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Circadian pacemaking beyond clock genes: Neural network-based coherent oscillation and adaptive phasing by the suprachiamatic nucleus

開催日 2014/9/11
時間 9:00 - 11:00
会場 Room F(302)
Chairperson(s) 本間 さと / Sato Honma (北海道大学大学院医学系研究科 時間医学講座 / Department of Physiol Chronomedicine, Hokkaido University Graduate School of Medicine, Japan)
土居 雅夫 / Masao Doi (京都大学大学院薬学研究科医薬創成情報科学専攻システムバイオロジー分野 / Department of Systems Biology, Graduate School of Pharmaceutical Sciences, Kyoto University, Japan)

Effect of MeCP2 on Molecular Clock Development in the SCN

  • S1-F-1-2
  • 八木田 和弘 / Kazuhiro Yagita:1 
  • 1:京都府立医科大学医学研究科 / Dept. of Physiology and Systems Bioscience, Kyoto Prefectural University of Medicine, Japan 

The circadian clock in mammalian cells is cell-autonomously generated during the cellular differentiation process, but the underlying mechanisms are not fully understood. To understand the role of the epigenetic regulation and transcriptional program on the circadian clock development in mammalian cells, we investigated the differentiation-coupled clock development using genetically modified mouse embryonic stem cell (ESC) models. Our established in vitro circadian clock formation assay clearly shows that the programmed DNA Methylation during the cellular differentiation is essential for circadian clock development. DNA methylation around the promoter region in turn suppresses the gene expression via recruitment of co-suppressor complex with methyl-DNA binding proteins such as methyl-CpG binding protein 2 (MeCP2). MeCP2 is known as a responsible gene of Rett Syndrome, which is one of the developmental disorders often accompanied with sleep disorder. Therefore, here we investigated the effect of MeCP2 deficiency on circadian molecular clock in mPER2::Luc knock-in mouse suprachiasmatic nucleus (SCN) by using CRISPR/Cas9-based genome engineering strategy. Although circadian molecular clock oscillation is observed in MeCP2 deficient mice SCN, our findings suggest that MeCP2 plays a distinct role in the SCN.

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