Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA298575 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3208750_1.fastq.gz | Fastqsanger.gz | |||
| SRR3208750_2.fastq.gz | Fastqsanger.gz | |||
| SRR3208760_1.fastq.gz | Fastqsanger.gz | |||
| SRR3208760_2.fastq.gz | Fastqsanger.gz | |||
| SRR3208770_1.fastq.gz | Fastqsanger.gz |
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Project description:Histone modifications play critical roles in regulating developmental genes expression during embryo development in mammals1,2. However, genome-wide analysis of histone modifications in pre-implantation embryos has been impeded by technical difficulties and the scarcity of required materials. Here, by using a small-scale chromatin immunoprecipitation sequencing (ChIP-seq) method3, for the first time, we mapped the genome-wide profile of histone H3 lysine 4 trimethylation (H3K4me3) and histone H3 lysine 27 trimethylation (H3K27me3), associated with gene activation and repression respectively, in mouse pre-implantation embryos. We found that the establishment of H3K4me3 mark occurs much more rapidly than that of H3K27me3 following fertilization. Furthermore, H3K4me3 and H3K27me3 possess distinct features in sequence preference and dynamics in pre-implantation embryos. Although most H3K4me3 signature constantly exists on transcription start site (TSS) region, the breadth of H3K4me3 domain is of high-dynamic feature. Interestingly, the broad H3K4me3 peak (wider than 5kb) is associated with higher transcription activity and cell identity not only in pre-implantation embryos but also in the process of deriving embryonic stem cells (ESCs) from the inner cell mass (ICM) and trophoblast stem cells (TSCs) from the trophectoderm (TE). Unlike those observed in ESCs, we found that the bivalency (containing both H3K4me3 and H3K27me3) is unstable and not frequently observed in early cleavage stage embryos until the morula to blastocyst transition. Taken all together, our study provides a genome-wide map of H3K4me3 and H3K27me3 modifications in pre-implantation embryos, which offers us opportunities to further understand the epigenetic regulation mechanism in early embryo development.
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Project description:Successful cloning through somatic cell nuclear transfer (SCNT) face significant challenges due to epigenetic obstacles. Recent studies have highlighted the roles of H3K4me3 and H3K27me3 as potential epigenetic barriers. However, the underlying mechanisms remain largely unclear. In this study, we generated genome-wide maps of H3K4me3 and H3K27me3 from mouse pre-implantation NT embryos. Our analysis revealed aberrant over-representation of H3K4me3 and H3K27me3 bivalent in 2-cell stage NT embryos, potentially linked to the deficiency of H3K36me3. Notably, the overexpression of Setd2, a H3K36me3 methyltransferase, successfully restored multiple epigenetic marks, including H3K36me3, H3K4me3 and H3K27me3. Additionally, it reinstated the expression levels of ZGA-related genes by re-establishing H3K36me3 at gene body regions to exclude H3K27me3 from bivalent regions, and ultimately improved cloning efficiency. These findings highlight the excessive bivalent state as a potent barrier and emphasize the removal of these barriers as a promising approach to achieving higher cloning efficiency.
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Project description:Successful cloning through somatic cell nuclear transfer (SCNT) face significant challenges due to epigenetic obstacles. Recent studies have highlighted the roles of H3K4me3 and H3K27me3 as potential epigenetic barriers. However, the underlying mechanisms remain largely unclear. In this study, we generated genome-wide maps of H3K4me3 and H3K27me3 from mouse pre-implantation NT embryos. Our analysis revealed aberrant over-representation of H3K4me3 and H3K27me3 bivalent in 2-cell stage NT embryos, potentially linked to the deficiency of H3K36me3. Notably, the overexpression of Setd2, a H3K36me3 methyltransferase, successfully restored multiple epigenetic marks, including H3K36me3, H3K4me3 and H3K27me3. Additionally, it reinstated the expression levels of ZGA-related genes by re-establishing H3K36me3 at gene body regions to exclude H3K27me3 from bivalent regions, and ultimately improved cloning efficiency. These findings highlight the excessive bivalent state as a potent barrier and emphasize the removal of these barriers as a promising approach to achieving higher cloning efficiency.
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Project description:Pluripotent stem cells provide a platform to interrogate control elements that function to generate all cell types of the body. Despite their utility for modeling development and disease, the relationship of mouse and human pluripotent stem cell states to one another remains largely undefined. We have shown that mouse embryonic stem (ES) cells and epiblast stem cells (EpiSCs) are distinct, pluripotent states isolated from pre- and post-implantation embryos respectively. Human ES cells are different than mouse ES cells and share defining features with EpiSCs, yet are derived from pre-implantation human embryos. Here we show that EpiSCs can be routinely derived from pre-implantation mouse embryos. The pre-implantation-derived EpiSCs exhibit molecular features and functional properties consistent with bona fide EpiSCs. These results provide a simple method for isolating EpiSCs and offer direct insight into the intrinsic and extrinsic mechanisms that regulate the acquisition of distinct pluripotent states.
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