Transactivation mechanisms of mouse clock transcription factors, mClock and mArnt3

@article{Takahata2000TransactivationMO,
  title={Transactivation mechanisms of mouse clock transcription factors, mClock and mArnt3},
  author={Shinya Takahata and Tomona Ozaki and Junsei Mimura and Yasuo Kikuchi and Kazuhiro Sogawa and Yoshiaki Fujii‐Kuriyama},
  journal={Genes to Cells},
  year={2000},
  volume={5}
}
The Arnt3 (also termed as BMAL1 or MOP3)/Clock heterodimer is a positive regulator of circadian rhythm and activates the transcription of target genes such as per1 and vasopressin. 
Cryptochrome 1 regulates the circadian clock through dynamic interactions with the BMAL1 C-terminus
TLDR
It is shown that, in mouse fibroblasts, CRY1 competes for binding with coactivators to the intrinsically unstructured C-terminal transactivation domain (TAD) of BMAL1 to establish a functional switch between activation and repression of CLOCK–BMAL1.
Machine Learning Helps Identify CHRONO as a Circadian Clock Component
Two independent studies, one of them using a computational approach, identified CHRONO, a gene shown to modulate the activity of circadian transcription factors and alter circadian behavior in mice.
Mutational scanning identified amino acids of the CLOCK exon 19‐domain essential for circadian rhythms
TLDR
The classical Clock mice, the first circadian mouse mutant discovered, are behaviourally arrhythmic and in this mutant, CLOCK lacks a 51 amino acid domain corresponding to exon 19 (CLOCKΔ19), which is required for normal transactivation.
Modulation Of Circadian Cycling By The C-Terminal Transactivation Domain Of BMAL1
TLDR
It is shown that the unstructured C-terminal transactivation domain (TAD) of BMAL1 is a regulatory hub where transcriptional activators and repressors compete for binding and undergoes significant and differing conformational rearrangements upon binding CBP KIX and CRY CC.
Posttranslational and epigenetic regulation of the CLOCK/BMAL1 complex in the mammalian
TLDR
How the CLOCK and BMAL1 activities are regulated by intracellular distribution, posttranslational modification, and the recruitment of various epigenetic regulators in response to circadian and cellular signaling pathways is reviewed.
Coactivation of the CLOCK–BMAL1 complex by CBP mediates resetting of the circadian clock
TLDR
It is demonstrated that the CREB-binding protein (CBP) plays a key role in rapid activation of the CLOCK–BMAL1 heterodimer that leads to phase resetting of the circadian clock.
The BMAL1 C terminus regulates the circadian transcription feedback loop.
TLDR
A molecular genetic screening assay for mutant circadian clock proteins that is based on real-time circadian rhythm monitoring in cultured fibroblasts suggests that the C-terminal region of BMAL1 is involved in determining the balance between circadian transcriptional activation and suppression.
Cancer/Testis Antigen PASD1 Silences the Circadian Clock.
Vertebrate-like CRYPTOCHROME 2 from monarch regulates circadian transcription via independent repression of CLOCK and BMAL1 activity
TLDR
CRISPR/Cas9-mediated mutagenesis in the monarch butterfly is applied to show that insect CRY2 regulates circadian repression through TAD α-helix–dependent and –independent mechanisms, providing evidence for independent mechanisms of vertebrate-like CRY circadian regulation on the BMAL1 C terminus and the CLK PAS-B domain.
Rhythmic histone acetylation underlies transcription in the mammalian circadian clock
TLDR
It is shown that transcriptional regulation of the core clock mechanism in mouse liver is accompanied by rhythms in H3 histone acetylation, and that H3 acetylations is a potential target of the inhibitory action of Cry.
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TLDR
CLOCK-BMAL1 heterodimers appear to drive the positive component of per transcriptional oscillations, which are thought to underlie circadian rhythmicity.
Role of CBP/P300 in nuclear receptor signalling
TLDR
In vitro and in vivo evidence is provided that identifies the CREB-binding protein (CBP) and its homologue P300 as cofactors mediating nuclear-receptor-activated gene transcription and may serve as integrators of extracellular and intracellular signalling pathways.
Closing the circadian loop: CLOCK-induced transcription of its own inhibitors per and tim.
TLDR
The Drosophila CLOCK protein was shown to induce transcription of the circadian rhythm genes period and timeless, and PERIOD and TIMELESS proteins blocked dCLOCK's ability to transactivate their promoters via the E-box.
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TLDR
The possibility arises that CBP/p300 is extensively involved as a coactivator in the transactivation process by bHLH/PAS heterodimer transcription factors through interaction with Arnt or Arnt2.
Human p300 Protein Is a Coactivator for the Transcription Factor MyoD (*)
TLDR
It is shown that the repression of MyoD-mediated E box (MyoD consensus) reporter activity by E1A is correlated with its interaction with p300, indicating that p300 participates in Myo D-dependent transactivation.
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TLDR
The Arnt homodimer binds the sequence of adenovirus major late promoter (MLP) with the E box core sequence CACGTG, suggesting that the CAC half of the XRE, CACGCN(A/T), recognized by the AhR-Arnt heterodimer is a target for Arnt.
Positional Cloning of the Mouse Circadian Clock Gene
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