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Homo sapiens

ABSTRACT: Replicative senescence is associated with nuclear reorganization and DNA methylation at specific transcription factor binding sites (MBD-seq)

OTHER RELATED OMICS DATASETS IN: E-GEOD-59966

PROVIDER: PRJNA257204 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1533800.fastq.gz	Fastqsanger.gz
	SRR1533797.fastq.gz	Fastqsanger.gz
	SRR1533798.fastq.gz	Fastqsanger.gz
	SRR1533799.fastq.gz	Fastqsanger.gz

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Project description:Replicative senescence is associated with nuclear reorganization and DNA methylation at specific transcription factor binding sites

| PRJNA257208 | ENA

Homo sapiens

Project description:Replicative senescence is associated with nuclear reorganization and DNA methylation at specific transcription factor binding sites (RNA-seq)

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Replicative senescence is associated with nuclear reorganization and DNA methylation at specific transcription factor binding sites (MBD-seq)

Project description:Primary cells enter replicative senescence after a limited number of cell divisions. This process is associated with reproducible changes in DNA methylation (DNAm) at specific sites in the genome. The mechanism that drives senescence-associated DNAm changes remains unknown and may arise through drift in DNAm or through regulated, senescence dependent modifications at specific sites in the genome. In this study, we analyzed the reorganization of nuclear architecture and DNA methylation during long-term culture of human fibroblasts and mesenchymal stromal cells (MSCs). [MethylCap-seq] Fibroblasts of two female donors (both 43 years old) were culture expanded and DNA was harvested of 10,000,000 cells at early passage (P3 or P5) and late passage (P30 and P33). DNA methylation changes were subsequently analyzed by MethylCap-Seq.

2015-03-26 | E-GEOD-59960 | biostudies-arrayexpress

Replicative senescence is associated with nuclear reorganization and DNA methylation at specific transcription factor binding sites (RNA-seq)

2015-03-26 | GSE59966 | GEO

Replicative senescence is associated with nuclear reorganization and DNA methylation at specific transcription factor binding sites (MBD-seq)

2015-03-26 | GSE59960 | GEO

Replicative senescence is associated with nuclear reorganization and DNA methylation at specific transcription factor binding sites (RNA-seq)

Project description:Primary cells enter replicative senescence after a limited number of cell divisions. This process is associated with reproducible changes in DNA methylation (DNAm) at specific sites in the genome. The mechanism that drives senescence-associated DNAm changes remains unknown and may arise through drift in DNAm or through regulated, senescence dependent modifications at specific sites in the genome. In this study, we analyzed the reorganization of nuclear architecture and DNA methylation during long-term culture of human fibroblasts and mesenchymal stromal cells (MSCs). [RNA-seq] RNA was isolated from 1,000,000 cells of three MSC donors (59, 64, and 73 years old) at passage 4 and passage 13 using the miRNeasy Mini Kit (Qiagen). Gene expression profiles were analzyed by deep sequencing with IlluminaHiSeq 2000 technology with a read length of 50 bases at EMBL gene core facility (Heidelberg, Germany).

2015-03-26 | E-GEOD-59966 | biostudies-arrayexpress

Senescent cells cluster CTCF on nuclear speckles to sustain their splicing program [APEX-seq]

Project description:Senescence —the endpoint of replicative lifespan for normal cells— is established via a complex sequence of molecular events. One such event is the dramatic reorganization of CTCF into senescence-induced clusters (SICCs). However, the molecular determinants, genomic consequences, and functional purpose of SICCs remained unknown. Here, we combine functional assays, super-resolution imaging, and 3D genomics with computational modelling to dissect SICC emergence. We establish that the competition between CTCF-bound and non-bound loci dictates clustering propensity. Upon senescence entry, cells repurpose SRRM2 —a key component of nuclear speckles— and BANF1 —a ‘molecular glue’ for chromosomes— to cluster CTCF and rewire genome architecture. This CTCF-centric reorganization in reference to nuclear speckles functionally sustains the senescence splicing program, as SICC disruption fully reverts alternative splicing patterns. We therefore uncover a new paradigm, whereby cells translate changes in nuclear biochemistry into architectural changes directing splicing choices so as to commit to the fate of senescence.

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Average_hypermethylation_TF_sites

Project description:Average hypermethylation on transcription factor binding sites based on nanopolish calls; only positions showing higher methylation than sampleÃ¢Â€Â™s average methylation at enhancers were included when defining the average methylation level. Data from 6 individuals at different time points.

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Methylation-dependent and -independent genomic targeting principles of the MBD protein family

Project description:In order to gain insight into DNA methylation readout, we have established a controlled strategy for profiling genomic targeting of chromatin-interacting factors in vivo. With this approach we determined binding preferences for the methyl-CpG binding domain (MBD) family of proteins, including disease relevant mutants, deletions and isoforms. In vivo binding of MBD proteins occurs as a linear function of local methylation density, and is dependent on functional MBD domain – methyl-CpG interactions. This directs specificity of MBD proteins to methylated, CpG dense and inactive regulatory regions. In contrast, binding to unmethylated sites is MBD protein specific and mediated via alternative domains or protein-protein interactions. The latter is observed for NuRD complex-mediated MBD2 tethering to a subset of unmethylated, tissue-specific regulatory regions, similar to MBD3. These functional binding maps reveal methylation-dependent and -independent binding modes determined by distinct protein domains and revise current models of DNA methylation readout through MBD proteins.

2013-04-01 | GSE39610 | GEO

Methylation-dependent and -independent genomic targeting principles of the MBD protein family

Project description:In order to gain insight into DNA methylation readout, we have established a controlled strategy for profiling genomic targeting of chromatin-interacting factors in vivo. With this approach we determined binding preferences for the methyl-CpG binding domain (MBD) family of proteins, including disease relevant mutants, deletions and isoforms. In vivo binding of MBD proteins occurs as a linear function of local methylation density, and is dependent on functional MBD domain M-bM-^@M-^S methyl-CpG interactions. This directs specificity of MBD proteins to methylated, CpG dense and inactive regulatory regions. In contrast, binding to unmethylated sites is MBD protein specific and mediated via alternative domains or protein-protein interactions. The latter is observed for NuRD complex-mediated MBD2 tethering to a subset of unmethylated, tissue-specific regulatory regions, similar to MBD3. These functional binding maps reveal methylation-dependent and -independent binding modes determined by distinct protein domains and revise current models of DNA methylation readout through MBD proteins. Comparative binding analysis for the MBD family of proteins utilizing recombinase-assisted mapping of biotin-tagged proteins (RAMBiO). This set contains maps for 29 samples including wild type MBD proteins, mutants and domain variants in mouse ES cells, derived neurons (NP and TN) and Dnmt1/3a/3b triple-KO ES cells (TKO).

2013-04-01 | E-GEOD-39610 | biostudies-arrayexpress

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