Ontology highlight
ABSTRACT:
PROVIDER: PRJNA135175 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR086201.fastq.gz | Fastqsanger.gz | |||
| SRR086202.fastq.gz | Fastqsanger.gz | |||
| SRR086203.fastq.gz | Fastqsanger.gz | |||
| SRR086204.fastq.gz | Fastqsanger.gz | |||
| SRR086205.fastq.gz | Fastqsanger.gz |
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Project description:Widespread targeted chromatin remodeling during the initial phase of somatic cell reprogramming [expression]
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Project description:Widespread targeted chromatin remodeling during the initial phase of somatic cell reprogramming [ChIP-Seq]
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Project description:Despite rapid progress in characterizing transcription factor-driven reprogramming of somatic cells to an induced pluripotent stem (iPS) cell state, many mechanistic questions still remain. To gain insight into the earliest events in the reprogramming process, we systematically analyzed the transcriptional and epigenetic changes that occur during early factor induction after discrete numbers of divisions. We observed rapid, genome-wide changes in the euchromatic histone modification, H3K4me2, at more than a thousand loci including large subsets of pluripotency or developmentally related gene promoters and enhancers. In contrast, patterns of the repressive H3K27me3 modification remained largely unchanged except for focused depletion specifically at positions where H3K4 methylation is gained. These chromatin regulatory events precede transcriptional changes within the corresponding loci. Our data provide evidence for an early, organized, and population-wide epigenetic response to ectopic reprogramming factors that clarify the temporal order through which somatic identity is reset during reprogramming. Gene expression was measured by Affymetric microarrays during the initial phase of the reprogramming of mouse embryonic fibroblasts.
2011-01-03 | E-GEOD-26096 | biostudies-arrayexpress
Project description:Despite rapid progress in characterizing transcription factor-driven reprogramming of somatic cells to an induced pluripotent stem (iPS) cell state, many mechanistic questions still remain. To gain insight into the earliest events in the reprogramming process, we systematically analyzed the transcriptional and epigenetic changes that occur during early factor induction after discrete numbers of divisions. We observed rapid, genome-wide changes in the euchromatic histone modification, H3K4me2, at more than a thousand loci including large subsets of pluripotency or developmentally related gene promoters and enhancers. In contrast, patterns of the repressive H3K27me3 modification remained largely unchanged except for focused depletion specifically at positions where H3K4 methylation is gained. These chromatin regulatory events precede transcriptional changes within the corresponding loci. Our data provide evidence for an early, organized, and population-wide epigenetic response to ectopic reprogramming factors that clarify the temporal order through which somatic identity is reset during reprogramming. Genome-scale DNA methylation was measured by reduced representation bisulfite sequencing (RRBS) during the initial phase in the reprogramming of mouse embryonic fibroblasts.
2011-01-03 | E-GEOD-26098 | biostudies-arrayexpress
Project description:Despite rapid progress in characterizing transcription factor-driven reprogramming of somatic cells to an induced pluripotent stem (iPS) cell state, many mechanistic questions still remain. To gain insight into the earliest events in the reprogramming process, we systematically analyzed the transcriptional and epigenetic changes that occur during early factor induction after discrete numbers of divisions. We observed rapid, genome-wide changes in the euchromatic histone modification, H3K4me2, at more than a thousand loci including large subsets of pluripotency or developmentally related gene promoters and enhancers. In contrast, patterns of the repressive H3K27me3 modification remained largely unchanged except for focused depletion specifically at positions where H3K4 methylation is gained. These chromatin regulatory events precede transcriptional changes within the corresponding loci. Our data provide evidence for an early, organized, and population-wide epigenetic response to ectopic reprogramming factors that clarify the temporal order through which somatic identity is reset during reprogramming. Covalent histone modifications were measured by ChIP-Seq during the initial phase in the reprogramming of mouse embryonic fibroblasts.
2011-01-03 | E-GEOD-26099 | biostudies-arrayexpress
Project description:Cellular reprogramming remodels the gene expression program by re-setting the epigenome of somatic cells into an embryonic-like state. Post-translational modifications of histones play an important role in this process. We previously used ChIP-seq to profile the distribution of specific histone H3 marks during the entire reprogramming process and found widespread loss of H3K27me3 in the initial stages[1]. Here, using an unbiased middle-down proteomics approach we have identified 74 unique isoforms of histone H4 and quantified them across nine stages of reprogramming. Our data showed substantial differences between the precursor cells and late-phase reprogramming cells. Also, ESCs and iPSCs displayed higher levels of H4 acetylation and tri-methylation concomitantly with lower levels of mono- and di-methylation when compared to cells undergoing reprogramming. These results suggest that during reprogramming, the histone H4 “PTM code” experiences dynamic changes in multiple waves, with a final reset taking place during the transition to an ESC-like state, in perfect agreement with the in-parallel generated multi-omics data[1]. Together, these data represent an invaluable resource to study PTMs of H4 and their potential cross-talk and extend our knowledge on the epigenetic mechanisms involved in acquisition of induced pluripotency.
2015-08-17 | PXD002062 | Pride
Project description:Mature oocyte cytoplasm can reprogram somatic cell nuclei to the pluripotent state through a series of sequential events including protein exchange between the donor nucleus and ooplasm, chromatin remodeling, and pluripotency gene reactivation. Maternal factors that are responsible for this reprogramming process remain largely unidentified. Here, we demonstrate that knockdown of histone variant H3.3 in mouse oocytes results in compromised reprogramming and down-regulation of key pluripotency genes; and this compromised reprogramming both for developmental potentials and transcription of pluripotency genes can be rescued by injecting exogenous H3.3 mRNA, but not H3.2 mRNA into oocytes in somatic cell nuclear transfer (SCNT) embryos. We show that maternal H3.3, and not H3.3 in the donor nucleus, is essential for successful reprogramming of somatic cell nucleus into the pluripotent state. Furthermore, H3.3 is involved in this reprogramming process by remodeling the donor nuclear chromatin through replacement of donor nucleus-derived H3 with de novo synthesized maternal H3.3 protein. Our study shows that H3.3 is a crucial maternal factor for oocyte reprogramming and provides a practical model to directly dissect the oocyte for its reprogramming capacity. Transcriptome sequencing of 4-cell NT embryos, Luciferase 4-cell SCNT embryos, 4-cell NT embryos_H3.3KD, 4-cell NT embryos_H3.3KD+H3.3mRNA, H3.3 KD + H3.2 mRNA SCNT embryos
2014-06-02 | E-GEOD-56762 | biostudies-arrayexpress
Project description:Somatic cell reprogramming into pluripotent stem cells (iPSC) through the forced expression of defined factors induces changes in genome architecture reflective of the embryonic stem cell state. However, only a small minority of cells typically transition to pluripotency, which has limited our understanding of what defines cells that successfully reprogram. Here, we characterize the changes that occur across the DNA regulatory landscape during reprogramming by time-course profiling of isolated sub-populations of reprogramming intermediates poised to become iPSC. Widespread reconfiguration of chromatin states and transcription factor occupancy occurs early during reprogramming, and cells that fail to reprogram partially retain regulatory elements active in their somatic cell state. A second wave of reconfiguration occurs just prior to cells achieving pluripotency, where a majority of early changes revert to the somatic cell state and many of the changes that define the pluripotent state become established. Our comprehensive characterization of the molecular changes that occur during reprogramming broaden our understanding of the reprogramming process by providing crucial insights into iPSC generation, and shed light on how transcription factors in general access and change the chromatin during cell fate transitions.
2017-12-06 | GSE101905 | GEO
Project description:Reactivation of the pluripotency network during somatic cell reprogramming by exogenous transcription factors involves chromatin remodeling and the recruitment of RNA polymerase II (Pol II) to target loci. Here, we report that Pol II is engaged at pluripotency promoters in reprogramming but remains paused and inefficiently released. We also show that bromodomain-containing protein 4 (BRD4) stimulates productive transcriptional elongation of pluripotency genes by dissociating the pause release factor P-TEFb from an inactive complex containing HEXIM1. Consequently, BRD4 overexpression enhances reprogramming efficiency and HEXIM1 suppresses it, whereas Brd4 and Hexim1 knockdown do the opposite. We further demonstrate that the reprogramming factor KLF4 helps recruit P-TEFb to pluripotency promoters. Our work thus provides a mechanism for explaining the reactivation of pluripotency genes in reprogramming and unveils an unanticipated role for KLF4 in transcriptional pause release. Examination of differential gene expression after overexpression of Cdk9-DN at 4 time points of somatic cell reprogramming
2014-10-07 | E-GEOD-59813 | biostudies-arrayexpress