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Mammalian PERIOD2 regulates H2A.Z incorporation into chromatin to orchestrate circadian negative feedback [RNA-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: GSE153937 | 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.

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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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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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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.

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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

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-02-17 | GSE153939 | GEO

ChIP-seq of H2A.Z and its histone chaperones during the cell cycle

Project description:The aim of this study was to uncover cell cycle dependent chromatin binding of H2A.Z and its histone chaperones. U2OS cells were stably transfected with Twin-Strep-tagged H2A.Z, ANP32e, or YL1 constructs, and WT cells were used as a negative/background control. U2OS cells were synchronised in G1 or G2-M phase using hydroxyurea or nocodazole, respectively, and protein-DNA complexes were isolated by affinity purification.

2023-06-29 | E-MTAB-11617 | biostudies-arrayexpress

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