English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Acetylation of BMAL1 by TIP60 controls BRD4-P-TEFb recruitment to circadian promoters.

MPS-Authors
/persons/resource/persons239770

Petkau,  N.
Department of Genes and Behavior, MPI for biophysical chemistry, Max Planck Society;

/persons/resource/persons15030

Eichele,  G.
Department of Genes and Behavior, MPI for biophysical chemistry, Max Planck Society;

Locator
There are no locators available
Fulltext (public)

3136041.pdf
(Publisher version), 5MB

Supplementary Material (public)
There is no public supplementary material available
Citation

Petkau, N., Budak, H., Zhou, X., Oster, H., & Eichele, G. (2019). Acetylation of BMAL1 by TIP60 controls BRD4-P-TEFb recruitment to circadian promoters. eLife, 8: e43235. doi:10.7554/eLife.43235.


Cite as: http://hdl.handle.net/21.11116/0000-0004-4278-B
Abstract
Many physiological processes exhibit circadian rhythms driven by cellular clocks composed of interlinked activating and repressing elements. To investigate temporal regulation in this molecular oscillator, we combined mouse genetic approaches and analyses of interactions of key circadian proteins with each other and with clock gene promoters. We show that transcriptional activators control BRD4-PTEFb recruitment to E-box-containing circadian promoters. During the activating phase of the circadian cycle, the lysine acetyltransferase TIP60 acetylates the transcriptional activator BMAL1 leading to recruitment of BRD4 and the pause release factor P-TEFb, followed by productive elongation of circadian transcripts. We propose that the control of BRD4-P-TEFb recruitment is a novel temporal checkpoint in the circadian clock cycle.