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MYC/MIZ1-dependent gene repression inversely coordinates the circadian clock with cell cycle and proliferation

Author

Listed:
  • Anton Shostak

    (Heidelberg University, Biochemistry Center)

  • Bianca Ruppert

    (Heidelberg University, Biochemistry Center)

  • Nati Ha

    (Heidelberg University, Biochemistry Center)

  • Philipp Bruns

    (German Cancer Research Center (DKFZ))

  • Umut H. Toprak

    (German Cancer Research Center (DKFZ))

  • Roland Eils

    (German Cancer Research Center (DKFZ)
    Institute for Pharmacy and Molecular Biotechnology (IPMB) and BioQuant, Heidelberg University)

  • Matthias Schlesner

    (German Cancer Research Center (DKFZ))

  • Axel Diernfellner

    (Heidelberg University, Biochemistry Center)

  • Michael Brunner

    (Heidelberg University, Biochemistry Center)

Abstract

The circadian clock and the cell cycle are major cellular systems that organize global physiology in temporal fashion. It seems conceivable that the potentially conflicting programs are coordinated. We show here that overexpression of MYC in U2OS cells attenuates the clock and conversely promotes cell proliferation while downregulation of MYC strengthens the clock and reduces proliferation. Inhibition of the circadian clock is crucially dependent on the formation of repressive complexes of MYC with MIZ1 and subsequent downregulation of the core clock genes BMAL1 (ARNTL), CLOCK and NPAS2. We show furthermore that BMAL1 expression levels correlate inversely with MYC levels in 102 human lymphomas. Our data suggest that MYC acts as a master coordinator that inversely modulates the impact of cell cycle and circadian clock on gene expression.

Suggested Citation

  • Anton Shostak & Bianca Ruppert & Nati Ha & Philipp Bruns & Umut H. Toprak & Roland Eils & Matthias Schlesner & Axel Diernfellner & Michael Brunner, 2016. "MYC/MIZ1-dependent gene repression inversely coordinates the circadian clock with cell cycle and proliferation," Nature Communications, Nature, vol. 7(1), pages 1-11, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11807
    DOI: 10.1038/ncomms11807
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