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CDK9 modulates circadian clock by attenuating REV-ERBα activity.

Jiali Ou1, Huilin Li1, Peiyuan Qiu2

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Cyclin-dependent kinase 9 (CDK9) modulates the circadian clock by regulating Bmal1 expression. This discovery offers new insights into circadian clock regulation and related diseases like cancer.

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Area of Science:

  • Molecular Biology
  • Chronobiology
  • Cellular Biology

Background:

  • The circadian clock and cell cycle are crucial, time-regulated cellular processes.
  • These two oscillators are interconnected to regulate biological functions.

Purpose of the Study:

  • To investigate the role of Cyclin-dependent kinase 9 (CDK9) in modulating the circadian clock.
  • To identify potential therapeutic targets for circadian and cell cycle-related disorders.

Main Methods:

  • Screening of CDK inhibitors to identify modulators of circadian clock gene expression (PER2:LUC).
  • Utilizing siRNA to confirm CDK9 as the effector of inhibitor LY2857785.
  • Investigating the interaction between CDK9 and REV-ERBα.
  • Performing in vivo studies by knocking down CDK9 in mice.

Main Results:

  • CDK inhibitor LY2857785 was identified to block PER2:LUC expression, with CDK9 confirmed as the primary target.
  • CDK9 knockdown or LY2857785 treatment resulted in decreased Bmal1 and increased Rev-Erbα expression.
  • CDK9 was found to associate with REV-ERBα, inhibiting its binding to RORE and suppressing Bmal1.
  • In vivo CDK9 knockdown in mice altered respiratory exchange ratio, daily activity, and circadian period.

Conclusions:

  • CDK9 acts as a novel modulator of the circadian clock.
  • CDK9's role in circadian regulation provides a potential basis for understanding and treating diseases involving circadian and cell cycle dysregulation, such as cancer.