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E2F2 and CREB cooperatively regulate transcriptional activity of cell cycle genes
Usua Laresgoiti1, Aintzane Apraiz, Miguel Olea
1Department of Genetics, Physical Anthropology and Animal Physiology, University of the Basque Country, UPV/EHU, Bilbao 48940, Spain and Department of Biochemistry and Molecular Biology, University of the Basque Country, UPV/EHU, Bilbao 48940, Spain.
Nucleic Acids Research
|September 17, 2013
Summary
The transcription factor E2F2 maintains T lymphocyte quiescence by silencing genes involved in DNA metabolism and cell cycle regulation. E2F2 cooperates with CREB to repress specific target genes, revealing a novel regulatory mechanism.
Area of Science:
- Molecular Biology
- Immunology
- Transcriptional Regulation
Background:
- E2F2 is crucial for maintaining T lymphocyte quiescence.
- Understanding E2F2's role in transcriptional regulation is essential.
Purpose of the Study:
- To identify all E2F2 target genes in T lymphocytes.
- To elucidate the mechanism of E2F2-mediated transcriptional control.
Main Methods:
- ChIP-chip analysis in lymph node-derived T lymphocytes.
- Gene expression profiling of E2F2-deficient T lymphocytes.
- Luciferase reporter assays and siRNA-mediated gene knockdown.
Main Results:
- E2F2 binds promoters of DNA metabolism and cell cycle genes during quiescence, leading to silencing.
- 51 E2F2-specific target genes were identified, mostly upregulated upon E2F2 loss.
- E2F2 represses target genes independently of retinoblastoma protein.
- CREB contributes to E2F2-mediated repression of Mcm5 and Chk1 promoters.
Conclusions:
- E2F2 plays a significant role in negative transcriptional regulation of T lymphocyte genes.
- E2F2 and CREB collaborate to repress a subset of E2F2 target genes.
- This study uncovers a novel cooperative regulatory mechanism in E2F-mediated transcriptional control.
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