Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA359751 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5138760_1.fastq.gz | Fastqsanger.gz | |||
| SRR5138760_2.fastq.gz | Fastqsanger.gz | |||
| SRR5138770_1.fastq.gz | Fastqsanger.gz | |||
| SRR5138770_2.fastq.gz | Fastqsanger.gz | |||
| SRR5138771_1.fastq.gz | Fastqsanger.gz |
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Project description:Dramatic change in DNA methylation patterns and levels both globally and/or locus-specifically is associated with the process of cell linage specification and somatic reprogramming. We found the expression of DNA methyltransferase 1 (Dnmt1) is tightly regulated by the features of cell cycle, which we referred as cell cycle-directed Dnmt1 expression adjustment. To further investigate how DNA methylation is affected by this mechanism, we applied reduced representation bisulphate sequencing (RRBS) to map genome-wide DNA methylation on mouse embryonic fibroblasts (MEFs). To characterize how this mechanism affects somatic reprogramming, samples of MEFs induced by Yamanaka factors (Sox2, Klf4, Oct4, cMyc) was included. The cell cycle was accelerated by shRNA targeted to p53, and the expression of Dnmt1 was manipulated genetically. We find 5mC level remains constant in regardless of cell proliferation rate, a result from the adjusted expression of Dnmt1. However, repressed expression of Dnmt1 in fast-proliferating cells results in global DNA demethylation. The patterns of DNA methylation and demethylation affected by this mechanism is sensitive to CpG densities. Generally, the results demonstrate cell cycle-directed Dnmt1 expression adjustment as an mechanism for the insurance of the stability of genomic 5mC inheritance.
2017-10-13 | GSE93058 | GEO
Project description:To generate association of DNA methylation level and gene expression profile, we applied RNA-sequencing on mouse embryonic fibroblasts (MEFs) after the modulation of cell cycle and Dnmt1 expression level. To characterize how these factors affect somatic reprogramming, samples of MEFs induced by Yamanaka factors (Sox2, Klf4, Oct4, cMyc) was also included. The cell cycle was accelerated by shRNA targeted to p53, and the expression of Dnmt1 was manipulated by either over expression or knock down.
2017-10-13 | GSE93416 | GEO
Project description:Dramatic change in DNA methylation patterns and levels both globally and/or locus-specifically is associated with the process of cell lineage specification and somatic reprogramming. We found the expression of DNA methyltransferase 1 (Dnmt1), the enzyme that maintains 5-methylcytosine (5mC) after DNA replication, is tightly regulated by the progression of cell cycle. Upregulation of Dnmt1 was observed in cells with shortened G1 and G2 phase. We hypothesize that 5mC level is not completely recovered by Dnmt1 immediately after DNA replication. In the attempt to clarify DNA methylation status before and after DNA replication, we performed Whole Genome Bisulfite Sequencing (WGBS) to map genome-wide DNA methylation separately in G1 and G2 phase of mouse embryonic fibroblasts (MEFs). Cells of different cell cycle phases were sorted by flow cytometry after Propidium iodide (PI) staining. We find an average of 2% decrease of global DNA methylation in G2 phase compared with G1, with the trend more magnificent in high CpG density regions. Generally, the results indicate that the G1 phase of cell cycle is an important time window for the stability of DNA methylation inheritance.
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Project description:DNA methylation is a key epigenetic modification involved in regulating gene expression and maintaining genomic integrity. Somatic patterns of DNA methylation are largely static, apart from focal dynamics at gene regulatory elements. To further advance our understanding of the role of DNA methylation in human development and disease, we inactivated all three catalytically active DNA methyltransferases in human embryonic stem cells (ESCs) using CRISPR/Cas9 genome editing. Disruption of DNMT3A or DNMT3B individually, as well as of both enzymes in tandem, creates viable, pluripotent cell lines with distinct effects on their DNA methylation landscape as assessed by whole-genome bisulfite sequencing. Surprisingly, in contrast to mouse, deletion of DNMT1 resulted in rapid cell death in human ESCs. To overcome the immediate lethality, we generated a doxycycline (DOX) responsive tTA-DNMT1* rescue line and readily obtained homozygous DNMT1 mutant lines. However, DOX-mediated repression of the exogenous DNMT1* initiates rapid, global loss of DNA methylation, followed by extensive cell death, demonstrating that DNA methylation is essential for human ESCs cultured in standard conditions. In summary, our data provide a comprehensive characterization of DNMT mutant ESCs, including single base genome-wide maps of their targets. RRBS methylation profiling of a time course of DNMT1* withdrawal in human ES cells
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2015-04-13 | E-GEOD-67811 | biostudies-arrayexpress
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Project description:Myelination in the CNS is modulated by interplay between transcription factors and recruitment of chromatin modifying enzymes. Using a network built from genome-wide DNA methylation and transcriptomic profiling of sorted oligodendrocyte lineage cells that integrates oligodendrocyte-specific ChIP-Seq data, we defined a crucial role of DNA methylation in coordinating the transition between progenitor cell cycle arrest and oligodendrocyte differentiation. We further identified DNA methyltransferase 1 (DNMT1) as key regulator of oligodendrocyte survival at this transition point, as we detected severe and extensive developmental hypomyelination only in Olig1cre/+;Dnmt1flox/flox but not in Olig1cre/+;Dnmt3aflox/flox mice or in Cnpcre/+;Dnmt1flox/flox. This phenotype was characterized by decreased expression of genes regulating myelination and lipid metabolism â despite the hypomethylation observed at these genetic loci  â and upregulation of cell cycle and DNA-damage pathways. Therefore DNMT1 is a nodal point regulating proliferation, survival, and differentiation in the oligodendrocyte lineage, and is critical for cell number regulation in the developing brain. Genome wide DNA methylation profiles of FAC-sorted P2 Pdgfra::GFP and P18 Plp1-GFP purified cell samples from mouse brains were generated by ERRBS analysis, in duplicate, using Illumina HiSeq 2000.
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Project description:DNA methylation is a key epigenetic modification involved in regulating gene expression and maintaining genomic integrity. Somatic patterns of DNA methylation are largely static, apart from focal dynamics at gene regulatory elements. To further advance our understanding of the role of DNA methylation in human development and disease, we inactivated all three catalytically active DNA methyltransferases in human embryonic stem cells (ESCs) using CRISPR/Cas9 genome editing. Disruption of DNMT3A or DNMT3B individually, as well as of both enzymes in tandem, creates viable, pluripotent cell lines with distinct effects on their DNA methylation landscape as assessed by whole-genome bisulfite sequencing. Surprisingly, in contrast to mouse, deletion of DNMT1 resulted in rapid cell death in human ESCs. To overcome the immediate lethality, we generated a doxycycline (DOX) responsive tTA-DNMT1* rescue line and readily obtained homozygous DNMT1 mutant lines. However, DOX-mediated repression of the exogenous DNMT1* initiates rapid, global loss of DNA methylation, followed by extensive cell death, demonstrating that DNA methylation is essential for human ESCs cultured in standard conditions. In summary, our data provide a comprehensive characterization of DNMT mutant ESCs, including single base genome-wide maps of their targets.
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