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Brain-specific deletion of histone variant H2A.z results in cortical neurogenesis defects and neurodevelopmental disorder

ABSTRACT: ChIP experiment was performed with antibody against H3K36me3 (active motif; 61101). we generated genome-wide characterization of H3K36me3 occupancy in E13 H2A.Z cKO forebrain. We found H3K36me3 is decreased throughout the whole genome in E13 H2A.Z cKO forebrain.

ORGANISM(S): Mus musculus

PROVIDER: GSE106679 | GEO | 2017/11/09

SECONDARY ACCESSION(S): PRJNA417668

REPOSITORIES: GEO

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Brain-specific deletion of histone variant H2A.z results in cortical neurogenesis defects and neurodevelopmental disorder.

Project description:Defects in neurogenesis alter brain circuit formations and may lead to neurodevelopmental disorders such as autism and schizophrenia. Histone H2A.z, a variant of histone H2A, plays critical roles in chromatin structure and epigenetic regulation, but its function and mechanism in brain development remain largely unknown. Here, we find that the deletion of H2A.z results in enhanced proliferation of neural progenitors but reduced neuronal differentiation. In addition, neurons in H2A.z knockout mice exhibit abnormal dendrites during brain development. Furthermore, H2A.zcKO mice exhibit serial behavioral deficits, such as decreased exploratory activity and impaired learning and memory. Mechanistically, H2A.z regulates embryonic neurogenesis by targeting Nkx2-4 through interaction with Setd2, thereby promoting H3K36me3 modification to activate the transcription of Nkx2-4. Furthermore, enforced expression of Nkx2-4 can rescue the defective neurogenesis in the H2A.z-knockdown embryonic brain. Together, our findings implicate the epigenetic regulation by H2A.z in embryonic neurogenesis and provide a framework for understanding how disruption in the H2A.z gene may contribute to neurological disorders.

| S-EPMC5861433 | biostudies-literature

Brain-specific deletion of histone variant H2A.z results in cortical neurogenesis defects and neurodevelopmental disorder

Project description:Brain-specific deletion of histone variant H2A.z results in cortical neurogenesis defects and neurodevelopmental disorder

| PRJNA417668 | ENA

ChIP-seq of H2A H2A.Z H2A.W H3 in Col-0, h2a, h2a.z, and h2a.w; ChIP-seq of H3K36me3 H3K9me2 in Col-0

Project description:ChIP-seq of H2A H2A.Z H2A.W H3 in Col-0, h2a, h2a.z, and h2a.w; ChIP-seq of H3K36me3 H3K9me2 in Col-0

2025-04-11 | GSE283046 | GEO

Expression data from H2A.Z-1 and H2A.Z-2 double KO cells

Project description:The histone variant H2A.Z is evolutionarily conserved from yeast to vertebrates. H2A.Z regulates gene expression when localized to promoter region. Recently, we identified two genes encoding H2A.Z, H2A.Z-1 and H2A.Z-2 in vertebrate genome. However, it is not clear that both H2A.Z-1 and H2A.Z-2 were required for the function of H2A.Z in gene regulation. To address this issue, we generated the H2A.Z-1 and H2A.Z-2 double knock out (KO) cells in chicken DT40 cells. The expression pattern of H2A.Z-1 and H2A.Z-2 double KO cells was compared with WT cells to characterize the genes regulated by H2A.Z-1 and H2A.Z-2. We used microarrays to analysis the alternation of gene expression between WT and H2A.Z double KO cells and identify classes of up or down regulated gene by H2A.Z-1 and H2A.Z-2. In H2A.Z-1 and H2A.Z-2 double KO cells, H2A.Z-2 is knocked out constitutively, but H2A.Z-1 conditionally by tetracycline. The expression of H2A.Z-1 transgene is suppressed completely when H2A.Z-1 and H2A.Z-2 double KO cells culture with tetracycline for three days. For this reason, we prepared the total RNA of WT cells and H2A.Z-1and H2A.Z-2 double KO cells treated with tetracycline for three days and hybridization on Affymetrix microarrays.

2015-11-04 | E-GEOD-35430 | biostudies-arrayexpress

H2A.Z regulates zygotic genome activation

Project description:Affinity Purification Mass Spectrometry (AP-MS) of Drosophila ovaries expressing an H2A.Z-FlagHA transgene to identify interacting partners of H2A.Z to elucidate potential maternally supplied histone chaperones that deposit H2A.Z on the transcription start site (TSS).

2022-02-15 | PXD029061 | Pride

H2A.Z regulates transcription, oocyte maturation and female fertility in mouse [RNA-seq]

Project description:Histone variants differ from canonical histones in their ability to be incorporated into chromatin independently of S-phase. H2A.Z is an evolutionarily conserved histone variant that plays critical roles in transcription regulation. However, its roles during mammalian oogenesis, a unique developmental stage marked by dynamic transcription activity without DNA replication, remain elusive. In this study, we demonstrated that oocyte-specific depletion of H2A.Z results in profound epigenetic and transcriptional alterations, impeding oocyte meiosis II resumption in mice, causing female infertility. Mechanistically, H2A.Z in mouse oocytes is enriched at active promoters and enhancers. Interestingly, H2A.Z is depleted from CG-rich silenced promoters in fully-grown oocytes (FGOs), unlike that in growing oocytes, early embryos and mESCs. In FGOs, the presence of H2A.Z correlates with H3K27ac, except in regions with DNA methylation and H3K36me3. Depletion of H2A.Z leads to partial loss of H3K27ac at both promoters and enhancers, correlated with impaired gene expression. Consistent with a role in gene activation, H2A.Z in FGOs is widely acetylated at the promoters and enhancers. Together, our findings uncover an essential role of H2A.Z in oocyte maturation and activation of cis-regulatory elements.

2025-04-23 | GSE263819 | GEO

H2A.Z regulates transcription, oocyte maturation and female fertility in mouse [ChIP-seq]

2025-04-23 | GSE263818 | GEO

Expression data from H2A.Z-1 and H2A.Z-2 double KO cells

2015-11-04 | GSE35430 | GEO

Identification of PWWP2A interactors using label-free quantitative affinity enrichment mass spectrometry

Project description:Chromatin structure and function is regulated by reader proteins recognizing histone modifications and/or histone variants. We recently identified PWWP2A, which tightly binds to H2A.Z-containing nucleosomes and is involved in mitotic progression and cranial-facial development. Here, using in vitro assays we show that distinct domains of PWWP2A moreover mediate binding to free linker DNA as well as H3K36me3 nucleosomes. In vivo, PWWP2A strongly recognizes H2A.Z-containing regulatory regions and weakly H3K36me3-containing gene bodies. Additionally, PWWP2A bind to an MTA1-specific core NuRD (M1HR) complex solely consisting of MTA1, HDAC1 and RBBP4/7, excluding CHD and MBD proteins. Depletion of PWWP2A leads to an increase of acetylation levels on H3K27 as well as H2A.Z, presumably by impaired chromatin recruitment of M1HR. Thus, this study identifies PWWP2A as an ever more complex chromatin binding protein serving as adapter for M1HR to H2A.Z-containing chromatin, thereby promoting changes in histone acetylation levels and likely fine-tuning the transcriptional balance.

2018-08-27 | PXD010424 | Pride

Replacement of Arabidopsis H2A.Z with human H2A.Z orthologs reveals extensive functional conservation and limited importance of the N-terminal tail sequence for Arabidopsis development (WT, h2a.z, h2a.z + AtHTA11 RNA-Seq)

Project description:To investigate the functional conservation of H2A.Z histones during eukaryotic evolution we transformed h2a.z deficient plants with three human H2A.Z proteins to assess their ability to rescue the mutant defects. We discovered that human H2A.Z.1 and H2A.Z.2.1 fully complement the phenotypic abnormalities of h2a.z plants even though Arabidopsis and human H2A.Z N-terminal tail sequences are divergent, while the brain-specific splice variant H2A.Z.2.2 has a dominant-negative effect in wild-type plants. Furthermore, H2A.Z.1 almost completely re-establishes normal H2A.Z chromatin occupancy in h2a.z plants and restores the expression of more than 84 % of misexpressed genes. Finally, our hypothesis that the N-terminal tail of Arabidopsis H2A.Z is not crucial for its overall function was supported by the ability of N-terminal end truncations of Arabidopsis HTA11 to largely rescue the defects of h2a.z mutants.

2024-05-13 | GSE263310 | GEO

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