CTCF is a Barrier for Totipotent-like Reprogramming [END-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA693454 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13489191.fastq.gz | Fastqsanger.gz | |||
| SRR13489192.fastq.gz | Fastqsanger.gz | |||
| SRR13489193.fastq.gz | Fastqsanger.gz | |||
| SRR13489194.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Totipotent cells have the ability of generating embryonic and extra-embryonic tissues. Interestingly, a rare population of cells with totipotent-like potential was identified within ESC cultures. These cells, known as 2 cell (2C)-like cells, arise from ESC and display similar features to those found in the totipotent 2 cell embryo. However, the molecular determinants of 2C like conversion have not been completely elucidated. Here, we show that CTCF is a barrier for 2C-like reprogramming. Indeed, forced conversion to a 2C-like state by DUX expression was associated with DNA damage at a subset of CTCF binding sites. Endogenous or DUX-induced 2C-like ESC showed decreased CTCF enrichment at known binding sites, suggesting that acquisition of a totipotent-like state is associated with a highly dynamic chromatin architecture. Accordingly, depletion of CTCF in ESC efficiently promoted spontaneous and asynchronous conversion to a totipotent-like state. This phenotypic reprogramming was reversible upon restoration of CTCF levels. Furthermore, we showed that transcriptional activation of the ZSCAN4 cluster was necessary for successful 2C-like reprogramming. In summary, we revealed the intimate relation between CTCF and totipotent-like reprogramming.
2021-06-07 | GSE165161 | GEO
Project description:Totipotent cells have the ability of generating embryonic and extra-embryonic tissues. Interestingly, a rare population of cells with totipotent-like potential was identified within ESC cultures. These cells, known as 2 cell (2C)-like cells, arise from ESC and display similar features to those found in the totipotent 2 cell embryo. However, the molecular determinants of 2C like conversion have not been completely elucidated. Here, we show that CTCF is a barrier for 2C-like reprogramming. Indeed, forced conversion to a 2C-like state by DUX expression was associated with DNA damage at a subset of CTCF binding sites. Endogenous or DUX-induced 2C-like ESC showed decreased CTCF enrichment at known binding sites, suggesting that acquisition of a totipotent-like state is associated with a highly dynamic chromatin architecture. Accordingly, depletion of CTCF in ESC efficiently promoted spontaneous and asynchronous conversion to a totipotent-like state. This phenotypic reprogramming was reversible upon restoration of CTCF levels. Furthermore, we showed that transcriptional activation of the ZSCAN4 cluster was necessary for successful 2C-like reprogramming. In summary, we revealed the intimate relation between CTCF and totipotent-like reprogramming.
2021-06-07 | GSE172073 | GEO
Project description:Totipotent cells have the ability of generating embryonic and extra-embryonic tissues. Interestingly, a rare population of cells with totipotent-like potential was identified within ESC cultures. These cells, known as 2 cell (2C)-like cells, arise from ESC and display similar features to those found in the totipotent 2 cell embryo. However, the molecular determinants of 2C like conversion have not been completely elucidated. Here, we show that CTCF is a barrier for 2C-like reprogramming. Indeed, forced conversion to a 2C-like state by DUX expression was associated with DNA damage at a subset of CTCF binding sites. Endogenous or DUX-induced 2C-like ESC showed decreased CTCF enrichment at known binding sites, suggesting that acquisition of a totipotent-like state is associated with a highly dynamic chromatin architecture. Accordingly, depletion of CTCF in ESC efficiently promoted spontaneous and asynchronous conversion to a totipotent-like state. This phenotypic reprogramming was reversible upon restoration of CTCF levels. Furthermore, we showed that transcriptional activation of the ZSCAN4 cluster was necessary for successful 2C-like reprogramming. In summary, we revealed the intimate relation between CTCF and totipotent-like reprogramming.
2021-06-07 | GSE165160 | GEO
Project description:CTCF is a Barrier for Totipotent-like Reprogramming
| PRJNA693449 | ENA
Project description:CTCF is a Barrier for Totipotent-like Reprogramming [ChIPseq]
| PRJNA721955 | ENA
Project description:CTCF is a Barrier for Totipotent-like Reprogramming [Cut&Run]
| PRJNA693448 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-06-07 | GSE165162 | GEO
Project description:Mammalian oocytes can reprogram somatic cells into totipotent state, which allows animal cloning through somatic cell nuclear transfer (SCNT). However, the great majority of SCNT embryos fail to develop to term due to poorly defined reprogramming defects. Here we demonstrate that histone H3 lysine 9 trimethylation (H3K9me3) in donor nuclei is a major epigenetic barrier that prevents efficient nuclear reprogramming in mouse oocytes. Comparative transcriptome analysis of early embryos revealed reprogramming resistant regions (RRRs) where transcriptional activation at 2-cell embryos is inhibited by SCNT compared to in vitro fertilization (IVF). RRRs significantly overlap with H3K9me3 enrichment in donor somatic cells. Importantly, removal of the H3K9me3 by ectopic expression of an H3K9me3 demethylase Kdm4d in recipient oocytes not only reactivates most RRRs, but also greatly improves development of SCNT embryos. Furthermore, the use of Suv39h1/2-depleted somatic nuclei as donors also greatly improves the development of SCNT embryos. Our study thus reveals H3K9me3 as an epigenetic barrier in SCNT-mediated reprogramming and provides a feasible method for improving mammalian cloning efficiency.
2014-11-07 | GSE59073 | GEO
Project description:To study the role of CGGBP1 in regulation of CTCF occupancy, we performed CTCF ChIP-seq in HEK293T cells with three different levels of CGGBP1: (i) endogenous levels of CGGBP1 (ii) CGGBP1 knockdown, and (iii) CGGBP1 overexpression. Here, we show that CTCF binds to repeats as well as canonical CTCF-motifs and CGGBP1 determines the CTCF occupancy preference for repeats over canonical CTCF-motif. By combining CTCF ChIP-seq with histone modifications ChIP-seq (for H3K4me3, H3K9me3 and H3K27me3) under conditions of normal or CGGBP1 knockdown, we demonstrate that CTCF binding sites regulated by CGGBP1 correspond to chromatin barrier elements with profound effects on H3K9me3 distribution. In conclusion, these finding shows that CGGBP1 is a regulator of CTCF occupancy and serve as a regulator of barrier functions of CTCF-binding sites.
2019-09-23 | GSE129548 | GEO
Project description:The pleiotropic CCCTC-binding factor (CTCF) plays a role in homologous recombination (HR) repair of DNA double-strand breaks (DSBs). However, the precise mechanistic role of CTCF in HR remains largely unclear. Here, we show that CTCF engages in DNA end resection, which is the initial, crucial step in HR, through its interactions with MRE11 and CtIP. Depletion of CTCF profoundly impairs HR and attenuates CtIP recruitment at DSBs. CTCF physically interacts with MRE11 and CtIP and promotes CtIP recruitment to sites of DNA damage. Subsequently, CTCF facilitates DNA end resection to allow HR, in conjunction with MRE11-CtIP. Notably, the zinc finger domain of CTCF binds to both MRE11 and CtIP and enables proficient CtIP recruitment, DNA end resection, and HR. The N-terminus of CTCF is able to bind to only MRE11 and its C-terminus is incapable of binding to MRE11 and CtIP, thereby resulting in compromised CtIP recruitment, DSB resection, and HR. Overall, this suggests an important function of CTCF in DNA end resection through the recruitment of CtIP at DSBs. Collectively, our findings identify a critical role of CTCF at the first control point in selecting the HR repair pathway
2019-11-12 | PXD014441 | Pride