Histone variant H2A.Z regulates zygotic genome activation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA678804 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13070800_1.fastq.gz | Fastqsanger.gz | |||
| SRR13070800_2.fastq.gz | Fastqsanger.gz | |||
| SRR13070801_1.fastq.gz | Fastqsanger.gz | |||
| SRR13070801_2.fastq.gz | Fastqsanger.gz | |||
| SRR13070802_1.fastq.gz | Fastqsanger.gz |
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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
Project description:During embryogenesis, the genome shifts from transcriptionally quiescent to extensively active in a process known as Zygotic Genome Activation (ZGA). In Drosophila, the pioneer factor Zelda is known to be essential for the progression of development; still, it regulates the activation of only a small subset of genes at ZGA. However, thousands of genes do not require Zelda, suggesting that other mechanisms exist. By conducting GRO-seq, HiC and ChIP-seq in Drosophila embryos, we demonstrate that up to 65% of zygotically activated genes are enriched for the histone variant H2A.Z. H2A.Z enrichment precedes ZGA and RNA Polymerase II loading onto chromatin. In vivo knockdown of maternally contributed Domino, a histone chaperone and ATPase, reduces H2A.Z deposition at transcription start sites, causes global downregulation of housekeeping genes at ZGA, and compromises the establishment of the 3D chromatin structure. We infer that H2A.Z is essential for the de novo establishment of transcriptional programs during ZGA via chromatin reorganization.
| S-EPMC8636486 | biostudies-literature
Project description:Early embryos undergo extensive epigenetic reprogramming to achieve gamete-to-embryo transition, which involves the loading and removal of histone variant H2A.Z on chromatin. Although the H2A.Z landscapes in sperm have been investigated, its dynamics during early development remain unrevealed. Here, by using ultra-low-input native chromatin immunoprecipitation and sequencing (ULI-NChIP-seq), we map the genome-wide distribution of H2A.Z in mouse oocytes and early embryos. We find that paternal H2A.Z is removed upon fertilization, followed by unbiased accumulation on parental genomes during zygotic genome activation (ZGA). More importantly, H2A.Z exhibits hierarchical accumulation as different peak types at promoters. We identify that double H2A.Z peaks co-localizes with H3K4me3 and facilitates transcriptional activation, bivalent markers (H3K4me3+H3K27me3) prefer to occupy single H2A.Z peak and inhibits developmental gene expression, while promoters with no H2A.Z accumulation exhibit gene silencing in early embryos. Remarkably, H2A.Z depletion changes the enrichments of histone modifications and RNA polymerase II (Pol II) binding at promoters, resulting in abnormal gene expression and developmental arrest during lineage commitment. Hence, H2A.Z plays dual roles in regulating the epigenomes required for proper gene expression during preimplantation development.
2022-06-24 | GSE188589 | GEO
Project description:Early embryos undergo extensive epigenetic reprogramming to achieve gamete-to-embryo transition, which involves the loading and removal of histone variant H2A.Z on chromatin. Although the H2A.Z landscapes in sperm have been investigated, its dynamics during early development remain unrevealed. Here, by using ultra-low-input native chromatin immunoprecipitation and sequencing (ULI-NChIP-seq), we map the genome-wide distribution of H2A.Z in mouse oocytes and early embryos. We find that paternal H2A.Z is removed upon fertilization, followed by unbiased accumulation on parental genomes during zygotic genome activation (ZGA). More importantly, H2A.Z exhibits hierarchical accumulation as different peak types at promoters. We identify that double H2A.Z peaks co-localizes with H3K4me3 and facilitates transcriptional activation, bivalent markers (H3K4me3+H3K27me3) prefer to occupy single H2A.Z peak and inhibits developmental gene expression, while promoters with no H2A.Z accumulation exhibit gene silencing in early embryos. Remarkably, H2A.Z depletion changes the enrichments of histone modifications and RNA polymerase II (Pol II) binding at promoters, resulting in abnormal gene expression and developmental arrest during lineage commitment. Hence, H2A.Z plays dual roles in regulating the epigenomes required for proper gene expression during preimplantation development.
2022-06-24 | GSE188588 | GEO
Project description:Nucleosome is the basic structural unit of chromatin, and its dynamics plays critical roles in the regulation of genome functions. However, how the nucleosome structure is regulated by histone variants in vivo is still largely uncharacterized. Here, by employing Micrococcal nuclease (MNase) digestion of crosslinked chromatin followed by chromatin immunoprecipitation (ChIP) and paired-end sequencing (MNase-X-ChIP-seq), we mapped genome-wide unwrapping states of nucleosomes containing histone variant H2A.Z in mouse embryonic stem (ES) cells. We found that H2A.Z is enriched with unwrapped nucleosomes. Interestingly, the function of +1 H2A.Z nucleosome in transcriptional regulation is correlated with the unwrapping states. We further showed that H2A.Z nucleosomes adjacent the CTCF binding sites (CBS) may adopt an open conformation. We confirmed the unwrapping state of H2A.Z nucleosomes under native condition by re-ChIP of H2A.Z after CTCF CUT&RUN in mouse ES cells. Importantly, we found that depletion of H2A.Z results in increased CTCF binding, indicating dynamic competition between the unwrapped H2A.Z nucleosomal intermediates and CTCF at the CBS. Taken together, our results showed that histone variant H2A.Z regulates transcription and CTCF binding through modulating the nucleosome unwrapping.
2020-04-27 | GSE146082 | GEO
Project description:The regulation of eukaryotic chromatin relies on interactions between many epigenetic factors, including histone modifications, DNA methylation, and the incorporation of histone variants. H2A.Z, one of the most conserved but enigmatic histone variants that is enriched at the transcriptional start sites of genes, has been implicated in a variety of chromosomal processes. Recently, we reported a genome-wide anticorrelation between H2A.Z and DNA methylation, an epigenetic hallmark of heterochromatin that has also been found in the bodies of active genes in plants and animals. Here, we investigate the basis of this anticorrelation using a novel h2a.z loss-of-function line in Arabidopsis thaliana. Through genome-wide bisulfite sequencing, we demonstrate that a loss of H2A.Z in Arabidopsis does not affect the level or profile of DNA methylation in genes, and we propose that the global anticorrelation between DNA methylation and H2A.Z is caused by the exclusion of H2A.Z from methylated DNA. RNA-seq and genomic mapping of H2A.Z show that H2A.Z enrichment across gene bodies, rather than at the TSS, is correlated with lower transcription levels and higher measures of gene responsiveness. We find that a loss of H2A.Z causes misregulation of many genes that are disproportionately associated with response to both endogenous and exogenous stimuli. We propose that H2A.Z deposition in gene bodies promotes variability in levels and patterns of gene expression, and that a major function of genic DNA methylation is to exclude H2A.Z from constitutively expressed genes. Examination of DNA methylation and transcription in an h2a.z mutant
2012-12-13 | E-GEOD-39045 | biostudies-arrayexpress
Project description:Histone variant H2A.Z-containing nucleosomes are incorporated at most eukaryotic promoters. This incorporation is mediated by the conserved SWR1 complex, which replaces histone H2A in canonical nucleosomes with H2A.Z in an ATP-dependent manner. Here, we show that promoter-proximal nucleosomes are highly heterogeneous for H2A.Z in Saccharomyces cerevisiae, with substantial representation of nucleosomes containing one, two, or no H2A.Z molecules. SWR1-catalyzed H2A.Z replacement in vitro occurs in a stepwise and unidirectional fashion, one H2A.Z-H2B dimer at a time, producing heterotypic nucleosomes as intermediates and homotypic H2A.Z nucleosomes as end products. The ATPase activity of SWR1 is specifically stimulated by H2A-containing nucleosomes without ensuing histone H2A eviction. Remarkably, further addition of free H2A.Z-H2B dimer leads to hyperstimulation of ATPase activity, eviction of nucleosomal H2A-H2B and deposition of H2A.Z-H2B. These results suggest that the combination of H2A-containing nucleosome and free H2A.Z-H2B dimer acting as both effector and substrate for SWR1 governs the specificity and outcome of the replacement reaction. Total nucleosomes from MNase-treated nuclear extracts were fractionated by sequential immunoprecipitation into homotypic H2A/H2A (AA), heterotypic H2A/H2A.Z (AZ), and homotypic H2A.Z/H2A.Z (ZZ) nucleosomes.
2010-10-12 | E-GEOD-24618 | biostudies-arrayexpress
Project description:NRP histone chaperones promote the removal of histone variant H2A.Z
| PRJNA525997 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-10-13 | GSE161594 | GEO
Project description:The histone variant H2A.Z plays key roles in gene expression, DNA repair, and centromere function. H2A.Z deposition is controlled by SWR-C chromatin remodeling enzymes that catalyze the nucleosomal exchange of canonical H2A with H2A.Z. Here we report that acetylation of histone H3 lysine 56 (H3-K56Ac) alters the substrate specificity of SWR-C, leading to promiscuous dimer exchange where either H2A.Z or H2A can be exchanged from nucleosomes. This result is confirmed in vivo, where genome-wide analysis demonstrates widespread decreases in H2A.Z levels in yeast mutants with hyperacetylated H3K56. Our work also suggests that a conserved SWR-C subunit may function as a M-bM-^@M-^\lockM-bM-^@M-^] that prevents removal of H2A.Z from nucleosomes. Our study identifies a histone modification that regulates a chromatin remodeling reaction and provides insights into how histone variants and nucleosome turnover can be controlled by chromatin regulators. H2A.Z ChIP seq experiments in mutants with constitutive H3K56ac
2013-04-15 | E-GEOD-43935 | biostudies-arrayexpress