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Mammalian PERIOD2 regulates H2A.Z incorporation into chromatin to orchestrate circadian negative feedback [Mnase-Seq]

ABSTRACT: We report the interdependance of PERIOD and H2A.Z to orchestrated the circadian negative feedback. H2A.Z is required for the circadian rhythm, it allows the binding of Bmal1 and PERIOD2 to the chromatin. And reciprocally, PERIOD2 aid H2A.Z deposition by interacting with the specific chaperone YL1.

ORGANISM(S): Mus musculus

PROVIDER: GSE153936 | GEO | 2022/02/17

REPOSITORIES: GEO

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Mammalian PERIOD2 regulates H2A.Z incorporation into chromatin to orchestrate circadian negative feedback [Mnase-seq]

Project description:We report the interdependance of PERIOD and H2A.Z to orchestrated the circadian negative feedback. H2A.Z is required for the circadian rhythm, it allows the binding of Bmal1 and PERIOD2 to the chromatin. And reciprocally, PERIOD2 aid H2A.Z deposition by interacting with the specific chaperone YL1.

2022-02-17 | GSE190862 | GEO

Mammalian PERIOD2 regulates H2A.Z incorporation into chromatin to orchestrate circadian negative feedback [RNA-Seq]

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Mammalian PERIOD2 regulates H2A.Z incorporation into chromatin to orchestrate circadian negative feedback [Mnase-seq]

Project description:Mammalian PERIOD2 regulates H2A.Z incorporation into chromatin to orchestrate circadian negative feedback [Mnase-seq]

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Mammalian PERIOD2 regulates H2A.Z incorporation into chromatin to orchestrate circadian negative feedback [Mnase-Seq]

Project description:Mammalian PERIOD2 regulates H2A.Z incorporation into chromatin to orchestrate circadian negative feedback [Mnase-Seq]

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Mammalian PERIOD2 regulates H2A.Z incorporation into chromatin to orchestrate circadian negative feedback

Project description:Mammalian PERIOD2 regulates H2A.Z incorporation into chromatin to orchestrate circadian negative feedback

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Mammalian PERIOD2 regulates H2A.Z incorporation into chromatin to orchestrate circadian negative feedback [RNA-Seq]

Project description:Mammalian PERIOD2 regulates H2A.Z incorporation into chromatin to orchestrate circadian negative feedback [RNA-Seq]

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CLK:BMAL1 is a pioneer-like transcription factor [MNase-Seq]

Project description:The mammalian circadian clock relies on the master genes CLOCK (CLK) and BMAL1 and drives rhythmic gene expression to regulate biological functions under circadian control. We recently uncovered a surprising disconnect between the rhythmic binding of CLK:BMAL1 on DNA and the transcription of its target genes, suggesting that they are regulated by as yet uncharacterized mechanisms. Here we show that rhythmic CLK:BMAL1 DNA binding promotes rhythmic chromatin opening. The underlying mechanisms include CLK:BMAL1 binding to nucleosomes and rhythmic chromatin modifications, including the incorporation of the histone variant H2A.Z. This rhythmic chromatin remodeling mediates the rhythmic binding of other transcription factors adjacent to CLK:BMAL1, suggesting that the activity and the tissue-specific expression of these other transcription factors contribute to the genome-wide CLK:BMAL1 heterogeneous transcriptional output. These data therefore indicate that the clock regulation of transcription relies on the rhythmic regulation of chromatin accessibility and suggest that the concept of pioneer function extends to acute gene regulation, well beyond the current confines of developmental/cell specification. Mouse liver nucleosome profile assayed by MNase-Seq over 6 time points of the 24h light:dark cycle (4 wild-type and 4 Bmal1-/- mice per time point). Illumina libraries containing a mononucleosome insert were sequenced using Ilumina HiSeq2000.

2014-01-06 | E-GEOD-47142 | biostudies-arrayexpress

CLK:BMAL1 is a pioneer-like transcription factor [MNase-Seq]

2014-01-06 | GSE47142 | GEO

The Circadian Clock Gene Bmal1 Controls Thyroid Hormone-Mediated Spectral Identity and Cone Photoreceptor Function

Project description:Here we reveal a novel role for the circadian clock gene Bmal1 and Period2 in regulating the spatial organization of the cone opsins. Deletion of Bmal1 and Per2 have opposing effects on S-opsin expression and patterning of the cone photoreceptors is disrupted in cone specific knockouts of these genes. Using ChIP analysis we show that BMAL1 directly binds to the promoter region of the thyroid activating enzyme type II deiodinase (Dio2).

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H2A.Z chaperones promote melanoma cell growth by facilitating transcription of E2F target genes through H2A.Z deposition and H4 acetylation

Project description:High levels of the histone variant H2A.Z are characteristic for melanoma progression and correlate with poor prognosis of melanoma patients. Two chaperone complexes are reported to deposit H2A.Z isoforms into chromatin: SRCAP and P400-TIP60. YL1 is a common subunit of both complexes and directly binds to the H2A.Z-H2B dimer. Here, we showed that the knockdown of SRCAP (SRCAP-specific), P400 (P400-TIP60-specific) and YL1 (shared subunit) results in loss of H2A.Z deposition into chromatin in melanoma cells, confirming them as H2A.Z chaperone subunits in this system. Further, we demonstrated that H2A.Z, YL1 and the SRCAP-specific subunit ZNHIT1 co-localize at active promoters of cell cycle-related genes, such as the transcription factor E2F1. Knockdown of YL1, SRCAP and P400 downregulates E2F1 and its targets, resulting in a loss of proliferation and cell cycle arrest in melanoma cells as seen after knockdown of H2A.Z (Vardabasso et al. 2015). Strikingly, besides H2A.Z loss, we observed a dramatic loss of H4 acetylation in melanoma chromatin upon knockdown of H2A.Z chaperone subunits. The majority of genes whose promoters showed a reduction in H4 acetylation were previously bound by H2A.Z, YL1 and ZNHIT1. This is suggestive of a direct link between H2A.Z deposition and H4 acetylation to promote the expression of underlying genes. In agreement, the genes that lost H4 acetylation were enriched for E2F1 target genes. Interestingly, we additionally found that knockdown of YL1 did not only prohibit cell cycle progression, but also induces apoptosis, which is in contrast to H2A.Z knockdown affecting cell cycle only. In addition, YL1 (but not SRCAP or P400) was found to be overexpressed in melanoma and high YL1 levels were a predictor of poor melanoma patient outcome. These findings provide a rationale for targeting the H2A.Z-YL1 interaction as novel epigenetic strategy for melanoma treatment.

2024-05-10 | GSE242227 | GEO

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