DEC2-E4BP4 heterodimer represses the transcriptional enhancer activity of the EE element in the Per2 promoter

Shintaro Tanoue, Katsumi Fujimoto, Jihwan Myung, Fumiyuki Hatanaka, Yukio Kato, Toru Takumi

研究成果: 雜誌貢獻文章同行評審

5 引文 斯高帕斯(Scopus)

摘要

The circadian oscillation of clock gene expression in mammals is based on the interconnected transcriptional/translational feedback loops of Period (Per) and Bmal1. The Per feedback loop initiates transcription through direct binding of the BMAL1-CLOCK (NPAS2) heterodimer to the E-box of the Per2 promoter region. Negative feedback of PER protein on this promoter subsequently represses transcription. Other circadian transcription regulators, particularly E4BP4 and DEC2, regulate the amplitude and phase of Per2 expression rhythms. Moreover, a direct repeat of E-box-like (EE) elements in the Per2 promoter is required for its cell-autonomous circadian rhythm. However, the detailed mechanism for repression of the two core sequences of the EE element in the Per2 promoter region is unknown. Here, we show that E4BP4 binds to the Per2 EE element with DEC2 to repress transcription and identify the DEC2-E4BP4 heterodimer as a key repressor of the tightly interlocked Per2 feedback loop in the mammalian circadian oscillator. Our results suggest an additional modulatory mechanism for tuning of the phase of cell-autonomous Per2 gene expression cycling.
原文英語
文章編號166
期刊Frontiers in Neurology
6
發行號JUL
DOIs
出版狀態已發佈 - 1月 1 2015
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ASJC Scopus subject areas

  • 神經內科
  • 神經病學(臨床)

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