophila circadian clock system has evolved a distinct mechanism to tightly regulate the robust transcriptional potency of the dCLK/CYC heterodimer. |
| Databáze: | OpenAIRE |
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