Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA176705 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR580529.fastq.gz | Fastqsanger.gz | |||
| SRR580530.fastq.gz | Fastqsanger.gz | |||
| SRR580531.fastq.gz | Fastqsanger.gz | |||
| SRR580532.fastq.gz | Fastqsanger.gz | |||
| SRR580533.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 18 |
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Project description:While it has been clearly established that well positioned H2A.Z-containing nucleosomes flank the nucleosome depleted region (NDR) at the transcriptional start site (TSS) of active mammalian genes 1,2, how this chromatin-based information is transmitted through the cell cycle is unknown. We show here that in trophoblast stem (TS) cells, the level of H2A.Z at promoters decreases during S phase coinciding with homotypic (H2A.Z/H2A.Z) nucleosomes flanking the TSS becoming heterotypic (H2A.Z/H2A). Surprisingly, these nucleosomes remain heterotypic at M phase. At the TSS, we identify an unstable heterotypic H2A.Z-containing nucleosome in G1 which, strikingly, is lost following DNA replication. These dynamic changes in H2A.Z at the TSS mirror a global expansion of the NDR at S and M which, unexpectedly, is unrelated to transcriptional activity. Coincident with the loss of H2A.Z at promoters, it is targeted to the centromere when mitosis begins. We surveyed whole genome expression using microarrays, in combination with H2A.Z ChIP-Seq (Illumina) data, to study the H2A.Z distribution on promoters of coding genes in different stages of the cell cycle in Trophoblast Stem (TS) cells. These data are published in Nekrasov et al., H2AZ inheritance during the cell cycle and it's impact on promoter organization and dynamics, Nature Structural and Molecular Biology (in press: accepted for publication on 24 Sep 2012).
2012-11-23 | GSE41370 | GEO
Project description:While it has been clearly established that well positioned H2A.Z-containing nucleosomes flank the nucleosome depleted region (NDR) at the transcriptional start site (TSS) of active mammalian genes 1,2, how this chromatin-based information is transmitted through the cell cycle is unknown. We show here that in trophoblast stem (TS) cells, the level of H2A.Z at promoters decreases during S phase coinciding with homotypic (H2A.Z/H2A.Z) nucleosomes flanking the TSS becoming heterotypic (H2A.Z/H2A). Surprisingly, these nucleosomes remain heterotypic at M phase. At the TSS, we identify an unstable heterotypic H2A.Z-containing nucleosome in G1 which, strikingly, is lost following DNA replication. These dynamic changes in H2A.Z at the TSS mirror a global expansion of the NDR at S and M which, unexpectedly, is unrelated to transcriptional activity. Coincident with the loss of H2A.Z at promoters, it is targeted to the centromere when mitosis begins. We surveyed whole genome expression using microarrays, in combination with H2A.Z ChIP-Seq (Illumina) data, to study the H2A.Z distribution on promoters of coding genes in different stages of the cell cycle in Trophoblast Stem (TS) cells. These data are published in Nekrasov et al., H2AZ inheritance during the cell cycle and it's impact on promoter organization and dynamics, Nature Structural and Molecular Biology (in press: accepted for publication on 24 Sep 2012). Mouse Trophoblast stem (TS) cells were grown in cell culture medium. By adding specific drugs cells were arrested at particular stages of the cell cycle: G1; S and M. Total RNA was extracted from TS cells arrested at G1; S and M stages of cell cycle using TRizol (Invitrogen) extraction protocol and purified further the by RNAeasy Extraction Kit (Qiagen). RNA quality was assesed on Bioanalyzer total RNA chip. RNA samples were reverse transcribed and resulted cDNA samples were subjected to DNA microarray analysis (in triplicate) using the GeneChip Mouse Gene 1.0 ST Array (Affymetrix). Robust Multichip Average (RMA) correction and probe set summaries were obtained using Affymetrix Power Tools software annotation (Affymetrix) based on the mm9 mouse genome. Unless otherwise stated, all subsequent expression analyses (see Supplementary Methods) were performed in the R statistical computing environment (version 2.11.1).
2012-11-23 | E-GEOD-41370 | biostudies-arrayexpress
Project description:H2A.Z inheritance during the cell cycle [expression array]
| PRJNA176704 | ENA
Project description:Female mammalian brains exhibit sex-hormone-driven plasticity during the reproductive period. Evidence implicates the role of chromatin dynamics in gene regulation underlying this plasticity. However, whether ovarian hormones impact higher-order chromatin organization in post-mitotic neurons in vivo is unknown. Here, we mapped 3D genome of ventral hippocampal neurons across the estrous cycle and by sex in mice. In females, we found cycle-driven dynamism in 3D chromatin organization, including in estrogen-response-elements-enriched X-chromosome compartments, autosomal CTCF loops, and enhancer-promoter interactions. With rising estrogen levels, the female 3D genome becomes more similar to males. Cyclical enhancer-promoter interactions are partially associated with gene expression and enriched for brain disorder-relevant genes. Our study reveals unique 3D genome dynamics in the female brain relevant to female-specific gene regulation, neuroplasticity, and disease risk.
2022-05-06 | GSE172228 | GEO
Project description:ANP32e, a chaperone of H2A.Z, is receiving increasing attention because of its link to cancer growth and progression. An unanswered question is whether ANP32e regulates H2A.Z dynamics during the cell cycle; if so, this could have clear implications for the proliferation of cancer cells. Using the human U2OS cancer cell line model system, we have confirmed that ANP32e regulates the growth of these cells. ANP32e preferentially interacts with H2A.Z during G1 phase of the cell cycle. Unexpectedly, however, ANP32e does not mediate the removal of H2A.Z from chromatin, is not a stable component of the p400 remodeling complex, and is not strongly associated with chromatin. Instead, most ANP32e is in the cytoplasm. Here, ANP32e preferentially interacts with H2A.Z in G1 phase in response to an increase in H2A.Z protein abundance and regulates its protein stability. This G1-specific interaction between ANP32e and H2A.Z is also observed in the nucleoplasm but is unrelated to any change in H2A.Z abundance. Collectively, these results challenge the idea that ANP32e is involved in regulating the abundance of H2A.Z in chromatin as part of a chromatin remodeling complex. Rather, we propose that ANP32e acts as a molecular chaperone that maintains the soluble pool of H2A.Z by regulating its protein stability and acting as a buffer in response to cell cycle-dependent changes in H2A.Z abundance.
2024-05-23 | PXD033229 | Pride
Project description:While it has been clearly established that well positioned H2A.Z-containing nucleosomes flank the nucleosome depleted region (NDR) at the transcriptional start site (TSS) of active mammalian genes, how this chromatin-based information is transmitted through the cell cycle is unknown. We show here that in trophoblast stem (TS) cells, the level of H2A.Z at promoters decreases during S phase coinciding with homotypic (H2A.Z/H2A.Z) nucleosomes flanking the TSS becoming heterotypic (H2A.Z/H2A). Surprisingly, these nucleosomes remain heterotypic at M phase. At the TSS, we identify an unstable heterotypic H2A.Z-containing nucleosome in G1 which, strikingly, is lost following DNA replication. These dynamic changes in H2A.Z at the TSS mirror a global expansion of the NDR at S and M which, unexpectedly, is unrelated to transcriptional activity. Coincident with the loss of H2A.Z at promoters, it is targeted to the centromere when mitosis begins We performed ChIP-Seq experiments (on mouse Trophoblast Stem cells arrested at G1; S and M stages of thecell cycle) using antibodies against histone variant H2A.Z and sequentional ChIP-re-ChIP-Seq experiments using H2A.Z antibody and H2A antibody in sequence. Combining those data sets with microarray gene expression expression data allowed us to see H2A.Z distribution over promoters of mouse coding genes in cell cycle dependant manner. Interestingly, Input also showed cell-cycle dependent effects, but histone H3 could be used as a cell-cycle independent normalisation factor. We also performed ChIP-seq with a CTCF pull-down to investigate its cell-cycle dependent relationship with heterochromatin.
2012-11-23 | E-GEOD-41371 | biostudies-arrayexpress
Project description:The global and promoter-centric 3D genome organization temporally resolved during a circadian cycle [ChIP-seq]
| PRJNA648852 | ENA
Project description:Nucleosome organization and dynamics play a central role in controlling the DNA accessibility to regulatory factors of many critical cellular functions, especially gene regulation. However, despite extensive studies, the main factors determining nucleosome positioning and its fluctuation during cell cycle still remain elusive. Here, we present a large-scale study of nucleosome plasticity throughout the cell cycle and its interplay with gene expression based on genome-wide nucleosome positioning and mRNA abundance. We have clusterized distinct nucleosome architectures around transcription start sites and replication origins and studied their dynamics during the cell cycle progression. The most significant cell cycle-dependent changes occur at G1-S and G2-M transitions due to a large changes in gene expression in cell cycle regulatory genes. Taken together, our accurate study provides a dynamic picture of chromatin organization along cell cycle and its interplay with gene expression.
2014-10-09 | E-MTAB-2839 | biostudies-arrayexpress
Project description:Plants are sessile organisms and therefore must sense and respond to changes of their surrounding conditions such as ambient temperature, which vary diurnally and seasonally. It is not yet clear how plants sense temperature and integrate this information into their development. We have previously shown that H2A.Z-nucleosomes are evicted in response to warmer temperatures. It is not clear however, whether the link between transcriptional responsiveness and changes in H2A.Z binding in context of temperature shifts is a global trend that can be seen throughout the genome, or the phenomenon is specific to a specialised set of temperature-responsive genes. In addition to the role of H2A.Z-nucleosome dynamics in the transcriptional response to temperature, it was shown that genes strongly misregulated in the h2a.z mutant are enriched for gene categories involved in response to multiple environmental cues. This suggests that H2A.Z could be implicated in the transcriptional response to various environmental inputs, raising the question: What brings the specificity of H2A.Z dynamics in response to temperature? To address this question we have profiled H2A.Z-nucleosome occupancy genome wide (using ChIP-seq) during a time course after temperature variation and compared its dynamics to transcriptional changes. We identified a fast, targeted and transient eviction of H2A.Z associated with transcriptional activation in response to temperature for a few hundreds genes. This eviction is associated with a reduction of the stability of the nucleosome. Moreover the genes with a fast H2A.Z eviction were strongly enriched in heat shock elements in their promoter and we observed a strong association between HSF1 binding and H2AZ eviction at warm temperature. These results highlight the importance of the interplay between transcription factors and chromatin to allow a controlled and dynamics response to temperature.
2017-09-29 | GSE79354 | GEO