Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA135477 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR094815.fastq.gz | Fastqsanger.gz | |||
| SRR094816.fastq.gz | Fastqsanger.gz | |||
| SRR094817.fastq.gz | Fastqsanger.gz | |||
| SRR094818.fastq.gz | Fastqsanger.gz |
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Project description:Cell fate specification is accompanied by global changes in gene expression from patterns of maintaining stem/progenitor cells to patterns for supporting differentiation. To ensure a proper transition, it is conceivable that genes important for differentiation are kept silent in stem/progenitor cells yet can be readily activated. RNA polymerase II (Pol II) pausing and bivalent chromatin marks are two paradigms that are suited for establishing such a poised state of gene expression, however, their contributions to gene regulation in development are not well understood. Here, using neural progenitor cells (NPCs) and their daughter neurons co-purified from the embryonic mouse cerebral cortex, we characterized Pol II pausing and H3K4me3/H3K27me3 marks in this in vivo setting of neurogenesis. We show that genes paused in NPCs or neurons are well correlated with their respective cell type-specific functions, but pausing and pause release did not predict gene activation. Bivalent chromatin marks, on the other hand, poised the marked genes in NPCs for activation in neurons. Interestingly, our data also revealed a positive correlation between H3K27me3 and paused Pol II. This study thus reveals cell-type specific Pol II pausing and gene activation-associated bivalency during mammalian neuronal differentiation.
2017-07-12 | GSE93010 | GEO
Project description:Cell fate specification is accompanied by global changes in gene expression from patterns of maintaining stem/progenitor cells to patterns for supporting differentiation. To ensure a proper transition, it is conceivable that genes important for differentiation are kept silent in stem/progenitor cells yet can be readily activated. RNA polymerase II (Pol II) pausing and bivalent chromatin marks are two paradigms that are suited for establishing such a poised state of gene expression, however, their contributions to gene regulation in development are not well understood. Here, using neural progenitor cells (NPCs) and their daughter neurons co-purified from the embryonic mouse cerebral cortex, we characterized Pol II pausing and H3K4me3/H3K27me3 marks in this in vivo setting of neurogenesis. We show that genes paused in NPCs or neurons are well correlated with their respective cell type-specific functions, but pausing and pause release did not predict gene activation. Bivalent chromatin marks, on the other hand, poised the marked genes in NPCs for activation in neurons. Interestingly, our data also revealed a positive correlation between H3K27me3 and paused Pol II. This study thus reveals cell-type specific Pol II pausing and gene activation-associated bivalency during mammalian neuronal differentiation.
2017-07-12 | GSE93009 | GEO
Project description:Proteomics reveals dynamic metabolic changes of human hematopoietic stem progenitor cells from fetal liver to adult stages
2024-05-10 | PXD052196 |
Project description:The formation of hematopoietic cells relies on the chromatin remodeling activities of ISWI ATPase SMARCA5 (SNF2H) and its complexes. The Smarca5 null and conditional alleles have been used to study its functions in embryonic and organ development in mice. These mouse model phenotypes vary from embryonic lethality of constitutive knockout to less severe phenotypes observed in tissue-specific Smarca5 deletions, e.g., in the hematopoietic system. Here we show that, in a gene dosage-dependent manner, the hypomorphic allele of SMARCA5 (S5tg) can rescue not only the developmental arrest in hematopoiesis in the hCD2iCre model but also the lethal phenotypes associated with constitutive Smarca5 deletion or Vav1iCre-driven conditional knockout in hematopoietic progenitor cells. Interestingly, the latter model also provided evidence for the role of SMARCA5 expression level in hematopoietic stem cells, as the Vav1iCre S5tg animals accumulate stem and progenitor cells. Furthermore, their hematopoietic stem cells exhibited impaired lymphoid lineage entry and differentiation. This observation contrasts with the myeloid lineage which is developing without significant disturbances. Our findings indicate that animals with low expression of SMARCA5 exhibit normal embryonic development with altered lymphoid entry within the hematopoietic stem cell compartment.
2025-10-27 | PXD048865 | panorama
Project description:Stem and progenitor cells undergo a global elevation of nascent transcription, or hypertranscription, during key developmental transitions involving rapid cell proliferation. The chromatin remodeler Chd1 binds to RNA Pol I and II genes and is required for hypertranscription in embryonic stem (ES) cells in vitro and the early post-implantation epiblast in vivo. Biochemically, Chd1 has been shown to facilitate transcription at least in part by removing nucleosomal barriers to elongation, but its mechanism of action in stem cells remains poorly understood. Here we report a novel role for Chd1 in the repair of promoter-proximal endogenous double-stranded DNA breaks (DSBs) in ES cells. An unbiased proteomics approach revealed that Chd1 interacts with several DNA repair factors including ATM, Parp1, Kap1 and Topoisomerase 2. We show that wild-type ES cells display high levels of phosphorylated H2AX and Kap1 at chromatin, notably at rDNA in the nucleolus, in a Chd1-dependent manner. Loss of Chd1 leads to an extensive accumulation of DSBs at Chd1 target Pol II genes and rDNA. Genes prone to DNA breaks in Chd1-null ES cells tend to be longer genes with GC-rich promoters, a more labile nucleosomal structure and roles in chromatin organization, transcription and signaling. These results reveal a vulnerability of hypertranscribing stem cells to endogenous DNA breaks, with important implications for developmental and cancer biology.
2021-06-14 | PXD024604 | Pride
Project description:Dosage compensation in mammals occurs at two levels. In addition to balancing X-chromosome dosage between males and females via X-inactivation, mammals also balance dosage of Xs and autosomes. It has been proposed that X-autosome equalization occurs by upregulation of Xa (active X). To investigate the mechanism, we perform allele-specific ChIP-seq for chromatin epitopes and analyze RNA-seq data (SRA010053). The hypertranscribed Xa demonstrates enrichment of active chromatin marks relative to autosomes. We derive predictive models for relationships among Pol II, active mark densities and gene expression, and we suggest that Xa upregulation involves increased transcription initiation and elongation. Enrichment of active marks on Xa does not scale proportionally with transcription output, a disparity explained by nonlinear quantitative dependencies among active histone marks, Pol II occupancy and transcription. Notably, the trend of nonlinear upregulation also occurs on autosomes. Thus, Xa upregulation involves combined increases of active histone marks and Pol II occupancy, without invoking X-specific dependencies between chromatin states and transcription. Examination of 4 marks of active transcription (H3K4me3, H3K36me3, POL-II-S2P, POL-II-S5P) in a transformed female mouse embryonic fibroblast cell line (EY.T4).
2012-01-06 | E-GEOD-33823 | biostudies-arrayexpress
Project description:We studied the chromatin modification patterns induced by the presence of the MLL-AF9 fusion protein in a model of human hematopoietic stem/progenitor cells (HSPC) transduced with retrovirus expressing MLL-AF9cDNA (HSPC-MA9). Comparative ChIP-seq analysis between HSPC-MA9 and control HSPC, revealed a massive hyperacetylation of histones that was consistent with the transcriptional profile in the presence of MLL-AF9 fusion protein. Furthermore, we identified 66 MLL-AF9 targets, and found that H4ac was present along with H3K4me3 and H3K79me2 chromatin marks in over 50% of the MLL-AF9 target genes. Examination of histone aceylation and methylation changes upon expression of MLL-AF9 fusion protein in human hematopoietic stem/progenitor cells.
2015-03-01 | E-GEOD-54344 | biostudies-arrayexpress
Project description:The AML1/ETO fusion protein, which is present in 10% to 15% of cases of acute myeloid leukemia, is known to repress myeloid differentiation genes through DNA binding and recruitment of chromatin-modifying proteins and transcription factors in target genes. ChIP-chip analysis of human hematopoietic stem/progenitor cells transduced with the AML1/ETO fusion gene enabled us to identify 1168 AML1/ETO target genes, 103 of which were co-occupied by HDAC1 and had lost the hyperacetylation at histone H4 marks and 264 of which showed a K9 trimethylation at histone H3. Enrichment of genes involved in hematopoietic differentiation and in specific signaling pathways was observed in the presence of these epigenetic modifications associated with an inactive chromatin status. Furthermore, AML1/ETO target genes had a significant correlation between the chromatin marks studied and transcriptional silencing. ChIP-chip comparison of human hematopoietic stem/progenitor cells (HSPCs) retrovirally transduced with the AML1/ETO fusion protein with HSPCs transduced with an empty vector (Mulloy et al., Blood, 2002) using antibodies tagging the AML1/ETO fusion protein, the HDAC1 protein, as well as H4Ac and H3K9m3 chromatin modifications.
2012-01-18 | E-GEOD-27663 | biostudies-arrayexpress
Project description:THOC5, a member of the THO complex, is essential for the 3´processing of some inducible genes, the export of a subset of genes and stem cell self-renewal. Utilising nanopore mRNA-sequencing we show that when THOC5 is depleted 50% of mRNAs undergo altered 3´end cleavage. Further, THOC5 depletion leads to increased RNA Polymerase II (Pol II) presence on the gene body and close to the 3’end. Moreover, THOC5 is recruited close to high density Pol II sites except those at the promotor regions suggesting that THOC5 is involved in transcriptional elongation. Indeed, THOC5 independent genes in cells expressing fast Pol II became THOC5 dependent in cells expressing slow Pol II. In cells expressing slow Pol II chromatin associated THOC5 interacts with CDK12 (a protein that modulates mRNA elongation rates), RNA helicases DDX5, DDX17, and THOC6. Importantly these interactions were not observed in cells expressing fast Pol II. The CDK12/THOC5 interaction promotes CDK12 recruitment to R-loops in a THOC6-dependent manner. These data demonstrate that THOC5/THOC6 play a part in transcription elongation. Given the role of THOC5 in primitive cell survival its phosphorylation by agonists, oxidative stress and oncogenes the pathway we identified has relevance in the physiology and pathology of stem cells
2022-12-12 | PXD035092 | Pride
Project description:Pol II and its associated epigenetic marks are present at pol III-transcribed non-coding RNA genes (II)
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