Bos taurus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA387179 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5575800_1.fastq.gz | Fastqsanger.gz | |||
| SRR5575800_2.fastq.gz | Fastqsanger.gz | |||
| SRR5575801_1.fastq.gz | Fastqsanger.gz | |||
| SRR5575801_2.fastq.gz | Fastqsanger.gz | |||
| SRR5575802_1.fastq.gz | Fastqsanger.gz |
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Project description:KMT1A prevents somatic cell nuclear transfer (SCNT) mediated reprogramming (Bovine)
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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:KMT1A (also known as SUV39H1)was involved in improving reprogramming efficiency during inducing pluripotent stem cells (iPSC). However, the knowledge about KMT1A regulating somatic cell nuclear transfer (SCNT) mediated reprogramming was limited. To understand the role of KMT1A during SCNT embryos in vitro development; we performed based transcriptome profiling in SCNT embryos at 8-cell stages and KMT1A knockdown 8-cell SCNT embryos. The data show the mRNAs regulated after KMT1A was down-regulated.
2017-07-31 | GSE99072 | GEO
Project description:The extremely low efficiency of human embryonic stem cell (hESC) derivation using somatic cell nuclear transfer (SCNT) limits potential application. Blastocyst formation from human SCNT embryos occurs at a low rate and with only some oocyte donors. We previously showed in mice that reduction of histone H3 lysine 9 trimethylation (H3K9me3) through ectopic expression of the H3K9me3 demethylase Kdm4d greatly improves SCNT embryo development. Here we show that overexpression of a related H3K9me3 demethylase KDM4A improves human SCNT, and that, as in mice, H3K9me3 in the human somatic cell genome is an SCNT reprogramming barrier. Overexpression of KDM4A significantly improves the blastocyst formation rate in human SCNT embryos by facilitating transcriptional reprogramming, allowing derivation of NTESCs from all oocyte donors tested using adult AMD patient somatic nuclei donors. This conserved mechanistic insight has potential applications for improving SCNT in a variety of contexts, including regenerative medicine. Here we perform RNA-seq based transcriptome profiling in human Donor (fibroblast cells), in vitro fertilized embryos at 8-cell stages (IVF_8Cell), somatic cell nuclear transfer embryos at 8-cell stages (SCNT_8Cell), SCNT assisted by KDM4A 8-cell embryos (SCNT_KDM4A_8Cell). Besides, we also perform RNA-seq in Control human ES cells (CTR_hES) and SCNT assisted by KDM4A derived human ES cells (NTK) with duplicates.Â
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Project description:Mammalian oocytes have the ability to reset the transcriptional program of differentiated somatic cells into that of totipotent embryos through somatic cell nuclear transfer (SCNT). However, the mechanisms underlying SCNT-mediated reprogramming are largely unknown. To understand the mechanisms governing chromatin reprogramming during SCNT, we profiled DNaseI hypersensitive sites (DHSs) in donor cumulus cells and 1-cell stage SCNT embryos. To our surprise, the chromatin accessibility landscape of the donor cells is drastically changed to recapitulate that of the in vitro fertilization (IVF)-derived zygotes within 12 hours. Interestingly, this DHS reprogramming takes place even in the presence of a DNA replication inhibitor, suggesting that SCNT-mediated DHS reprogramming is independent of DNA replication. Thus, the study not only reveals the rapid and drastic nature of the changes in chromatin accessibility through SCNT, but also provides a DNA replication-independent model for studying cellular reprogramming.
2018-05-14 | GSE110851 | GEO
Project description:Placental gene expression in pregnancies established after the transfer of day 7 blastocysts derived from in vitro (IVP), somatic cell nuclear transfer (SCNT) and in vivo (AI) embryos
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Project description:Trichostatin A does not correct specific errors of somatic cell nuclear transfer on the transcriptomic level highlighing the non-random nature of oocyte-mediated reprogramming errors.
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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:Cloning mammals by somatic cell nuclear transfer (SCNT) is highly inefficient because of aberrant genomic reprogramming. In addition to random reprogramming errors, we hypothesized the presence of specific errors as evidenced by common anomalies among clones. We found that Xist, which normally inactivates one of the two X chromosomes in females, was ectopically expressed from the active X (Xa) chromosome in cloned mouse embryos of both sexes. Deletion of Xist on Xa normalized global gene expression and produced about a 10-fold increase in cloning efficiency. We also identified an Xist-independent mechanism that specifically downregulated a subset of X-linked genes through somatic-type repressive histone blocks. Thus, we have identified nonrandom reprogramming errors in mouse cloning, which provide promising targets for breakthroughs in SCNT cloning technology. Gene expression were measured in mouse in vitro fertilized and somatic cell cloned blastocysts. More than three biological replicates were performed in each group using defferent nuclear donor cells.
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Project description:Bovine endometrium at day 18 of pregnancy after transfer of in vitro produced or somatic cell nuclear transfer embryos
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